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Knowledge and best practice in this eld are constantly changing. As new research and experience broaden
our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate.
Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or formula, the method
and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on
their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of
the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or
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The Publisher

Previous editions copyrighted 2001, 1995, 1985.

Library of Congress Control Number: 2007928036

Vice President and Publisher: Linda Duncan

Senior Acquisitions Editor: Anthony Winkel
Developmental Editor: Shelly Stringer
Publishing Services Manager: Pat Joiner-Myers
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Design Direction: Karen OKeefe Owens

Printed in Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

To my wife, Jeri, my son, Kyle, mother, Dorothy
In honor of that secret correspondence and love within our hearts

Larry P. Tilley

To the ever-popular Ben Smith and his charming sister Jade,

thanks for keeping life fun. You are the best! To my wife May,
who warms my heart every day, thanks for always being there.

Francis W. K. Smith, Jr.

To my parents, who made this all possible.

To Emi, K.A., Miya, and Audrey, who keep the kid in me alive.

Mark A. Oyama

To Dave, whose support enables my dreams; and my father, who inspired them.

Meg M. Sleeper

Jonathan A. Abbott, DVM, DACVIM Kathleen E. Cavanagh, BSc, DVM

(Cardiology) Haskell Valley Veterinary Hospital
Associate Professor Orleans, New York;
Department of Small Animal Clinical Sciences Niagara Veterinary Emergency Clinic
Virginia-Maryland Regional College of Veterinary St. Catharines, Ontario, Canada
Medicine Appendix 1: Canine Breed Predilections for Heart
Virginia Polytechnic Institute and State University Disease
Blacksburg, Virginia
Acquired Valvular Disease Steven G. Cole, DVM, DACVECC, DACVIM
Janice McIntosh Bright, BSN, MS, DVM, Section of Critical Care
DACVIM (Cardiology and Internal Department of Clinical Studies Philadelphia
School of Veterinary Medicine
University of Pennsylvania
Professor of Cardiology Philadelphia, Pennsylvania
Department of Clinical Sciences
Cardiopulmonary Resuscitation
College of Veterinary Medicine and
Emergency Management and Critical Care
Biomedical Sciences
Colorado State University
Fort Collins, Colorado Thomas K. Day, DVM, MS, DACVA,
Pacemaker Therapy DACVECC
Owner, Emergency and Critical Care Veterinarian,
Scott A. Brown, VMD, PhD, DACVIM Anesthesiologist
Louisville Veterinary Specialty and Emergency Services
(Internal Medicine)
Louisville, Kentucky
Josiah Meigs Distinguished Professor
Anesthesia of the Cardiac Patient
Associate Dean for Academic Affairs
Department of Physiology and Pharmacology
University of Georgia Kenneth J. Drobatz, DVM, MSCE, DACVIM
College of Veterinary Medicine (Internal Medicine), DACVECC
Athens, Georgia Professor, Section of Critical Care
Systemic Hypertension Department of Clinical Studies Philadelphia
School of Veterinary Medicine
Clay A. Calvert, DVM, DACVIM University of Pennsylvania;
Director, Emergency Service
(Internal Medicine)
Ryan Veterinary Hospital of the University of
Small Animal Medicine and Surgery
Philadelphia, Pennsylvania
College of Veterinary Medicine
Cardiopulmonary Resuscitation
The University of Georgia
Athens, Georgia Emergency Management and Critical Care
Heartworm Disease

viii Contributors

Virginia Luis Fuentes, MA, VETMB, PhD, Marc S. Kraus, DVM, DACVIM
CertVR, DVC, DACVIM (Cardiology), (Cardiology and Internal Medicine)
DECVIM-CA (Cardiology), MRCVS Lecturer
Senior Lecturer in Small Animal Medicine Department of Clinical Sciences
Veterinary Clinical Sciences College of Veterinary Medicine
Royal Veterinary College Cornell University
Hatfield, United Kingdom Ithaca, New York
Echocardiography and Doppler Ultrasound Treatment of Cardiac Arrhythmias and Conduction
Anna R. M. Gelzer, Dr.med.vet., DACVIM
(Cardiology) Elizabeth A. McNiel, DVM, PhD,
Assistant Professor DACVIM (Oncology), ACVR
Department of Clinical Sciences (Radiation Oncology)
College of Veterinary Medicine Assistant Professor
Cornell University Department of Veterinary Clinical Sciences
Ithaca, New York College of Veterinary Medicine
Treatment of Cardiac Arrhythmias and Conduction University of Minnesota
Disturbances St. Paul, Minnesota
Pericardial Disorders and Cardiac Tumors
Rebecca E. Gompf, DVM, MS, DACVIM
(Cardiology) Sydney Moise, DVM, MS, DACVIM
Associate Professor of Cardiology (Cardiology and Internal Medicine)
Department of Small Animal Clinical Sciences Professor of Medicine, Section Chief Cardiology
University of Tennessee Department of Clinical Sciences
College of Veterinary Medicine College of Veterinary Medicine
Knoxville, Tennessee Cornell University
The History and Physical Examination Ithaca, New York
Treatment of Cardiac Arrhythmias and Conduction
Rosemary A. Henik, DVM, MS, DACVIM Disturbances
(Internal Medicine)
Clinical Associate Professor E. Christopher Orton, DVM, PhD, DACVS
Department of Medical Sciences Professor
University of Wisconsin Madison Department of Clinical Sciences
Madison, Wisconsin Veterinary Medical Center
Systemic Hypertension Colorado State University
Fort Collins, Colorado
Lynelle R. Johnson, DVM, PhD, DACVIM Cardiac Surgery
(Internal Medicine)
Assistant Professor Mark A. Oyama, DVM, DACVIM
Department of Veterinary Medicine and Epidemiology (Cardiology)
College of Veterinary Medicine Associate Professor
University of CaliforniaDavis Department of Clinical Studies
Davis, California School of Veterinary Medicine
Cor Pulmonale and Pulmonary Thromboembolism University of Pennsylvania
Philadelphia, Pennsylvania
Richard D. Kienle, DVM, DACVIM Canine Cardiomyopathy
(Cardiology) Appendix 2: Common Cardiovascular Drugs
Staff Cardiologist
Bay Area Veterinary Specialists Brian A. Poteet, MS, DVM, DACVR, ABSVM
San Leandro, California; Director,
Owner Gulf Coast Veterinary Diagnostic Imaging
Mission Valley Veterinary Cardiology Gulf Coast Veterinary Specialists
Gilroy, California Houston, Texas
Feline Cardiomyopathy Radiology of the Heart
Contributors ix

Carl D. Sammarco, BVSc, DACVIM Keith N. Strickland, DVM, DACVIM

(Cardiology) (Cardiology)
Senior Cardiologist Clinical Associate Professor of Veterinary Cardiology
Department of Cardiology Department of Veterinary Clinical Sciences
Red Bank Veterinary Hospital School of Veterinary Medicine
Tinton Falls, New Jersey Louisiana State University
Cardiovascular Effects of Systemic Diseases Baton Rouge, Louisiana
Congenital Heart Disease
Donald P. Schrope, DVM, DACVIM Pathophysiology and Therapy of Heart Failure
Oradell Animal Hospital Justin David Thomason, DVM, DACVIM
Department of Cardiology (Internal Medicine)
Paramus, New Jersey Assistant Professor
Cardiovascular Effects of Systemic Diseases Department of Veterinary Clinical Science
Center for Veterinary Health Sciences
Meg M. Sleeper, VMD, DACVIM Oklahoma State University
(Cardiology) Stillwater, Oklahoma
Assistant Professor and Section Chief, Cardiology Heartworm Disease
Department of Clinical Studies
School of Veterinary Medicine Larry P. Tilley, DVM, DAVCIM
University of Pennsylvania (Internal Medicine)
Philadelphia, Pennsylvania President, VetMed Consultants, Inc.
Special Diagnostic Techniques for Evaluation of Consultant, New Mexico
Cardiac Disease Veterinary Specialty Referral Center
Appendix 2: Common Cardiovascular Drugs Santa Fe, New Mexico
Francis W. K. Smith, Jr., DVM, DACVIM Appendix 2: Common Cardiovascular Drugs
(Internal Medicine and Cardiology)
Vice President Anthony H. Tobias, BVSc, PhD, DACVIM
VetMed Consultants, Inc. (Cardiology)
Lexington, Massachusetts; Associate Professor
Clinical Assistant Professor Department of Clinical Sciences
Department of Medicine College of Veterinary Medicine
Cummings School of Veterinary Medicine University of Minnesota
Tufts University St. Paul, Minnesota
North Grafton, Massachusetts Pericardial Disorders and Cardiac Tumors
Cardiovascular Effects of Systemic Diseases
Appendix 1: Canine Breed Predilections for Heart
Appendix 2: Common Cardiovascular Drugs

In the last 5 years there have been a number of field of canine and feline cardiology. The fourth edi-
excellent textbook chapters and journal articles tion has been carefully revised, edited, and updated
describing new findings in the field of canine and to reflect the latest technologies and approaches to
feline cardiology. However, for the practicing vet- cardiac care.
erinarian and veterinary student, the amount of The methods of diagnosis of heart diseases in the
information is overwhelming. Many veterinarians dog and the cat are described in Section I The first
and students have stated, in past surveys, the diffi- five chapters follow the sequence that the veterinar-
culty in keeping up with cardiovascular advances in ian uses in approaching the patient. Chapter 1 cov-
the most time-effective way. The Manual of Canine ers the history and physical examination; Chapter
and Feline Cardiology, now in its fourth edition, has 2, radiology of the heart; Chapter 3, electrocardi-
been updated to continue to meet the need for a cur- ography; Chapter 4, echocardiography and Doppler
rent textbook that can provide useful and practical ultrasound; and Chapter 5, special diagnostic tech-
information on cardiac disease in the dog and cat. niques for evaluation of cardiac disease.
We have worked hard to make this book a most reli- Section II presents in a step-by-step fashion a
able source for practicing cardiovascular medicine description of the various cardiac disorders that oc-
in the dog and cat. For the new edition, we have cur in the dog and cat, starting in each chapter with
expanded the number of contributors, with each general considerations (e.g., definitions, incidence,
chapter written by an expert. We have also worked pathophysiology, etiology), history, physical exam-
to conserve reading time by using an easy-to-use ination, electrocardiography, thoracic radiography,
format. The Manual of Canine and Feline Cardiol- special diagnostic techniques, differential diagno-
ogy, Fourth Edition, is unique as a quick reference sis, and finally, the therapeutic approach.
with consistency of presentation. The new edition Section III includes chapters describing the
now also has generous use of figures and charts, treatment of cardiac failure, treatment of arrhyth-
with many in color. mias and conduction disturbances, and two sepa-
This practical approach to the diagnosis and rate chapters on cardiopulmonary arrest and resus-
therapy of cardiac disease will be useful to a wide citation and on emergency management and critical
audience, from the veterinary student to the fully care in cardiology. Chapters on anesthesia of the
trained cardiologist. The approach is largely clini- cardiac patient, cardiac surgery, and pacemaker
cal and includes the practical as well as the most therapy complete this section.
sophisticated methods for diagnosis and therapy. Appendix 1, Canine Breed Predilections for
Cardiovascular disorders in the dog and cat Heart Disease, represents the most current listing
represent a substantial portion of diseases seen of breed-associated cardiac disorders.
in the average veterinary practice. It is important Appendix 2 is a cardiopulmonary drug formu-
for veterinary students and practitioners to under- lary that contains extensive cardiopulmonary drug
stand the principles of diagnosis and treatment of tables with indications, dosages, side effects, con-
the numerous cardiovascular disorders. New chap- traindications, and drug interactions. An extraordi-
ters that have been added include cardiac surgery, nary array of new cardiovascular drugs has become
cor pulmonale, pulmonary thromboembolism, and available, and both students and veterinarians have
pacemaker therapy. A table of canine breed pre- difficulty deciding which drugs from various drug
dilections for heart disease has been added to the classes should be prescribed.
appendixes. Appendix 3, Echocardiographic Normals, is
Since the third edition of this textbook was pub- an easy-to-refer-to list of normal values by body
lished, there has been tremendous growth in the weight and breed.
xii Preface

The Manual of Canine and Feline Cardiology, as a reference for the advanced student and the vet-
Fourth Edition, will help to eliminate the aura of erinarian with expertise in cardiology.
mystery that surrounds the diagnostic and thera-
peutic principles of veterinary cardiology. The Larry P. Tilley
teaching principles that are presented will allow Francis W. K. Smith, JR.
even the novice to make an intelligent assessment Mark A. Oyama
of a cardiac case. This manual will be useful to a Meg M. Sleeper
wide audience, but comprehensive enough to serve

The completion of this manual provides a welcome much you know until they know how much you
opportunity to recognize in writing the many indi- care. That saying was Johns philosophy and one
viduals who have helped along the way. All authors that all of us should follow.
have board certification and are uniquely qualified Finally, a special thank you goes to Tony Winkel,
to give an update or review of their respective dis- Editor, Elsevier, whose vision and support were
ciplines. critical for this fourth edition. The unique format
In addition to thanking veterinarians who have and use of numerous images demonstrates the edu-
referred cases to us, we would like to express our cational vision he had. For this edition, we would
gratitude to each of the veterinary students, interns, also like to thank Shelly Stringer, Developmental
and residents whom we have had the pleasure of Editor and the rest of the Elsevier staff, including
teaching. Their curiosity and intellectual stimula- everyone in the Production Department. They are
tion have enabled us to grow and prompted us to all meticulous workers and kind people who made
undertake the task of writing this manual. the final stages of preparing this book both inspir-
The last edition was co-edited by John Karl ing and fun.
Goodwin, and since then he has unfortunately
passed away. Johns teaching principles in vet- Larry P. Tilley
erinary medicine were clearly drawn from clinical Francis W. K. Smith, JR.
experience, and this edition continues to maintain Mark A. Oyama
that focus. I will always remember what John had Meg M. Sleeper
posted on a wall at his office: No one cares how


Diagnosis of Heart Disease

1. The History and Physical Examination 4. Echocardiography and Doppler

Rebecca E. Gompf Ultrasound
Virginia Luis Fuentes
2. Radiology of the Heart
Brian A. Poteet 5. Special Diagnostic Techniques for
Evaluation of Cardiac Disease
3. Electrocardiography
Meg M. Sleeper
Larry P. Tilley and Francis W. K. Smith, Jr.
Chapter 1

The History and Physical

Rebecca E. Gompf

Medical History
Despite the technical nature of many cardiovascu-
lar diagnostics, such as electrocardiography and
echocardiography, the history and physical exami- Age
nation remain the most crucial steps in establish- Young animals usually present with congenital
ing the correct diagnosis. Findings from a careful diseases (e.g., patent ductus arteriosus [PDA]),
history and physical examination prompt the clini- whereas older animals usually present with ac-
cian to the probability or presence of heart disease. quired diseases, such as degenerative diseases
Results of the cardiovascular physical examination (e.g., mitral and tricuspid regurgitations) or neo-
will usually allow the clinician to make a tentative plastic diseases (e.g., heart base tumor). Excep-
diagnosis or formulate a specific differential diag- tions can occur because cardiomyopathies can
nosis. The history and physical examination also occur in young dogs and cats (aged 6 months
provide important information regarding the stage oryounger), and older dogs can have congeni-
of heart disease present, which may significantly tal heart defects that were not diagnosed when
impact therapy. theywere young (e.g., PDA, atrial septal de-
A good history and physical exam are invalu- fect). Also, cardiac disease in older animals can
able in making a diagnosis of heart disease and be modified or affected by other concurrent dis-
helping to differentiate heart disease from pul- ease processes (e.g., collapsing trachea, renal or
monary disease. liverdisease).
Besides helping to make the diagnosis, a good
history and physical exam help to tell the extent Breed
of the problem, how well the animal is respond- Certain cardiac defects are more common in some
ing to previous therapy, if the owner is able to breeds of animals; however there can be a regional
medicate the animal consistently, and if other difference in the rate of occurrence of cardiac prob-
medical problems are present. lems. See Appendix for a summary of some of the
cardiac defects found in certain breeds of dogs and
Key Point
Clinicians should do a thorough history and Sex
physical exam in order to properly diagnose Males are more susceptible to certain cardiac dis-
and treat an animal with heart disease. eases (e.g., male cocker spaniels to endocardiosis
of the mitral valve, and large-breed males to dilated

Chapter 1 The History and Physical Examination 

cardiomyopathy). However, sick sinus syndrome It will also define the animals attitude and be-
occurs in the female miniature schnauzer and PDA havior by asking if the animal is listless and
is more common in females than in males. depressed or alert and playful. Does the animal
tire easily with exercise?
Weight It covers the family history of the siblings and
The animals weight influences several aspects of parents, especially if congenital disease is present
treatment including the dose of cardiac medication in the patient.
to use, evaluation of the response to diuretic medi- It will ask about the health of other pets in the
cation, and the monitoring of cardiac cachexia. A household.
Pickwickian syndrome (characterized by severe It includes the results of previous tests done on
obesity, somnolence, and hypoventilation) can oc- the patient.
cur in an animal that is so obese that its ability to It covers other relevant information that may help
breathe is restricted. to identify the patients problem(s), such as what
and how much is being fed and the patients ap-
Utilization of the Animal petite and water consumption. How frequently is
It is important to know how an animal is going to the animal urinating, and does it have any diar-
be used when giving a long term prognosis for a rhea? Does the patient have any vomiting or re-
cardiac disease. For example, hunting dogs with gurgitation? Has the patient had any seizures or
severe heartworm disease may not be able to hunt syncopal episodes? What is the patients repro-
again after treatment. Also, some animals with con- ductive status? Does the patient have any lame-
genital heart defects may have normal life spans ness or paresis? Is the patient coughing, sneezing,
and may make good pets; however, they should not or having difficulty breathing? Has the patient
be used for breeding purposes, because the defect had any previous trauma? Where is the animal
could be perpetuated. housed (e.g., indoors, outdoors, fenced-in yard)?
It includes information about other diseases such
as hyperthyroidism, chronic renal disease, respi-
ratory diseases, or other diseases that can also af-
Key Point fect the heart or can affect how the animals heart
The age, breed, and sex of the animal may disease is treated.
help the clinician to make an accurate diag- Once a problem is identified, more specific ques-
nosis; however, there are always exceptions tions can be asked such as the character of a
to every rule, so a clinician should not ignore cough, when the cough occurs, and stimuli evok-
the fact that an animal could have an atypical ing the cough.
problem for its age, breed, or sex. Common presenting complaints for cardiac dis-
ease include dyspnea or tachypnea, coughing,
exercise intolerance, syncope, abdominal swell-
ing, cyanosis, anorexia or decreased appetite, and
poor growth or performance.
A good history will establish the presence of a Other symptoms can be associated with cardio-
cardiac problem, help to differentiate between vascular disease. Polydipsia and polyuria are
cardiac and respiratory problems, and help to common in animals on diuretics or that have a
monitor the course of the disease and the re- concurrent disease (e.g., renal disease), whereas
sponse to therapy. It must be done carefully oliguria occurs with severe left-heart failure. He-
to prevent an owner from giving a misleading moglobinuria is found with the postcaval syn-
history. drome of heartworm disease.
It includes several key questions such as the rea- Cardiac drugs such as digitalis, quinidine, and
son the animal is being presented, the problems procainamide can cause vomiting and diarrhea.
noted by the owner, the onset and duration of the Regurgitation occurs with congenital vascular
problem(s), the progression of the disease, any ring anomalies. Right-heart failure can cause in-
known exposure to infectious diseases, vaccina- testinal edema and a protein-losing enteropathy
tion history, any current medications the animal resulting in diarrhea. Cats with cardiomyopathy
is receiving, the animals response to any medica- can develop hemorrhagic enteritis secondary to
tions that have been given, and the owners ability thromboembolism of the gastric or mesenteric
to give the medication(s). arteries.
 Section I Diagnosis of Heart Disease

Key Point Dogs with chronic heart disease usually have

mild, intermittent coughs. They may also have
A good history will uncover all of the animals nocturnal dyspnea, coughing, and restlessness.
symptoms and problems whether they are
Their coughs tend to be harsh and lower pitched.
due to a cardiac problem or to another con-
current problem. Also, by the end of a good Dogs with fulminant left-heart failure may have
history, an astute clinician will have a good pink foam in their mouth and nose and be dys-
idea as to the potential causes of the animals pneic, but they may or may not be coughing.
problems. Dogs with a loud, harsh, dry cough of sudden on-
set followed by a nonproductive gag commonly
have tracheobronchitis.
Specific Symptoms Dogs with a honking, high-pitched cough often have
a collapsing trachea and/or collapsed bronchi.
Small breeds of dogs with large airway disease will
Coughing is the most common complaint in dogs have a chronic, paroxysmal cough that is hard, loud,
with significant heart disease, but cats rarely cough and honking, and usually occurs with excitement.
even when they have an enlarged left atrium. Dogs that cough after drinking may have cardiac
Coughing is a sudden, forced expiration and is a disease, collapsing trachea, chronic tracheitis,
normal defense mechanism to clear debris from tracheobronchitis, laryngeal problems, or other
the tracheobronchial tree. It can originate from causes of dysphagia.
many different areas such as the pharynx, tra- Dog that cough without an inciting factor may have
chea, bronchi, bronchioli, pleura, pericardium, cardiac, pulmonary, or extrapulmonary disease.
and diaphragm. Dogs that cough after eating have pharyngeal
A cardiac cough can be difficult to differentiate dysphagia, megaesophagus, vascular ring anom-
from a respiratory cough. Table 1-1 lists some of the alies, esophageal diverticula, esophageal foreign
characteristic coughs and their associated causes. bodies, or esophageal tumors.
Dogs with pulmonary edema often have an acute It is unusual for cats to cough with congestive
onset of coughing that progresses rapidly to a severe heart failure; however, they will cough with
cough and dyspnea. These coughs are usually soft. heartworm disease. If the clinician compresses

Table 1-1 Characteristics of Coughs and Their Associated Causes in Dogs and Cats
Type of Cough Causes
Acute cough Tonsillitis, pharyngitis, tracheobronchitis, acutebronchitis,
pleuritis, acute left heart failure (dogs)
Chronic cough Right or left heart disease, heartworms, enlarged left
atrium compressing the left mainstem bronchus (dog
only), pulmonary neoplasia, asthma (cat only), chronic
respiratory problem, chronic bronchitis (dog only)
Acute onset, soft that rapidly becomes Pulmonary edema
worse in dogs with dyspnea
Mild, intermittent cough, harsh, low Chronic heart disease
pitched in dogs
Loud, harsh, dry, sudden onset followed Tracheobronchitis
by gag in dogs
Honking, high-pitched in dogs Collapsing trachea or bronchi
Chronic, paroxysmal, loud, honking Large airway disease
with excitement in dogs
Cough after drinking in dogs Cardiac disease, collapsing trachea, chronic tracheitis,
tracheobronchitis, laryngeal paralysis, dysphagia
Cough after eating in dogs Pharyngeal dysfunction, megaesophagus, vascular ring
anomalies, esophageal diverticula, esophageal foreign
bodies, esophageal tumors
Cough without an inciting factor Cardiac, pulmonary, or extrapulmonary disease
Chapter 1 The History and Physical Examination 

Key Point Box 1-1 Causes of Dyspnea

It is important to distinguish between a cough Acidosis
due to cardiac disease versus one due to re- Anemia
spiratory disease. The history can be the first Central nervous system disorders
step in differentiating between the two major Excitement
causes of coughing. High altitude
Pericardial effusions
the cats trachea and the cat has a prolonged bout Pleural effusions
of coughing, then coughing is likely to be part of Primary cardiac diseases causing pulmonary edema
the cats problem. or pleural effusion
Pulmonary edema
Secondary cardiac diseases
Dyspnea Strenuous exercise
Thoracic wall problems (e.g., fractured ribs)
Dyspnea is difficult, labored, or painful breathing.
It is usually preceded by tachypnea (an increased
rate of breathing), which owners may miss. It is a into heart failure. It can also be associated with
good idea to have the owner of a cardiac patient chronic, obstructive lung disease.
learn to count his or her pets respiratory rate at Expiratory dyspnea is prolonged and labored ex-
rest. The respiratory rate should be less than 30 piration and is due to lower respiratory tract ob-
per minute in a dog at rest, and if it goes over 50 struction or disease.
per minute, then the dog has tachypnea. Inspiratory dyspnea is prolonged and labored in-
Dyspnea will occur whenever anything increases the spiration and is due to upper airway obstruction.
amount of air that must be breathed by the animal. Mixed dyspnea is due to severe pulmonary edema
Box 1-1 lists the problems that can cause dyspnea. caused by left-heart failure or severe pneumonia.
The most common cardiac cause of dyspnea in Orthopnea means that the dyspnea occurs when
the dog is left-heart failure causing pulmonary the animal lies down but not when it is standing.
edema. The most common cardiac cause of It is associated with severe pulmonary edema,
dyspnea in the cat is right-heart failure causing pleural effusion, pericardial effusion, pneumo-
pleural effusion or left-heart failure causing pul- thorax, diaphragmatic hernia, and severe respira-
monary edema. tory problems.
Dyspnea can be accompanied in cardiac patients by Paroxysmal dyspnea means that the dyspnea
stridor, which is a harsh, high-pitched respiratory comes and goes. It can be associated with ar-
sound. Other sounds include rhonchi, which sound rhythmias that cause either bradycardia or
like dry, coarse crackles. Also, dyspnea can be ac- tachycardia.
companied by wheezing, which is more typical of Simple dyspnea, or polypnea, is an increased
respiratory problems than cardiac problems. rate of respiration due to fever, fear, pain, or
Table 1-2 lists the different types of dyspnea and excitement.
the problems associated with each type. Cats with severe hyperthyroidism can also be
Acute dyspnea is usually caused by pulmonary dyspneic.
edema (cardiac and noncardiac), severe pneu Dyspnea that improves when treated with diuret-
monia, airway obstruction, pneumothorax, or ics and angiotensin-converting enzyme inhibitors
pulmonary embolism.
Chronic, progressive dyspnea is caused by right-
heart failure with ascites and/or pleural effusion,
Key Point
pericardial diseases, bronchial disease, lung
diseases such as emphysema, pleural effusions, Dyspnea is a sign of significant cardiac, respi-
progressive anemia, and primary or secondary ratory, or other systemic problems. It requires
pulmonary neoplasia. immediate diagnostic tests to identify the
cause of the dyspnea so that specific therapy
Dyspnea at rest occurs with pneumothorax, pulmo-
can be started. However, all tests should be
nary embolism, and severe left- or right-heart failure. done with minimal stress to the animal as
Exertional dyspnea occurs after or during activity these patients are very fragile and could die
and can be associated with heart diseases, such with stress.
as dilated cardiomyopathy, when the animal goes
 Section I Diagnosis of Heart Disease

Table 1-2 Types of Dyspnea and Their Associated Diseases or Problems

Type of Dyspnea Disease or Problem
Acute dyspnea Pulmonary edema (cardiogenic and noncardiogenic), severe pneumonia, airway
obstruction, pneumothorax, pulmonary embolism
Chronic, progressive Right heart failure with ascites and/or pleural effusion, pericardial diseases, bronchial
dyspnea disease, lung diseases (e.g., emphysema), pleural effusions, progressive anemia,
primary and secondary neoplasia
Dyspnea at rest Pneumothorax, pulmonary embolism, severe left or right heart failure
Exertional dyspnea Heart disease (e.g., dilated cardiomyopathy) or chronic obstructive lung disease
Expiratory dyspnea Lower respiratory tract obstruction or disease
Inspiratory dyspnea Upper airway obstruction
Mixed dyspnea Pulmonary edema due to left heart failure or severe pneumonia
Orthopnea Severe pulmonary edema, pericardial effusion, pleural effusion, diaphragmatic hernia,
pneumothorax, severe pulmonary disease
Paroxysmal dyspnea Arrhythmias (e.g., bradycardia or tachycardia)
Simple dyspnea Fever, fear, pain, or excitement

plus or minus digoxin is suggestive of left-heart

Box 1-2 Causes of Hemoptysis
failure as the cause of the dyspnea.
Dyspnea that improves when treated with bron- Acute and chronic bronchitis
chodilators, antibiotics, or steroids is sugges- Chronic pulmonary granulomas
tive of respiratory disease as the cause of the Clotting disorders
dyspnea. Disseminated intravascular coagulopathy
Lung abscesses
Lung lobe torsions
Hemoptysis Oral or other neoplasia
Pulmonary embolism
Hemoptysis is coughing up of blood. It is uncom- Pulmonary fungal infections
mon in animals, as they usually swallow their Pulmonary neoplasia
sputum. It is a sign of very severe pulmonary Respiratory foreign bodies
disease. Severe heartworm disease with pulmonary embo-
The causes of hemoptysis are listed in Box 1-2.
Severe pneumonia
Cardiac causes of hemoptysis include severe pul- Severe pulmonary edema (e.g., from ruptured chor-
monary edema (e.g., ruptured chordae tendineae) dae tendineae)
and severe heartworm disease, usually with pul- Trauma with severe pulmonary contusions
monary embolism.

Key Point
back up quickly, and are normal before and after
Hemoptysis is a sign of a very serious underly-
ing abnormality in the lungs, which may be the syncopal episode.
caused by either a severe cardiac or respira- Box 1-3 lists the causes of syncope in dogs and
tory problem. cats.
In a dog with no other cardiac problems, syncope
may be associated with severe bradycardias (e.g.,
third degree heart block or sick sinus syndrome),
or with marked sustained tachycardias (e.g., atrial
Syncope is a loss of consciousness due to inad- or ventricular tachycardias), which are usually
equate cerebral blood flow. It can reoccur and is paroxysmal (i.e., they come and go).
usually brief. Small dogs with chronic, severe mitral regurgita-
Syncope can be hard to differentiate from sei- tion that cough when they get excited can have
zures. Animals usually fall over suddenly, get syncopal episodes.
Chapter 1 The History and Physical Examination 

Box 1-3 Causes of Syncope in Dogs and Box 1-4 Causes of Weakness and
Cats Exercise Intolerance

Disease with very poor cardiac output (e.g., dilated Cardiac disease with myocardial dysfunction (e.g.,
cardiomyopathy) dilated cardiomyopathy)
Severe bradycardia (e.g., complete heart block, sick Cardiac disease with obstruction to left ventricular
sinus syndrome) outflow (e.g., subaortic stenosis, hypertrophic
Severe sustained tachycardias (e.g., atrial or ventri obstructive cardiomyopathy)
cular tachycardia) Decreased arterial oxygen (e.g., pulmonary edema,
Severe hypertrophic cardiomyopathy in cats pleural effusion or other pulmonary diseases)
Systemic hypotension including arteriolar dilator Inadequate ventricular filling (e.g., arrhythmias, peri-
therapy cardial diseases)
Severe pulmonary hypertension Drug toxicities
Severe subaortic stenosis Severe anemia
Severe pulmonic stenosis Severe metabolic disease
Small dogs with severe mitral regurgitation that Severe respiratory diseases
cough when excited Severe systemic diseases
Tetralogy of Fallot

that their animal is slowing down due to old age

Dogs with severe subaortic stenosis, pulmonic and not due to heart disease or other problems.
stenosis, pulmonary hypertension, or tetralogy of Both complaints can be an early sign of decom-
Fallot can have arrhythmias associated with their pensated heart failure, as the heart cannot pump
ventricular hypertrophy and myocardial hypoxia. enough blood to the muscles due to:
Syncope can also occur in cats with severe hyper- Myocardial dysfunction (e.g., dilated cardio-
trophic cardiomyopathy. myopathy or advanced mitral valve disease)
Animals with poor cardiac output due to di- Obstruction to left ventricular outflow (e.g.,
lated cardiomyopathy can have syncope, espe- subaortic stenosis or hypertrophic obstructive
cially if they also have arrhythmias such as atrial cardiomyopathy)
fibrillation or ventricular premature beats that Inadequate ventricular filling (e.g., arrhyth-
further reduce their cardiac output. mias, pericardial diseases, hypertrophic
Vasodilators, especially arterial dilators, can result cardiomyopathy)
in systemic hypotension, which can cause syncope. Decreased arterial oxygen (e.g., pulmonary
edema or pleural effusion).
Key Point
Syncope must be distinguished from seizures
by careful history and physical examination. Key Point
Having the owner videotape an episode can It is important to distinguish between exer-
also help the clinician to distinguish between cise intolerance due to heart disease versus
the two. Further tests such as Holter or event other causes.
monitoring may be necessary to determine if
an arrhythmia is causing the syncope.

Weakness and Exercise Intolerance
Ascites is an accumulation of fluid in the
Weakness and exercise intolerance are nonspe- abdomen.
cific signs of heart disease. Many diseases such Ascites caused by cardiac problems is either
as severe anemia, systemic diseases, metabolic due to the right heart being unable to pump the
diseases (e.g., hyperadrenocorticism), drug tox- blood presented to it or because of pericardial
icities, and severe respiratory diseases can cause disease, in which the blood cannot get into the
these signs. See Box 1-4 for causes of weakness right heart. In either case the blood accumulates
and exercise intolerance. in the liver and spleen and causes congestion
Because most animals do not exercise very hard, and increased venous pressure. Eventually fluid
weakness and exercise intolerance are uncom- leaks out of the capsule of the liver causing the
mon presenting complaints. Some owners think ascites.
 Section I Diagnosis of Heart Disease

Ascites is seen more frequently with right-heart Box 1-5 Causes of Ascites in the Dog
failure in dogs due to acquired diseases (e.g.,
tricuspid regurgitation due to endocardiosis, ad- Advanced heartworm disease
vanced heartworm disease, dilated cardiomyopa- Dilated cardiomyopathy
thy, pericardial effusions, restrictive pericarditis) Large atrial septal defect
Large ventricular septal defect
and congenital heart defects (e.g., tricuspid dys- Pericardial effusion
plasia, large ventricular septal defect, large atrial Restrictive pericarditis
septal defect). See Figure 1-1 for an example of Tricuspid dysplasia
ascites and Box 1-5 for a list of causes of ascites Tricuspid regurgitation due to endocardiosis
in the dog.
Ascites is less common in cats and is usually
due to tricuspid dysplasia but occasionally can
be seen with other problems such as dilated Cyanosis is a very insensitive way of detecting
cardiomyopathy. hypoxemia in dogs and cats because the oxy-
Large amounts of ascites will put pressure on the gen saturation has to be very low to cause it and
diaphragm, resulting in tachypnea or dyspnea. animals have darker mucous membranes, which
Ascites associated with right-heart failure is makes cyanosis harder to detect until it is severe.
usually a modified transudate and accumulates Right-to-left shunting cardiac defects such as
slowly. tetralogy of Fallot result in low oxygen satura-
tion plus high deoxygenated hemoglobin levels,
Key Point which make affected animals cyanotic. These pa-
Decompensated heart diseases that result in tients also have polycythemia, and the increased
ascites may not have an associated murmur number of red blood cells has increased amounts
(e.g., pericardial effusion, some dilated cardio- of reduced hemoglobin, which contributes to the
myopathies, heartworm disease). Thus, any cyanosis.
time ascites occurs, right-heart failure must be Cyanosis gets worse with exercise because the
included in the differential diagnosis. peripheral vascular resistance will decrease while
the pulmonary vascular pressure is unchanged
so more deoxygenated venous blood will go
Cyanosis is blue-tinged mucous membranes
of the gums, tongue, eyes, ears, and so on and Key Point
is associated most commonly with right-to-left
shunting congenital heart defects. Occasionally it Cyanosis is a very late finding in severe car-
diac disease, except in right to left shunting
is seen with severe left-heart failure or severe re-
congenital heart defects, and so it is an in-
spiratory disease. It is rarely seen with abnormal sensitive indicator of membrane oxygenation
hemoglobin production. and cardiac function.

Weight Loss
Weight loss occurs in dogs with chronic, severe
right-heart failure (e.g., severe tricuspid regurgi-
tation, dilated cardiomyopathy, advanced heart-
worm disease).
Weight loss in cats is usually associated with
hyperthyroidism or infiltrative bowel disease, al-
though cats with chronic right-heart failure can
also lose weight.
Cardiac cachexia is the loss of total body fat and
lean body mass, especially skeletal muscle, de-
spite a normal appetite and adequate therapy for
Figure 1-1. Notice the severe ascites in this dog with right-
heart failure due to severe pulmonic stenosis and severe tri- the underlying heart disease. It can be a rapid
cuspid dysplasia. loss of body condition in some dogs with dilated
Chapter 1 The History and Physical Examination 

cardiomyopathy (Figure 1-2). See Box 1-6 for a Box 1-6 Problems Contributing to Cardiac
list of the problems that contribute to cardiac ca- Cachexia in the Dog
chexia in dogs.
Weight loss is associated with: Ascites
Ascites. Dogs with ascites may have mild discom- Cardiac medications causing anorexia and vomiting
fort from the fluid which makes them reluctant Electrolyte imbalance causing anorexia
to eat. Also, the ascites and congested liver will Increased energy use by the body
compress the stomach so that the animal feels Increased tumor necrosis factor
full after eating only a small amount of food. The
fluid also restricts gastric emptying. Finally, if an Protein losing enteropathy
unpalatable diet is fed, the animal is even more
reluctant to eat and does not consume enough
calories to keep from losing weight.
Malabsorption caused by the congestion of the
intestines secondary to the ascites.
Congestion of the pancreas, which may decrease
its function of secreting enzymes for digestion,
resulting in maldigestion.
Systemic venous and lymphatic hypertension
from right-heart failure causing a secondary in-
testinal lymphangiectasia that results in a pro-
tein-losing enteropathy.
Increased effort to breath and increased myocar-
dial oxygen consumption that result from the de-
creased cardiac output. These two problems result
in an increased use of energy and therefore calories
by the heart and lungs. The activation of the sym-
pathetic nervous system, which also results from
the decreased cardiac output, causes increased en-
ergy use by the rest of the body.
Use of cardiac medications such as digoxin, mex-
iletine, quinidine, procainamide, diltiazem, and
occasionally other drugs that can cause anorexia
and/or vomiting. Digoxin also has a direct effect
on the small bowel, where it inhibits sugar and
amino acid transport.
Electrolytes, especially sodium and potassium,
are adversely affected by diuretics, angiotensin
converting enzyme inhibitors, and digoxin. When

Key Point
Weight loss and cardiac cachexia are due to
multiple factors. It is very important to make
sure that an animal with ascites is being treat-
ed appropriately for heart failure and that the
animals digoxin levels, electrolytes, and renal
function are being monitored. It is also impor-
tant to calculate the animals caloric require-
ment and make sure it is eating enough to
meet its requirements. Special high caloric di-
ets and multiple small meals may be needed to
insure adequate caloric intake. Appetite stimu-
Figure 1-2. Great Dane with cardiac cachexia secondary to lants have been tried with varying success.
dilated cardiomyopathy.
10 Section I Diagnosis of Heart Disease

potassium levels are abnormal, they contribute to dilated left atrium or left ventricle, and pieces
anorexia. break off and lodge in the distal aorta or other
Dogs with chronic congestive heart failure have artery. When the thrombus lodges in the aortic
increased tumor necrosis factor that inhibits the bifurcation, the cat will exhibit severe pain in
activity of lipoprotein lipase (hydrolyzes chylo- the first few hours after the embolism and the
microns) and therefore interferes with the con- distal limbs will be cold and may be slightly
version of triglycerides to free fatty acids. swollen. The pads on the rear feet will be cya-
notic (Figure 1-5). The cats pulses cannot be
detected, and the nails on the affected legs do
not bleed when cut short.
Cats with acute, posterior paresis (Figure 1-3) Acute, posterior paresis is rare in dogs but it has
or paresis of one front leg (Figure 1-4) often been associated with emboli from severe, vegeta-
have thromboembolism secondary to cardio- tive endocarditis of the aortic or mitral valve.
myopathy. The thrombi tend to form in the Shifting leg lameness in dogs has also been as-
sociated with bacterial endocarditis.

Key Point
Paresis in the rear limbs of the cat is usually
due to emboli that form in the left atrium sec-
ondary to left atrial enlargement secondary
to cardiomyopathies. Shifting leg lameness
or posterior paresis in the dog can be due to
emboli from vegetations on either the mitral
or aortic valve.

Figure 1-3. Cat with a saddle thrombus secondary to a left Physical Examination
atrial thrombus due to hypertrophic cardiomyopathy.
The animals attitude and behavior can give clues
as to the severity and kind of problems that the
animal is having. It is important to note whether
the animal is depressed or alert, and listless or

Figure 1-5. Comparison of the front and rear leg footpads

in a cat with a saddle thrombus. Note the purple color of the
rear leg due to the complete occlusion of blood flow to the
Figure 1-4. Cat with a front leg thrombus secondary to a rear limbs secondary to the saddle thrombus and constriction
left atrial thrombus due to hypertrophic cardiomyopathy. of the collateral circulation.
Chapter 1 The History and Physical Examination 11

An animal that refuses to lie down may have Hypertension in cats will cause decreased pu-
severe pulmonary edema, pleural effusion, peri- pillary responses due to retinal detachment or
cardial effusion, pneumothorax, diaphragmatic hemorrhage. Also, a fundic exam may reveal pap-
hernia, or respiratory disease (Box 1-7). illedema (swelling of the optic disc) along with
An animal that stands with elbows abducted and hemorrhage or retinal detachment.
head extended as well as open-mouth breathing Retinal hemorrhages also can occur with polycy-
with flared nostrils has severe respiratory distress themia and bacterial endocarditis.
and needs immediate therapy. Central retinal degeneration occurs in about one
The rate and rhythm of respirations can help de- third of cats with dilated cardiomyopathy caused
termine the underlying problem. Tachypnea and by taurine deficiency. The areas of degeneration
panting are usually due to excitement; however, are horizontal, linear, and hyperreflective.
expiratory dyspnea usually indicates lower air- The ears have no significant changes associated
way disease, and inspiratory dyspnea usually in- with the cardiovascular system.
dicates upper airway disease. Cyanosis can sometimes be recognized by evalu-
The nature and type of coughing is helpful if it ating the color of the pinna.
occurs during the course of the physical exam. Examine the nose for signs of disease and for
The presence of dependent ventral edema can patency.
give the clinician an idea as to the source of In the mouth, mucous membrane color and perfu-
theanimals problem. If edema is present in sion should be noted. A perfusion time of greater
the neck, head, and forelimbs only, then it usu- than 2 seconds suggests decreased cardiac out-
ally indicates an obstruction of the cranial vena put; however, most animals with congestive heart
cava or a mediastinal mass. If edema is present failure have normal mucous membrane color un-
in the entire body, then pleural effusion with or til their heart failure is severe. So, mucous mem-
without ascites is usually present. Other causes brane color and perfusion are very insensitive
of edema (e.g., hypoproteinemia) should also be ways to evaluate adequate circulation.
considered. Cyanosis is due to hypoventilation or poor dif-
Elevated temperature may be seen with an infec- fusion across the alveoli produced by multiple
tious disease or subacute bacterial endocarditis. different factors (see history section discussed
Hyperemic mucous membranes (dark red to
Key Point muddy) may indicate an increased packed cell
By observing an animal, the presence and se-
volume (polycythemia), which can be second-
verity of a respiratory problem can be deter- aryto a chronic right-to-left vascular shunt
mined quickly. Animals with severe dyspnea (Figure 1-6).
should be handled gently to avoid stress and Pale mucous membranes indicate anemia or poor
should be treated immediately. perfusion.
The mucous membranes of the mouth should
becompared with the posterior membranes
Check for any asymmetry and swellings.
The eyes should be examined for changes that
could indicate systemic diseases.

Box 1-7 Reasons an Animal Will Not Lie


Diaphragmatic hernia
Severe pericardial effusion
Severe pleural effusion
Severe pulmonary edema
Severe respiratory disease Figure 1-6. Hyperemic mucous membranes in a dog with
polycythemia due to Tetralogy of Fallot.
12 Section I Diagnosis of Heart Disease

(e.g., vagina, prepuce), because differential cya- The entire jugular vein can be distended indicat-
nosis can occur in a right-to-left shunting PDA. ing increased systemic venous pressure caused
Check the oral cavity for severe dental tartar, gin- by right-heart failure, pericardial disease, or ob-
givitis, or pyorrhea, which can serve as sources struction of the cranial vena cava (e.g., heart base
of sepsis leading to bacteremia and possibly tumor). Only about 70% of dogs with right-heart
endocarditis. failure have distended jugular veins, and cats
rarely have distended jugular veins with right-
Key Point heart failure. See Box 1-9 for causes of jugular
Mucous membrane color and perfusion are distension.
insensitive signs of cardiac function, so when Mediastinal masses such as lymphosarcoma can
they are abnormal, the animals cardiac or re- compress the cranial vena cava causing a dis-
spiratory problem is severe. tended jugular vein; however, they also usually
cause pleural effusion and head and neck edema.
Arterial pulses can mimic a jugular pulse; how-
ever, when light pressure is applied to the area of
The jugular pulse should be evaluated while the the jugular pulse, the arterial pulse will continue,
animal is standing with its head in a normal posi- whereas the jugular pulse will stop.
tion. Any pulse going over one third of the way The hepatojugular reflex is a distension of the jug-
up the neck is abnormal and can be due to any of ular veins that occurs when the abdomen is com-
several factors. See Box 1-8 for causes of abnor- pressed for 10 to 30 seconds. It is caused by an
mal jugular pulses. increased return of blood to the right heart from the
Abnormal jugular pulses occur in right-heart fail- abdomen. However, the right heart is not normal
ure due to tricuspid regurgitation or dilated car- and cannot handle the increased venous return, so
diomyopathy, when the right ventricle contracts the blood from the cranial vena cava cannot enter
and the blood flows back into the right atrium and the heart and the jugular veins become distended.
up the jugular veins due to the insufficient tricus- This reflex is present with both right- and left-heart
pid valve. failure and indicates increased blood volume in the
Abnormal jugular pulses occur with pulmonic peripheral venous system due to an inability of the
stenosis and pulmonary hypertension, when the heart to circulate the blood properly.
right atrium contracts against a hypertrophied, Cats with left-heart failure may have distended
noncompliant right ventricle so that only some of jugular veins only when lying down and the jugu-
the blood enters the right ventricle and the rest lar veins return to normal when they sit or stand.
goes back up the jugular veins.
With heartworm disease, abnormal jugular pulses
occur because there is both a stiff, hypertrophied
Box 1-9 Causes of Distended Jugular Veins
right ventricle and tricuspid regurgitation which
both contribute to the jugular pulses. Right-heart failure (e.g., tricuspid regurgitation,
Arrhythmias such as second or third degree heart dilated cardiomyopathy)
block or premature beats cause abnormal jugular Pericardial diseases
Heart base tumor
pulses because the sequence of atrial and ven-
Mediastinal mass
tricular activation is disrupted so that the atrium
contracts against a closed tricuspid valve sending
blood back up the jugular veins.
Key Point
Box 1-8 Causes of Abnormal Jugular Jugular vein distention can be present with
Pulses both right- and left-heart failure, but may be
present in only 70% of these cases. Abdominal
Arrhythmias ultrasound is a sensitive, noninvasive method
Heartworm disease of determining increased venous pressure by
Pulmonary hypertension detecting distended hepatic veins; however,
Pulmonic stenosis the ultrasound only confirms the presence of
Right-heart failure (e.g., tricuspid regurgitation, di- increased venous pressure and not the cause
lated cardiomyopathy) of it.
Chapter 1 The History and Physical Examination 13

A central venous pressure can be obtained on Box 1-10 Causes of Shifting of the
animals with distended jugular veins. It is most Palpable Apex Beat or Point
useful in the diagnosis of restrictive pericardial of Maximum Intensity
disease where less invasive tests have not con-
firmed the diagnosis. Cardiac enlargement
A young dog with regurgitation due to a mega- Collapsed lung lobes on the right
esophagus may have a congenital vascular ring Diaphragmatic hernias
anomaly. Pectus excavatum
Lying down
Masses displacing the heart
Tracheal Palpation Pleural effusions

The trachea should be palpated for abnormali-

ties such as collapsing, masses, or increased
sensitivity. Box 1-11 Causes of Changes in Heart
This step is best postponed until after ausculta- Sounds
tion of the thorax, because a cough may be elic-
ited that makes auscultation difficult. Decreased intensity due to:
Lymph nodes should be palpated to see if they are Decreased left ventricular contractility
enlarged. Diaphragmatic hernias
The thyroids may be enlarged in cats with hyper- Emphysema
thyroidism (thyroid slip). Pleural or pericardial effusions
An old dog having a mass near the larynx with Pneumothorax
an associated thrill usually has thyroid carcinoma Thoracic masses
with an arteriovenous fistula causing the thrill Increased intensity due to:
(murmur that can be felt as well as heard). Hyperdynamic states (e.g., anemia, hyperthyroid-
ism, fever)
Key Point Increased heart rates
Young, thin animals
Palpation of the neck can reveal primary or
secondary problems that affect the heart and
can mimic heart disease (collapsing trachea).
with increased heart rates or with hyperdynamic
states such as anemia, hyperthyroidism, or fever.
Thoracic Palpation
The heart sometimes appears to be beating on the
The apex beat (sometimes called the point of chest wall. The heart is not actually hitting the
maximum intensity [PMI]) is where the cardiac chest wall; the appearance is due to the increased
impulse is felt strongest on the chest wall. It wall tension of the thoracic wall for an indeter-
should be on the left side of the thorax between minate reason. It does not mean that the heart is
the fourth and sixth intercostal spaces. Shifting contracting normally or better than normal.
of the PMI is due to cardiac enlargement, masses Loud cardiac murmurs can be palpated as thrills,
displacing the heart, collapsed lung lobes al- which are due to vibrations caused by blood flow. A
lowing the heart to shift, diaphragmatic hernias, thrill is always located where a murmur is loudest.
pleural effusions associated with collapsed lung
lobes or fibrin, or lying down in right lateral re- Key Point
cumbency such that the heart falls to the right. It is important to locate both the PMI
Pectus excavatum, a deformity of the sternum, of the heartbeat and the presence of thrills
can also shift the heart to the right (Box 1-10). due to heart murmurs on the thoracic
A decreased intensity of heartbeat or heart wall.
sounds may be due to obesity, pleural effusion,
pericardial effusion, thoracic masses, pneumo-
Abdominal Palpation
thorax, emphysema, diaphragmatic hernias, or
decreased left ventricular contractility with de- Abdominal palpation is done to check for ascites,
creased cardiac output (Box 1-11). the presence of fluid in the abdomen. Ascites can
There can be an increased intensity of the PMI or be due to right-heart failure but also can be due to
heart sounds in young, thin animals or in animals multiple other causes.
14 Section I Diagnosis of Heart Disease

The presence of ascites can be difficult to ascer- The femoral pulse rate should be taken. Nor-
tain in obese animals. The clinician should put mal rates in dogs are 70 to 180 beats per minute
one hand on one side of the abdomen and the (bpm). Puppies can have a normal rate of 220
other hand on the other side, and then tap the bpm. Normal rates in cats are 160 to 240 bpm.
abdomen. If a fluid wave is felt by the hand on The rhythm of the pulses should be noted. There
the opposite side of the abdomen, then ascites is should be a pulse for every heartbeat. Pulse defi-
present. cits usually indicate incomplete ventricular fill-
Check for signs of hepatomegaly and splenomeg- ing, as seen in arrhythmias.
aly. The presence of ascites, splenomegaly and Arterial pulse pressure (femoral pulse quality) is
hepatomegaly, usually indicates right-heart failure the difference between the arterial systolic pres-
due to dilated cardiomyopathy, tricuspid regurgi- sure and the diastolic pressure. Pulse quality can
tation, heartworm disease, pericardial disease, or normally vary depending on the animals confor-
congenital heart disease. Another possibility is an mation, age, hydration, heart rate, cardiac func-
obstruction of the posterior vena cava. tion, and level of excitement or activity.
Palpate for any masses. The intensity of the pulse should be palpated.
Palpate the kidneys as chronic renal failure can Normal pulses are strong and have a rapid rate of
lead to systemic hypertension that can affect the rise and fall.
heart. Table 1-3 lists the pulse quality and the cause for
Most ascites due to right-heart failure is a modi- each type of pulse.
fied transudate on cytology and accumulates Hypokinetic (weak) pulses are due to decreased
slowly. cardiac output (e.g., congestive heart failure, hy-
povolemia), decreased peripheral vascular resis-
Key Point tance, increased arterial compliance, or slower
Ascites can be due to right-heart failure or rate of rise due to delayed emptying of the left
other heart problems such as pericardial effu ventricle (e.g., subaortic stenosis). Dogs will
sion; however, it can also be due to other have normal pulses until the stroke volume is
noncardiac problems. Further tests are indicted markedly decreased with severe congestive heart
to determine the cause of ascites.

Table 1-3 Types of Pulses and Their

Skin Associated Causes
Palpate for evidence of edema due to right-heart
Pulse Cause
failure or venous obstruction.
Absent pulses Thromboembolism
Abrupt pulses Mitral regurgitation
Femoral Pulses
Ventricular septal defects
Both pulses should be felt with the dog or cat Erratic pulses Atrial fibrillation
standing, and they should be compared to each
Hypokinetic pulses Heart failure
other because one could be obstructed. Hypotension
It is difficult to palpate the femoral pulse in a Hypovolemia
normal cat; therefore, the absence of palpable Subaortic stenosis
femoral pulses in a cat should not be interpreted Hyperkinetic pulses Aortic regurgitation
as definite arterial obstruction. Fear
Partial or complete occlusion of the pulses so that Fever
they cannot be felt is usually due to thrombo- Patent ductus arteriosus
embolism. In dogs this can occur with bacterial Severe anemia
endocarditis of the mitral or aortic valves, hyper- Severe bradycardia
adrenocorticism, and protein-losing glomerulo-
nephritis (especially amyloidosis). Cavalier King Pulse deficits Arrhythmias
Charles Spaniels with mitral regurgitation some- Pulsus alternans Severe dilated cardiomy-
times lack a pulse for unknown reasons. In cats, opathy
absent pulses are associated with cardiomyopa- Pulsus bigeminus Arrhythmias
thy but can also occasionally be due to bacterial
Pulsus paradoxus Cardiac tamponade
endocarditis or extra cardiac disease.
Chapter 1 The History and Physical Examination 15

failure so pulses are an insensitive indicator of If an area, especially dorsally, in the thorax sounds
cardiac output. hyperresonant, then pneumothorax may be present.
Hyperkinetic (strong) pulses rise and fall quickly If an area, especially ventrally, sounds hyporeso-
and are due to large left ventricular stroke vol- nant, then pleural effusion may be present.
umes with rapid diastolic runoffs (e.g., PDA,
aortic regurgitation). They are called B-B shot Key Point
or water-hammer pulses. Fear, fever, severe Percussion can be a rapid way of determining
bradycardia, thyrotoxicosis, and anemia can also the presence or absence of pleural effusion.
produce this type of pulse.
The pulses can be abrupt or jerky with mitral regur-
gitation and ventricular septal defects as a greater
volume of blood is ejected in early systole. The main components of the stethoscope are the
Pulsus alternans occurs when the pulse is alternately bell, diaphragm, tubing, and ear pieces. The bell
weak and then strong in patients with normal si- transmits both low-frequency (20 to 300 cycles
nus rhythm. It is frequently associated with severe per second [cps]) sounds when light pressure is
myocardial failure (e.g., dilated cardiomyopathy). used and high-frequency (300 to 1000 cps) sounds
Pulsus bigeminus occurs when weak pulses alter- when firm pressure is used to apply it to the thorax.
nate with strong pulses. This is associated with It is best for hearing third and fourth heart sounds.
arrhythmias such as ventricular bigeminy where The diaphragm attenuates low frequencies and se-
a normal heart beat alternates with a ventricular lectively transmits the high frequencies. It is best
premature beat. The weak pulses occur because for hearing the first and second heart sounds.
the premature beat causes the ventricles to con- Most stethoscopes combine the bell and dia-
tract before they are adequately filled so a smaller phragm into a dual-sided, combination-style
than normal volume of blood is ejected by the left chest piece. Some stethoscopes have the bell and
ventricle, causing weak pulses. The difference diaphragm as one piece. With these stethoscopes,
between the normal and abnormal pulses may simple fingertip pressure allows one to switch
be accentuated due to the fact the ventricles have from low- to high-frequency sounds. There is no
more time to fill on the normal beats so that the interruption in sound as there is in a traditional
normal pulses feel even stronger. two-sided stethoscope, resulting in added conve-
Pulsus paradoxus is an alteration of the pulse nience and efficiency in auscultation.
strength during respiration due to changes in A practical tubing length on a stethoscope is ap-
ventricular filling. There is an increase in pulse proximately 14 to 18 inches. If the tubing is too
strength on expiration and a decrease in strength long, then it will attenuate all the heart and lung
on inspiration in normal animals; however, this sounds.
change is exaggerated and easier to feel when Ear tubes should angle forward to conform to the
cardiac tamponade is present. anatomy of the ear canals. A stethoscope with
Pulses feel erratic when an animal has atrial variable sizes of ear pieces is ideal because each
fibrillation. person can find the correct size earpiece that fits
comfortably in the ear canal and shuts out extra-
Key Point neous sounds.
The quality of an animals pulse is not a good For dogs and cats less than 15 pounds, a pediatric
indication of the severity of its cardiac prob- stethoscope that has a smaller headpiece should
lem because only very advanced heart disease be used.
will cause weak pulses; however, pulse defi- Electronic stethoscopes have improved dramati-
cits are very good indicators of the presence cally in the past 10 years. In addition to electronic
of an arrhythmia. amplification of heart sounds and murmurs, most
electronic stethoscopes currently allow the user to
record and play back sounds at either normal or
half speed. This feature is useful for judging and
Percussion can be used to determine the presence timing the shape or quality of murmurs in tachy-
of masses or fluid lines, especially in the thorax. cardic patients and for judging the timing of tran-
It will elicit a hollow sound (hyperresonance) sient heart sounds such as clicks or gallops. Some
over the lungs and a dull sound over solid struc- models also provide the ability to record graphic
tures (hyporesonant). representations of sounds in a digital file format
16 Section I Diagnosis of Heart Disease

(i.e., a phonocardiogram) that can be stored on crackling due to the rubbing of hair. Extraneous
a computer, possibly even becoming part of the sounds will occur if auscultation is not performed
patients medical record. A new electronic stetho- in a quiet area.
scope (Figure 1-7), the 3M Littman Model 3000, Auscult the heart and lungs separately.
features useful ambient noise reduction circuitry Auscult the entire thorax on both sides.
that appears to overcome most if not all of the The areas of auscultation of the heart are
problems of background noise amplification that shown in Figure 1-8. Table 1-4 lists the areas of
plagued previous models. auscultation.
The pulmonic valve area is on the left side. In
Key Point the dog, it is between the second and the fourth
Not every stethoscope is ideal for everyone. intercostal spaces just above the sternum. In the
Ideally, a clinician should try various stetho-
scopes to find the one that works best for him
or her.

This is the most helpful part of the cardiac exami-
nation; it should be done carefully and systemati-
cally. The animal should be standing so that the
heart is in its normal position. This avoids the
problem of positional murmurs caused by the
heart rubbing against the chest wall when an ani-
mal is lying down.
Common artifacts heard include respiratory
clicks and murmurs, rumbles due to shivering Figure 1-7. 3M Littman electronic stethoscope.
and twitching, and movement sounds such as (Courtesy 3M Health Care, St. Paul, Minn.)

Figure 1-8. Areas of auscultation in the dog. M is the mitral valve area, A is the aortic valve area, P is the pulmonic valve area,
and T is the tricuspid valve area. (From Gompf RE: The clinical approach to heart disease: history and physical examination. In Fox
PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Chapter 1 The History and Physical Examination 17

Table 1-4 Areas of Auscultation in the Dog

Alternate areas of auscultation include the tho-
and Cat racic inlets for radiation of the murmur of sub-
aortic stenosis and the left axillary area for the
Structure Location murmurs of PDA.
Mitral valve Dogleft side, fifth intercostal Heart rate and rhythm should be identified. The
space at the costochondral effects of inspiration and expiration on heart rate,
junction rhythm, and heart sounds should be noted.
Catleft side, fifth to sixth inter- The presence or absence of heart sounds should
costal space near sternum be noted.
Aortic valve Dogleft side, fourth intercostal
space just above costochondral Key Point
Catleft side, second to third The lungs and heart should be ausculted sep-
intercostal space just dorsal to arately to avoid missing or confusing any ab-
pulmonic area normal sounds. All valve areas should be aus-
culted in all animals. Congenital heart defects
Pulmonic valve Dogleft side, between second
have been missed when clinicians only listen
and fourth intercostal space just
to the mitral valve area in a young animal.
above the sternum
Catleft side, second to third
intercostal space one-third way
up from sternum
Normal Heart Sounds
Tricuspid valve Dogright side, third to fifth Heart sounds are due to the abrupt acceleration
intercostal space near costo- or deceleration of blood and the vibrations of the
chondral junction heart and vessels.
Catright side, fourth to fifth The first heart sound (S1) (Figure 1-9) is due to
intercostal space near sternum passive closure of the mitral (left AV) and tricus-
pid (right AV) valves resulting in the sudden ac-
celeration and deceleration of blood. It has four
cat, it is located at the second to the third inter- parts that can be seen on a phonocardiogram.
costal space one third to one half of the way up S1 is longer, louder, duller, and lower-pitched
the thorax from the sternum. than the second heart sound. It is loudest over the
The aortic valve area is on the left side. In the mitral and tricuspid areas. It is loudest in young,
dog, it is at the fourth intercostal space just above thin animals and those with high sympathetic
the costochondral junction. In the cat, it is at the tone (e.g., fear), tachycardia, systemic hyperten-
second to the third intercostal space just dorsal to sion, anemia, or mitral regurgitation.
the pulmonic area. The intensity of S1 decreases owing to obesity,
In cats and small dogs, it may be impossible to pleural or pericardial effusion, thoracic masses,
distinguish the pulmonic and aortic areas, so diaphragmatic hernias, bradycardia, emphysema,
these two areas are referred to as the left heart shock and insufficient filling of the ventricles.
base. S1 varies in intensity with arrhythmias.
The mitral valve area is on the left side. In the Splitting of S1 (see Figure 1-9) is due to asynchro-
dog, it is at the fifth intercostal space at the cos- nous closure of the mitral and tricuspid valves. It
tochondral junction. In the cat, it is at the fifth to can be split normally in large breeds of dogs or
the sixth intercostal space one fourth of the way abnormally with right bundle branch block, atrial
up the thorax from the sternum. In cats and small or ventricular premature beats, cardiac pacing, or
dogs, this area may also be referred to as the left stenosis of the mitral or tricuspid valve.
heart apex. Box 1-12 lists the causes of changes in the first
The tricuspid valve area is on the right side. In the heart sound.
dog, it is at the third to the fifth intercostal space The second heart sound (S2) (see Figure 1-9) is
near the costochondral junction. In the cat, it is produced by passive closure of the aortic and pul-
at the fourth or fifth intercostal space, at a level monic valves. It is short, high pitched, and sharp.
opposite the mitral area. It is loudest over the aortic and pulmonic areas.
The areas in which murmurs are loudest (PMI) A split S2 (see Figure 1-9) is due to closure of
and to which they radiate should be noted. This the pulmonic valve after the aortic valve. This
can help identify the heart problem. occurs in pulmonary hypertension (e.g., severe
18 Section I Diagnosis of Heart Disease

Figure 1-9. Heart sounds and their relationship to the ECG. The first heart sound is S1. The second heart sound is S2. The third
heart sound is S3 and the fourth heart sound is S4. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)

heartworm disease or right-to-left PDA), right

Abnormal Heart Sounds
bundle branch block, ventricular premature beats
originating in the left ventricle, atrial septal de- The third heart sound (S3) (Figure 1-9) is due to
fect, pulmonic stenosis, and mitral stenosis. rapid ventricular filling and is not heard in normal
Paradoxical splitting of S2 is due to delayed dogs or cats. It is lower pitched than the second
closure of the aortic valve. This results from left heart sound. It is heard best in the mitral valve
bundle branch block, premature beats originating area and occurs during diastole after the second
from the right ventricle, subaortic stenosis, se- heart sound (S2).
vere systemic hypertension, and left ventricular An S3 in dogs indicates dilated ventricles, which
failure. most commonly occur with dilated cardiomyopa-
S2 may be absent in arrhythmias where there is thy, decompensated mitral or tricuspid regurgi-
incomplete filling of the ventricles and insuffi- tation, large ventricular or atrial septal defects,
cient pressure to open the semilunar valves. and large PDA. In cats it is associated with di-
Box 1-13 lists the causes of changes in the second lated cardiomyopathy, severe anemia, and severe
heart sound. hyperthyroidism.
Table 1-5 lists the causes of abnormal heart sounds.
Key Point The fourth heart sound (S4) (see Figure 1-9)isdue
to atrial contraction into an already over-distended
It is critical to identify the first and second ventricle or into a stiff ventricle in dogs and cats.
heart sounds in all patients in order to use
It is heard best over the aortic or pulmonic areas
auscultation as an effective tool in the diag-
but sometimes can be heard over the mitral valve
nosis of heart disease. If extraneous sounds
are present, then the clinician may need to area as well. It occurs in diastole just prior to the
move to another area of the thorax in order first heart sound.
to identify these sounds properly. An S4 is present in dogs or cats when the atria dilate
in response to ventricular diastolic dysfunction,
Chapter 1 The History and Physical Examination 19

Box 1-12 Causes of Changes in the First Box 1-13 Causes of Changes in the Second
(S1) Heart Sound (S2) Heart Sound

Loud S1 Loud S2
Anemia Atrial septal defect
Excitement Mild valvular pulmonic stenosis
Exercise Patent ductus arteriosus
Fear Pulmonary embolism
Fever Pulmonary hypertension
Hyperthyroidism Systemic hypertension
Mitral regurgitation Valvular aortic stenosis
Positive inotropic agents Ventricular septal defect
Pregnancy Soft S2
Systemic hypertension Dilated cardiomyopathy
Tachycardia Hypothyroidism
Thin animals Marked aortic regurgitation
Soft S1 Shock
Bradycardias Significant pulmonic stenosis
Decreased cardiac output Valvular aortic stenosis
Diaphragmatic hernias Split S2
Emphysema Atrial septal defect
Hypothyroidism Heartworms
Left bundle branch block Mitral stenosis
Negative inotropic agents Pulmonary hypertensionmoderate to severe
Obesity Pulmonic stenosis
Pericardial effusion Right bundle branch block
Pleural effusion Right to left patent ductus arteriosus
Severe aortic or mitral regurgitation Ventricular premature beat from left ventricle
Severe heart failure Paradoxical split S2
Shock Left bundle branch block
Thoracic masses Left ventricular failure
Variable S1 Severe systemic hypertension
Arrhythmias Significant aortic regurgitation
Split S1 Subaortic stenosis
Atrial or ventricular premature beats Ventricular premature beats from the right ven-
Cardiac pacing tricle
Right bundle branch block Absent S2
Stenosis of mitral or tricuspid valve Arrhythmias

such as hypertrophic cardiomyopathy or third The precise cause of the click is unknown, but it
degree heart block. It may also be heard in dogs may be due to the mitral valve buckling into the
with ruptured chordae tendineae. left atrium (mitral valve prolapse) in dogs with
A gallop rhythm is an S3, S4, or combination early mitral regurgitation because many of these
(summation) of the two. Gallops are of a low fre- animals develop a mitral regurgitation murmur
quency and can be difficult to hear. A gallop can later in life. This is a benign finding and is not
be a very early sign of heart failure, preceding usually associated with heart failure.
clinical signs. Ejection sounds are high frequency sounds gen-
Systolic clicks are short, mid- to high-frequency erated in early systole due to hypertension, dila-
clicking noises that occur in systole between S1 tion of the great vessels, or opening of abnormal
and S2 (see Figure 1-9). They are usually loud- semilunar valves such as in valvular pulmonic
est over the mitral and tricuspid areas. A sys- stenosis.
tolic click may come and go and may change its
position in systole (gets closer to or further away Key Point
from S2) and may change its intensity. The presence of a gallop is an indication of
A systolic click can be hard to differentiate from a cardiac disease in small animals.
gallop, especially if the animals heart rate is fast.
20 Section I Diagnosis of Heart Disease

Table 1-5 Causes of Abnormal Heart Sounds

beats as well as S3 and S4 on physical examina-
tion. An electrocardiogram and phonocardiogram
Sound Cause may be necessary.
Gallop sounds Both atrial and ventricular premature beats inter-
S3 Decompensated mitral or rupt the normal rhythm and are usually followed
tricuspid regurgitation by a pause. Usually only an S1 is heard with a
Dilated cardiomyopathy premature beat and S2 is absent. However, some-
Large atrial septal defect times S1 and S2 can be heard very close together.
Large patent ductus arteriosus Premature beats can also cause a split S1 or S2.
Large ventricular septal defect
Sinus arrhythmia has a cyclical pattern. The heart
Severe anemia in cats
Severe hyperthyroidism in rate will increase during inspiration and decrease
cats during expiration owing to changes in vagal tone.
Significant aortic regurgitation The intensity of the pulse and heart sounds may
S4 Anemia vary. It is normal in dogs, but in cats it is usually
Hypertrophic cardiomyopathy associated with heart disease. Sinus arrhythmia
Dogs with ruptured chordae occurs at normal heart rates in dogs and cats and
tendineae tends to disappear as the heart rate increases.
Pulmonary hypertension Arrhythmias that decrease the heart rate are
Systemic hypertension called bradycardias and examples include both
Third degree heart block
sinus bradycardia and heart blocks.
Sinus bradycardia has a very slow rhythm. The
Systolic click Mitral valve prolapse heart sounds may vary. The heart rate in dogs is be-
Ejection sounds Anemia tween 50 to 70 bpm, depending on the size of the
Atrial septal defect dog. The heart rate in cats is less than 120 bpm.
Dilation of great vessels Second and third degree heart blocks result in
slow heart rates. The heart sounds will vary in
Hyperthyroidism intensity. A fourth heart sound may be present
Pulmonary embolism in third degree block. The pulses will be slow
Pulmonary hypertension and hyperkinetic, but there are no pulse deficits.
Systemic hypertension A jugular pulse is usually present. Extra sounds
Valvular aortic stenosis may be generated by escape beats.
Valvular pulmonic stenosis An electrocardiogram is necessary to diagnose
the type of bradycardia present.
Unexpected pauses can occur with sinoatrial (SA or
Arrhythmias Heard on Auscultation
sinus) arrest. Sinus arrest occurs when an impulse
Arrhythmias that increase the heart rate (tachy- does not leave the SA node. The pause continues
cardias) include both atrial and ventricular until the next normal beat or an escape beat occurs.
arrhythmias. The heart sound following a pause may be louder
Animals with atrial fibrillation have a rapid, ir- than usual as the ventricles have had longer to fill
regular rhythm with heart sounds that vary in and eject a larger amount of blood. An electrocar-
intensity. Pulse deficits are present. It has been diogram is necessary to diagnose sinus arrest.
described as being irregularly irregular and rarely
is mistaken for other tachycardias.
Ventricular tachycardias are usually intermittent
and tend to be more regular than atrial fibrilla- Murmurs are caused by turbulent blood flow through
tion. Pulse deficits are frequently present. the heart and vessels. The turbulence can be caused
Sinus and atrial tachycardias are rapid and regu- by disruptions of blood flow through holes in the
lar. All the heart sounds are of a uniform intensity, heart (e.g., ventricular septal or atrial septal defect),
but an atrial tachycardia tends to be intermittent. a stenotic valve (e.g., aortic, pulmonic, mitral or
An electrocardiogram is necessary to distinguish tricuspid stenosis), an insufficient valve (e.g.,
among sinus, atrial, and ventricular tachycardia. mitral, tricuspid, aortic, or pulmonic regurgitation),
Atrial and ventricular premature beats generate an abnormal arterial venous connection near the
extra sounds that mimic S3 and S4. It is difficult to heart (e.g., PDA), or can be due to altered blood vis-
differentiate between the two types of premature cosity or changes in blood vessel diameter.
Chapter 1 The History and Physical Examination 21

Functional murmurs are divided into physiologic The loudness of a murmur does not indicate the
and innocent murmurs. severity of the underlying problem.
Physiologic murmurs have a known cause such as A murmur should be described by using the
increased cardiac output or decreased blood vis- following classification. First, the murmur
cosity and occur with anemia, hypoproteinemia, should be identified as to its timing in the car-
fever, increased blood pressure, pregnancy, hyper- diac cycle (e.g., systolic, diastolic, continuous).
thyroidism, and an athletic heart. These are high Also, the duration of the murmur (e.g., early
frequency murmurs occurring in the early to mid- systolic, holosystolic, pansystolic) should be
systolic phase, are loudest over the aortic and pul- noted (Figures 1-10 and 1-11).
monic areas and rarely radiate to other areas. Table Next the site at which the murmur is loudest
1-6 lists the types of murmurs and their causes. (PMI) (e.g., valve area) and where it radiates due
Innocent murmurs have no known cause and are to blood flow through the defect (e.g., other valve
not associated with any cardiac problem. These areas where it can be heard) should be noted.
murmurs are soft systolic murmurs (no louder than The intensity or loudness of the murmur can be
grade 3) and usually just occur in young animals. evaluated based on the following scale: grade I/
They can be located over any valve area but are VI can only be heard after listening for several
most frequent over the mitral and aortic areas. Also, minutes and sounds like a prolonged first heart
these murmurs should disappear by the time of the sound; grade II/VI is very soft, but can be heard
animals last vaccinations (5 months of age). immediately; grade III/VI is low to moderate in
Pathologic murmurs are caused by underlying intensity; grade IV/VI is very loud, but a thrill
heart or vessel disease such as stenosis of valves cannot be palpated on the thorax; grade V/VI is
or outflow tract or great vessels, valvular regur- very loud, and a thrill can be palpated on the tho-
gitation, or abnormal intracardiac or extracardiac rax; grade VI/VI can be heard without the use of
shunts. Refer to individual defects in the follow- a stethoscope or with the stethoscope slightly off
ing chapters for a description of the murmurs as- the thoracic wall.
sociated with each defect. The quality or shape of the murmur is subjective,
but can be evaluated according to graphic appear-
ance on phonocardiogram (see Figures 1-10 and
Table 1-6 Types of Heart Murmurs and Their 1-11). Regurgitant murmurs are plateau shaped
(e.g., equal loudness throughout). Ejection murmurs
Murmur Cause are usually decrescendo, crescendo, or diamond
shaped. Machinery or continuous murmurs are
Physiologic Anemia
Athletic heart
diamond-shaped and peak at S2, continuing
Fever through all of systole and most of diastole. Blow-
Hypoproteinemia ing murmurs are decrescendo murmurs (e.g., de-
Hypertension crease in intensity).
Hyperthyroidism The pitch or frequency of the murmur can also
Pregnancy be described. Some murmurs are high, medium
Innocent No known cause or low pitched, or a mix. Also, they can be harsh,
Pathologic Aortic regurgitation blowing, or musical.
Aorticopulmonary septal defect
Arteriovenous fistula
Atrial septal defect Other Sounds Auscultated in the Thorax
Mitral dysplasia Normal respiratory sounds include referred
Mitral regurgitation
sounds from the trachea that are commonly heard
Mitral stenosis
Patent ductus arteriosus over the lungs. Vesicular sounds are due to air
Pulmonic regurgitation moving through the small bronchi and are louder
Pulmonic stenosis on inspiration. Bronchial sounds are due to air
Subaortic stenosis moving through the large bronchi and trachea
Tetralogy of Fallot and are heard best on expiration. Bronchovesicu-
Tricuspid Dysplasia lar sounds are the combination of the above two
Tricuspid regurgitation and are heard best over the hilar area.
Tricuspid stenosis
Abnormal respiratory sounds include attenuated
Ventricular septal defect
sounds as well as increased, abnormal sounds.
22 Section I Diagnosis of Heart Disease

Figure 1-10. Timing and duration of murmurs. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)

Figure 1-11. Timing and quality of murmurs. (From Gompf RE: The clinical approach to heart disease: history and physical
examination. In Fox PR, ed: Canine and feline cardiology. New York, 1988, Churchill Livingstone.)
Chapter 1 The History and Physical Examination 23

Attenuated bronchovesicular lung sounds are due pericarditis. Wheezes are relatively high pitched,
to thoracic masses, pleural effusion, pneumothorax, musical sounds and are often a sign of pulmonary
obesity, pneumonia, shallow breathing, or early pathology.
consolidation of the pulmonary parenchyma.
Rhonchi are due to air passing through partially
Suggested ReadingS
obstructed airways in the bronchial tubes or
smallest airways. Rhonchi from the large bronchi Buchanan J: Prevalence of cardiovascular disorders. In
are low pitched, sonorous, and almost continu- Fox PR, Sisson DD, Moise NS, eds: Textbook of ca-
ous. They are heard best on inspiration. Rhonchi nine and feline cardiology, ed 2, Philadelphia, 1992,
from the small bronchi are high pitched, sibilant, WB Saunders.
or squeaky, and are heard best on expiration. Gompf RE: The clinical approach to heart disease: his-
tory and physical examination. In Fox PR, ed: Canine
Crackles are interrupted, crepitant, inspiratory
and feline cardiology. New York, 1988, Churchill
sounds heard in many disease conditions and are Livingstone.
not pathognomonic for pulmonary edema. They Kittleson MD: Signalment, history, and physical ex
are due to opening of alveoli or airways that are amination. In Kittleson MD, Kienle RD, eds: Small
collapsed or partially filled with fluid or bubbles animal cardiovascular medicine. St Louis, 1998,
bursting in the airways. They are further defined Mosby.
as fine or coarse in quality. Sisson DD, Ettinger SJ: The physical examination. In
Other sounds which can be ausculted include Fox PR, Sisson DD, Moise NS, eds: Textbook of ca-
pleural friction rubs. Pleural friction rubs are nine and feline cardiology, ed 2, Philadelphia, 1999,
grating, rubbing sounds heard during inspira- WB Saunders.
tionandexpiration owing to the moving of two Smith FWK, Keene B, Tilley LP: Heart sounds. In
Smith FWK, Keene B, Tilley LP, eds: Interpretation
relatively dry, roughened pleural surfaces against
of heart sounds, murmurs, arrhythmias, and lung
each other.Pericardial friction rubs are short, sounds: a guide to cardiac auscultation in dogs and
scratchy noises produced by pericarditis and catsCD ROM and manual. Philadelphia, 2006,
heart movement. Pericardial knocks are diastolic WB Saunders.
sounds that occur in animals with constrictive
Chapter 2

Radiology of the Heart

Brian A. Poteet

s0010 Introduction Use of a grid is imperative for adequate image

p0010 Thoracic radiography is a key component of the car- quality when chest thickness exceeds 10 cm.
diovascular evaluation. Careful attention to proper Table 2-1 is a representative thoracic technique
positioning is of primary importance to the use of chart using a 400-speed imaging system and 300
radiographic guidelines for interpretation. Radio- mA/125 kVp radiographic equipment.
graphic interpretation relies heavily on possible
Radiographic Projections s0040
disease considerations (i.e., differential diagnosis)
derived from signalment, physical examination, Lateral Projection s0050
and clinical pathology. Radiographic findings are There are subtle differences in cardiac conforma- u0020
not consistently specific enough to lead to the deri- tion and position when comparing the right ver-
vation of a definitive diagnosis without supportive sus the left lateral radiographic projection. These
clinical evidence. The radiographic study isolated differences are not significant enough to warrant
from clinical information will not provide a diagno- further discussion except to note that the same
sis. The clinician must be aware of certain param- projection should be used on all serial radio-
eters and guidelines for interpretation in order to graphic examinations when repeated evaluation
derive information from the radiographic image. is required.
Patient positioning and adequate radiographic
exposure are critical to an accurate radiographic
s0020 Radiographic Technique interpretation in the lateral projection.
s0030 Exposure Technique and Film Quality Key Point b0010

u0010 Exposure technique will vary depending on equip- A normal heart can appear diseased and vice
ment and film-screen combinations. The current versa when positioning is not adequate.
standard for veterinary radiographic equipment is
a 300 mA/125 to 75 kVp machine. Guidelines for proper exposure and positioning of p0020
The current standard for economic film-screen a lateral thoracic radiograph (Figure 2-1) include:
combination imaging systems is the rare earth Radiographic exposure should be adequate to u0030
systems. Because of the motion created by res- define the dorsal spinous process of the cranial
piration, relatively high-speed (400) film-screen thoracic vertebrae superimposed on the scapula.
combinations that allow shorter exposure times To ensure a lateral projection, the dorsal heads of
are best suited for thoracic radiography. the ribs should be superimposed.
Chapter 2 Radiology of the Heart 25
TABLE 2-1 Small Animal Thoracic Radiographic Technique Chart Using a 400-Speed Film-Screen
System and Standard Radiographic Equipment*

Thickness (cm)
mA Time mAs kVp
Table Top

Thorax 100 1/60 1.7 3 4 5 6 7 8 9 10 cm

48 50 52 54 56 58 60 62
In the Table (using Grid)

Thorax 200 1/60 3.3 4 5 6 7 8 9 10 11 12 13 14 15 16 cm

52 54 56 58 60 62 64 66 68 70 72 74 76

300 1/60 5 17 18 19 20 21 22 23 24 25 26 27 28 cm
76 78 80 82 84 86 88 90 92 95 90 101

Technique rules of thumb: Change exposure(1) 10% KVp; (2) two thirds of mAs.
*Single-phase fully rectified 300mA 125 KVp generator focal-film distance = 38.

1 3

A 2

2 3

Figure 2-1. A, Guidelines for proper exposure and positioning of a lateral thoracic radiographic projection. (1) Exposure should
allow delineation of the thoracic vertebral dorsal spinous process superimposed over the scapula. (2) The forelimbs should be pulled
forward to provide an unsuperimposed view of the cranial thorax. (3) The dorsal rib heads should be superimposed (compare with
B). (4) The exposure should be performed during inspiration, which provides maximum separation between caudal cardiac margin
and diaphragmatic cupula. B, Improperly positioned lateral thoracic radiographic projection (compare with A). (1) Nonsuperimposed
left and right rib heads. (2) The oblique projection markedly distorts cardiac silhouette conformation and intrathoracic position. (3)
Expiratory phase radiographic exposure with poor lung volume between caudal cardiac margin and cupula of the diaphragm.
26 Section I Diagnosis of Heart Disease



A 1 B


Figure 2-2. A, Guidelines for proper exposure and positioning of a dorsoventral/ventrodorsal thoracic radiographic projection.
L, Lateral; DV, dorsoventral. (1) The radiographic exposure should provide outline definition of thoracic vertebra superimposed
over the cardiac silhouette. (2) Exposure should be increased (usually a 10% kVp increase with obesity as suggested by an increase
in thoracic body wall thickness). (3) The thoracic vertebral dorsal spinous processes should be superimposed over the body por-
tions for the entire length of the thoracic spine. (4) Adequate lung volume between caudal cardiac margin and cupula indicates
an inspiratory phase radiographic exposure. B, Improperly positioned dorsoventral radiographic projection. Thoracic vertebral
dorsal spinous processes projected over the left hemithorax (1) and the sternal vertebra projected over the right hemithorax (2),
indicating an oblique thoracic dorsoventral radiographic projection. A lack of lung volume between caudal cardiac margin (3) and
cupula (4) indicates an expiratory phase radiographic exposure.

The forelimbs should be pulled forward so that The dorsal lung fields are hyperinflated, and the
they are not superimposed over the cranial thorax vessels to the caudal lung fields are magnified
or cranial margin of the heart. owing to increased object-film distance. This
The radiographic exposure is taken during full produces an improved radiographic definition
inspiration, identified as an adequate lung field of the large pulmonary arteries and veins of
spacing between the caudal margin of the heart the caudal lung fields. The DV projection also
and the cupula of the diagram. Two primary allows increased detection of early pulmonary
disease considerations for consistent expiratory infiltrates (most commonly with cardiac dis-
phase radiographs are: ease in the hilar and caudodorsal lung fields).
Obesity and Pickwickian syndrome, where the However, an improperly positioned DV/VD
overabundance of abdominal fat prevents ade- projection is worthless for cardiac radiographic
quate inspiratory distraction of the diaphragm interpretation.
Upper airway disease, which most commonly
causes obstruction during the inspiratory phase
of respiration Key Point b0020
Although the DV projection is preferred, a
Dorsoventral/Ventrodorsal Projection straight (symmetric) projection is the ultimate s0060
The dorsoventral (DV) radiographic projection is goal, with patient compliance determining p0030
preferred over the ventrodorsal (VD) for cardiac which projection (DV vs. VD) is attainable.
evaluation for two reasons:
The anatomic positioning of the heart in the DV u0040
p0040 projection is less dependent on thoracic cavity con- Guidelines for proper exposure and positioning for
formation (deep-chested vs. barrel-chested breeds). the DV/VD projections (Figure 2-2) include:
Chapter 2 Radiology of the Heart 27

u0050 Radiographic exposure should be sufficient to formation of early cardiogenic pulmonary edema.
define the outline of the thoracic vertebrae super- Adequate exposure is critical to ensure definition
imposed over the cardiac silhouette. of caudal pulmonary vasculature superimposed
The kVp should be increased 10% from tech- over the cupula of the diaphragm.
nique-chart values for obese patients. Examina- The radiographic detection of caudodorsal pul-
tion of the thoracic body wall thickness on the monary vasculature is the best objective parame-
VD view should assist in evaluation of obesity. ter for the detection of pulmonary edema. Vessels
The dorsal spinous processes of the thoracic in the normal lung are detected by their soft tissue
vertebrae should be centered over the vertebral opacity contrasting with the normal radiolucent
bodies along the full length of the thoracic spine. gas-filled lung parenchyma surrounding them.
The thoracic sternal vertebrae also should be su- As pulmonary parenchyma (interstitial spaces as
perimposed over the thoracic spine and be essen- well as alveoli) become filled with edema fluid,
tially indistinguishable radiographically. the normal radiographic soft tissuegas contrast
The radiograph is taken during full inspiration, is lost, and delineation of the vessels diminishes.
identified as an adequate lung field spacing be- In other words, the vessels start to disappear
tween caudal cardiac margin and cupula of the from radiographic detection with the increased
diaphragm. opacity of the surrounding edematous lung pa-
renchyma (Figure 2-3).
The phase of inspiration is critical when using this
s0070 Projection Selection in method for interpretation both in the DV/VD and
Cardiac-Related Pathology in the lateral projections. Pulmonary pathology
can be mimicked when underinflation decreases
s0080 Pulmonary Edema
the parenchymal gas content per unit volume,
u0060 The DV is preferred over the VD projection for thus decreasing the radiographic contrast be-
radiographic detection of pulmonary edema. The tween lung parenchyma and associated vascu-
DV view accentuates pathology in the dorsal lung lature. This is especially true in older patients,
field, which is the most common location for the which already have slightly increased pulmonary


Heart Heart

Figure 2-3. A, Normal radiographic definition and contrast of pulmonary venous vasculature (PV) with surrounding normal
radiolucent lung parenchyma. L, Lateral; DV, dorsoventral; LA, left atrium; LAa, left atrial auricular appendage. B, Radiographic
obliteration of pulmonary venous vasculature (PV) by alveolar consolidation (Alv) of hilar and caudal lung lobes, a characteristic
distribution for cardiogenic pulmonary edema.
28 Section I Diagnosis of Heart Disease

parenchymal radiographic opacity owing to age- degree of respiratory compromise should always
related pulmonary degenerative changes (intersti- be assessed prior to thoracic imaging.
tial fibrosis, bronchial mineralization, heterotopic If significant amounts of pleural effusion are sus-
pulmonary bone formation). pected, increasing radiographic exposure to ab-
dominal technique-chart levels results in better
intrathoracic radiographic contrast. When pos-
s0090 Pleural Effusion
sible, thoracocentesis and fluid drainage prior to
u0070 Pleural effusion is radiographically evident as fo- radiography is always preferred.
cal areas of increased soft tissue opacity located
within the thoracic cavity. It causes separation of
lung lobes from both the thoracic wall and the ad- Radiographic Anatomy s0100
jacent lobes. This is seen on the lateral projection
Lateral Thoracic Radiographic Projection s0110
as an increase in the soft tissue thickness of the
caudodorsal thoracophrenic angle and diaphragm Cardiac Parameters s0120
as well as linear soft tissue opacities (pleural fis- Even though the lateral radiographic projection de- p0050
sures) at anatomic locations comparable with fines the cranial-caudal and dorsal-ventral dimen-
interlobar fissures (Figure 2-4). Pleural effusion sions of the thorax, the anatomy of the heart of the
also contributes to loss of definition of the cra- dog and the cat as it resides in the thorax also al-
nial and caudal margins of the heart, producing a lows this projection to detail the left and right as-
radiographic positive-silhouette sign. pects of the heart. This is because in the dog and the
In cases of pleural effusion, the VD projection is cat the heart is slightly rotated along its base-apex
much preferred over the DV view for detection axis, such that the right cardiac chambers are posi-
and delineation of cardiac size and shape. If intra- tioned more cranially and the left chambers posi-
thoracic fluid volumes are severe enough, the heart tioned more caudally. Thus, the cardiac silhouette
can effectively disappear on the DV view because as it appears on the lateral projection defines the
of the relative distribution of the fluid and heart right side of the heart along the cranial margin and
in the thoracic cavity. The positive-silhouette the left side is defined by its caudal margin (Figures
phenomenon is accentuated in the DV compared 2-6 to 2-8).
with the VD view (Figure 2-5). However, patient The canine and feline heart shape or radiographic p0060
positioning for the DV projection puts less silhouette is ovoid, with the apex more pointed in
physiologic demand on the patient compromised conformation than the broader base. This base-
by pleural effusion and thus is favored over theVD apex difference in conformation is accentuated
projection. The patients physiologic stability and in the cat. The heart axis is defined by drawing a

1 1

f0040 Trachea Heart

Figure 2-4. Lateral thoracic radiographic projection of pleural effusion. Intrathoracic fluid accumulation causes separation of
adjacent lung lobes by (1) linear interlobar opacities, radiographically defined as pleural fissures, and (2) separation of lung lobes
from the thoracic wall.
Chapter 2 Radiology of the Heart 29




Figure 2-5. A, Ventrodorsal (VD) thoracic radiographic projection of pleural effusion consisting of pleural fissure lines (closed
arrows) with blunting of the thoracophrenic angles (open arrows). Note that the cardiac silhouette is still well outlined. B, Dorso-
ventral (DV) thoracic radiographic projection of pleural effusion. The intrathoracic fluid distribution creates a positive silhouette
sign where a complete loss of the cardiac silhouette has occurred. Thus, the VD projection (A) is preferred for cardiac silhouette
definition in the presence of pleural effusion. L, Lateral.





f0060 ra PV RV
Figure 2-6. Schematic lateral thoracic radiographic projection of the relative position and size of the right-side structures of the
heart. Note the more cranial position of the right chambers of the heart. CrVC, Cranial vena cava; PAS, main pulmonary artery;
PV, pulmonic valve; ra, right atrial auricular appendage; RV, right ventricle; RA, right atrium; LP, left pulmonary artery; RP, right
pulmonary artery; TV, tricuspid valve; CaVC, caudal vena cava.
30 Section I Diagnosis of Heart Disease





f0070 Aor AV Aot LV

Figure 2-7. Schematic lateral thoracic radiographic projection of the relative position and size of the left-side structures of the
heart. Note the more caudal position of the left chambers of the heart. Aa, Aortic arch; AOr, aorta; AV, aortic valve; Aot, aortic
outflow tract; LV, left ventricle; LVi, left ventricular inflow tract; LA, left atrium; MV, mitral valve; CVC, caudal vena cava.

Trachea TB CVC


RV Abdomen

Figure 2-8. Schematic lateral thoracic radiographic projection outlining the approximate location of the four heart chambers.
TB, Tracheal bifurcation; CVC, caudal vena cava; RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle.

line from the tracheal bifurcation (carina) to the Apso, Bulldog) tend to have more globular-shaped
apex at an angle approximately 45 degrees to the hearts, with increased sternal contact of the cra-
sternal vertebrae. This angle can decrease in the cat nial margin of the heart. The heart chambers can
with age and is often called a lazy heart. It has be roughly defined by a line connecting the apex
been postulated that this may be related to a loss to the tracheal bifurcation and a second line per-
of aortic connective tissue elasticity. This is most pendicular to the base-apex axis and positioned at
often seen in cats older than 7 years. Shallow, the level of the ventral aspect of the caudal vena
barrel-chested dog breeds (Dachshund, Lhasa cava (see Figure 2-8).
Chapter 2 Radiology of the Heart 31

Trachea T4 Unit measuring site CVC

VHS = S + L
f0090 Measured in vertebral units beginning at T4.
Figure 2-9. Schematic representation parameters for the vertebral scale system of cardiac size. The vertebral heart sum (VHS) is
the sum of the long axis cardiac dimension (L) and the maximal perpendicular short axis dimension (S). S and L are measured in
vertebral units beginning at T4. CVC, Caudal vena cava.

p0100 The dorsal cardiac margin includes both atria, A more objective determination of cardiac size
pulmonary arteries and veins, the cranial and caudal has been formulated for the dog and uses a verte-
vena cavae, and the aortic arch (see Figures 2-6 to bral scale system in which cardiac dimensions are
2-8). The cranial border is formed by both the right scaled against the length of specific thoracic ver-
ventricle and the right atrial appendage, resulting in tebrae (Figure 2-9). In lateral radiographs the long
the radiographically defined cranial waist (see Fig- axis of the heart (L) is measured with a caliper
ures 2-6 and 2-8). The caudal margin is formed by the extending from the ventral aspect of the left main
left atrium and left ventricle, with the atrioventricular stem bronchus (tracheal bifurcation hilus, carina) to
junction defined as the radiographic caudal waist. the left ventricular apex. The caliper is repositioned
p0080 The base-to-apex cardiac dimension or length along the vertebral column beginning at the cranial
occupies approximately 70% of the DV distance of edge of the fourth thoracic vertebra. The length of
the thoracic cavity at its position within the thorax. the heart is recorded as the number of vertebrae cau-
For objective measurements it is important to mea- dal to that point and estimated to the nearest tenth
sure thoracic cavity distance between the thoracic of a vertebra. The maximum perpendicular short
spine and the sternum at an axis perpendicular to axis (S) is measured in the same manner beginning
the thoracic spine. at the fourth thoracic vertebra. If obvious left atrial
The cranial-caudal dimension or width as it ap- enlargement is present, the short axis measurement p0090
pears on the lateral projection is measured at its is made at the ventral juncture of left atrial and cau-
maximum width (which is usually at the level of dal vena caval silhouettes.
the ventral aspect of the insertion of the caudal vena The lengths in vertebrae (v) of the long and p0110
cava) and perpendicular to the base-apex axis. This short axes are then added to obtain a vertebral
classically has been defined as between 2.5 (deep- heart sum (VHS), which provides a single number
chested conformation breeds [Setters, Afghans, representing heart size proportionate to the size
Collies]) and 3.5 (barrel-chested conformation of the dog. The average VHS in the dog is 9.7 v
breeds [Dachshunds, Bulldogs]) intercostal spaces (range 8.5 to 10.5 v). Caution must be exercised in
(ICS) in the dog and 2.5 to 3.0 ICS in the cat. The somebreedsthathave excessively disproportionate
ICS measurement is made at an axis perpendicular skeletalbody weight conformations. An example is
to the long axis of the ribs. Thus, the cardiac width the English Bulldog, which has relatively small tho-
distance determination may have to be shifted in racic vertebrae and commonly has hemivertebrae
axis angle before comparison to ICS length. as well; thus, a normal heart may be interpreted
32 Section I Diagnosis of Heart Disease



f0100 PA PV
Figure 2-10. Pulmonary vascular anatomy in the lateral thoracic projection. Cranial lung lobe branch of the pulmonary artery
(PA), cranial lung lobe branch of the pulmonary vein (PV), end-on view of the right main pulmonary artery (RPA) as it traverses
the thorax from left to right, and left main pulmonary artery (LPA). TB, tracheal bifurcation (carina); BCrL, Bronchus to a cranial
lung lobe.

as large with the VHS method. Although the VHS The pulmonary arteries and veins should be equal
concept is more precise, clinical judgment is still in size. The width of the vessels where they cross
necessary to avoid over diagnosing or under diag- the fourth rib should not exceed the width of the
nosing heart disease. narrowest portion of that rib at its juncture with the
rib head (the dorsal aspect of the rib near the tho-
s0130 Vessel Parameters racic spine). The dorsal section of the rib is used as
p0120 The main pulmonary artery (pulmonary trunk) can- a reference to adjust for radiographic magnification
not be seen on the lateral projection owing to a pos- owing to thoracic conformation.
itive-silhouette sign with the craniodorsal base of
Dorsoventral and Ventrodorsal Projections s0140
the heart. The left pulmonary artery can sometimes
be seen extending dorsal and caudal to the tracheal Cardiac Parameters s0150
bifurcation (carina). The right pulmonary artery is The heart is rotated on its long axis such that the p0150
frequently seen end-on as it leaves the main pul- right chambers are oriented both right and cranially,
monary artery immediately ventral to the carina and the left chambers reside both left and caudal.
(Figure 2-10). This end-on appearance may be con- The degree of rotation is less in the cat. The cranial-
fused with a mass lesion on normal radiographs and caudal rotation is most significant when defining
is accentuated in cases of pulmonary hypertension the location of the left and right atria, respectively.
such as heartworm disease. The pulmonary veins The canine heart appears radiographically as an p0160
are best identified as they enter the left atrium cau- elliptical opacity with its base-apex axis orientation
dal to the heart base. approximately 30 degrees to the left of the midline.
p0130 Using the larger, more proximal segments of the The width of the heart across its widest point is usu-
mainstem bronchi as a reference, the pulmonary ar- ally 60% to 65% of the thoracic width at its loca-
teries are dorsal to the bronchus, and the pulmonary tion within the thorax. In the cat the cardiac axis
veins are ventral to the bronchus (see Figure 2-10). is most commonly on or close to midline, and its
p0140 The vessels to the cranial lung lobes are usu- width does not usually exceed 50% of the width
ally seen as two pairs of vessels, each with their of the thoracic cavity during full inspiration. The
respective bronchi. The more cranial pair of vessels cardiac silhouette may be artificially increased in
generally corresponds to the side on which the lat- the obese patient owing to an excessive amount of
eral projection was made. Thus, in the right lateral pericardial fat. In these cases, the cardiac silhouette
projection, the right cranial lobar vessels are more margin appears to be less well defined or blurred
cranial than vessels of the left cranial lung lobe. because the margin of contrast between soft tissue
Chapter 2 Radiology of the Heart 33





Figure 2-11. Schematic anatomy of the chambers and vasculature of the left ventricular outflow tract of the heart in the dorso-
ventral radiographic projection. LV, Left ventricle; Aot, aortic outflow tract; AV, aortic valve; AA, aortic arch; PAS, pulmonary artery
segment; Da, descending aorta.


rpa lpa



Figure 2-12. Schematic anatomy of the pulmonary vasculature in the dorsoventral projection. PAS, Main pulmonary artery
(radiographic descriptionpulmonary artery segment); lpa, left pulmonary artery; rpa, right pulmonary artery; LA, left atrium; Pv,
pulmonary veins.

(heart), fat (pericardial), and air is not as distinct as vertical in the thorax and thus produces a smaller
that between soft tissue and air. and more circular cardiac silhouette conformation.
Evaluating the obesity of the patient by evalu- The broad, barrel-chested breeds produce a radio- p0170
ating the thickness of the abaxial thoracic wall graphic silhouette that appears wider than that of
and width of the mediastinum (as well as exam- standard breeds.
ining the patient) will assist in the determination The margins of the heart that create the car- p0180
of pericardial fat contribution to cardiac size. In diac silhouette contain a number of structures that
deep, narrow-chested breeds, the heart stands more often overlap. A clock face analogy can be used to
34 Section I Diagnosis of Heart Disease



Figure 2-13. Dorsoventral thoracic radiographic projection of a dog with severe left atrial (LA) enlargement. The left atrial
auricular appendage (LAu) contributes to the cardiac silhouette at the 2 to 3 oclock position (1). The body of the left atrium su-
perimposed over the caudal cardiac silhouette produces a radiolucent mach line, a radiographic edge effect caused by an acute
change in soft tissue thickness (2).





Figure 2-14. Schematic anatomy of the chambers and outflow tract of the right side of the heart in the dorsoventral radio-
graphic projection. RV, Right ventricle; RA, right atrium; RAa, right atrial auricular appendage; PV, pulmonic valve; PAS, mainstem
pulmonary artery segment; CVC, caudal vena cava.

s implify the location of these structures. The aortic segment (PAS) (Figures 2-12 and 2-13). In the
arch extends from the 11 oclock to 1 oclock posi- cat, the body of the left atrium proper forms the 2
tion (Figure 2-11). The main pulmonary artery is to 3 oclock position of the cardiac silhouette. In
located from the 1 to 2 oclock position, with its the dog, the left atrium is superimposed over the
radiographic designation as the pulmonary artery caudal portion of the cardiac silhouette in the DV
Chapter 2 Radiology of the Heart 35

p rojection (see Figure 2-12). With severe cases of substantiated on multiple radiographic views where
left atrial enlargement in the dog, the left auricular applicable.
u0080 appendage contributes to the definition and enlarge- Evaluate the radiographs for technical quality,
ment of the cardiac silhouette at the 2 to 3 oclock positioning, and proper exposure. If the study is
position (Figure 2-13). The left ventricle forms the substandard, then stop right here and repeat the
left heart margin from the 2 to 6 oclock position radiographic study.
(see Figure 2-11). The right ventricle is located Determine the phase of respiration.
from the 7 to 11 oclock position (the right ven- Review the entire thoracic cavity: spine, sternum,
tricle does not extend to the apex of the heart) (Fig- diaphragm, thoracic wall, ribs, cranial and caudal
ure 2-14). The right atrium is located at the 9 to 11 mediastinum, conformation and position of the
oclock position (see Figure 2-14). Pericardial fat diaphragm.
in the dog can asymmetrically contribute to cardiac Review the portion of the cranial abdomen in-
silhouette enlargement at the 4 to 5 oclock and 8 to cluded in the projection. Thoracic radiographic
11 oclock positions. exposure is usually half of that required for ab-
dominal imaging but a cursory evaluation of ab-
s0160 Vessel Parameters dominal contrast, detail, and hepatic size (using
p0190 The pulmonary arteries originate from the main gastric axis) can be performed.
pulmonary artery or the PAS with the right branch Evaluate the position, course, and diameter of the
coursing transversely, superimposed over the trachea and mainstem bifurcations.
cranial portion of the heart silhouette, extending Evaluate the position of the cardiac apex and cau-
beyond the right heart margin at approximately the dal mediastinum.
8 oclock position (see Figure 2-12). The left pul- Evaluate the size, shape, and course of the main
monary artery branch courses caudally, superim- pulmonary artery and peripheral pulmonary ar-
posed over the caudal left ventricular portion of the teries and veins.
heart, and extends beyond the left heart margin at Evaluate the lung fields for hyperinflation or un-
approximately the 4 oclock position. The pulmo- derinflation and for distribution and pattern of
nary veins are best seen as they enter the left atrium increased or decreased opacity.
along the caudal margin of the cardiac silhouette Evaluate the cardiac margin (cranial, caudal, right,
(see Figure 2-12). Compared with the pulmonary left, clock position segmentation) for enlarge-
arteries, they are clustered in a more axial position. ment, abnormal position, or conformation.
Thus, the pulmonary arteries extend to both the cra-
nial and caudal lung fields in a more abaxial posi-
tion relative to the pulmonary veins. NoncardiacRelated s0180
p0200 The aortic arch is within the cranial mediasti- Variables that can Mimic
num at the cranial heart margin and is normally Radiographic Signs of
not visible. The descending aorta is superimposed Cardiac Disease
over the heart and extends caudally, dorsally, and
Cardiac Position s0190
medially. The left lateral margin of the aorta can
be seen to the left of the vertebral column on both Pulmonary pathology (such as lung consolida- u0090
DV and VD views (see Figure 2-11). The caudal tion, atelectasis, or pleural disease) can cause a
vena cava courses cranially from the diaphragm mediastinal shift and alter the position and axis
to the right of midline and into the right caudal of the heart in the thoracic cavity.
margin of the heart (see Figure 2-14). This is one Mediastinal mass lesions can affect the cardiac
of the most useful landmarks for determination position and axis, as well as obscure the cranial and
of proper orientation of the DV radiograph on a cardiac margins when in contact with the heart, by
viewbox. producing a radiographic positive-silhouette sign.
Pneumothorax can produce disproportionate
hemithoracic volume changes, altering cardiac
s0170 Radiographic position and axis. Pneumothorax commonly
Interpretation produces elevation of the cardiac apex from the
p0210 A systematic evaluation of the entire thoracic sternum. This is supported by other radiographic
cavity involves adherence to and inclusion of the signs of pneumothorax:
following steps with each radiographic interpreta- Premature termination of lung vasculature into
tion. Abnormalities supportive of disease should be the periphery of the thoracic cavity
36 Section I Diagnosis of Heart Disease

Lung lobe margin detection as it contrasts with Uneven lung inflation secondary to disease or
nonparenchymal free intrathoracic gas previous lobectomy can produce a mediastinal
Sternal conformational abnormalities due to con- shift and resultant apex shift.
genital defects or previous trauma can alter car- If radiographs are taken on diseased, recumbent pa-
diac position and axis. tients or patients during or immediately following
general anesthesia, then hypostatic congestion and
atelectasis of the dependent lung fields can produce
Cardiac Size and Lateral Projection s0200
a mediastinal shift, altering cardiac position.
Younger animals appear to have larger hearts Pectus excavatum or funnel chest sternal con- u0100
relative to their thoracic size than do mature formation due to congenital deformities
The heart appears smaller on inspiration than
s0230 on expiration. During expiration increased ster- Evaluation of Heart
nal contact of the right heart margin and dorsal Chamber Enlargement
elevation of the trachea occurs, falsely suggesting
s0240 Right atrial enlargement
right-heart enlargement.
s0250 Anemic or emaciated patients often have small Radiographic Signs
u0120 hearts owing to hypovolemia and are hyperin- Lateral projection (Figure 2-15):
flated to compensate for hypoxemia. In deep- Elevation of the trachea as it courses dorsally
chested conformation breeds, the cardiac apex over the right atrium
can be elevated far enough from the sternum to Accentuation of the cranial waist. Preferential
mimic pneumothorax. enlargement of the more dorsal margin of the
cranial margin of the cardiac silhouette defines
s0210 Cardiac Position, Dorsoventral/
selective enlargement of the right atrial auricu-
Ventrodorsal Projection
lar appendage.
s0220 Malposition of the Cardiac Apex to the Right Increased soft tissue opacity of the cranial
or Left aspect of the cardiac silhouette owing to in-
u0110 Malposition of the heart to the right is normal creased soft tissue thickness of the right atrium
variant in the cat. superimposed over the right ventricle



Trachea RV Normal cardiac LV

Figure 2-15. Cardiac silhouette changes associated with vessel and chamber enlargement in the lateral thoracic radiographic
0150 projection. Ao, Aortic arch; Pa, main pulmonary artery; RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle; CVC,
caudal vena cava. Dotted line, area of right atrial superimposition over the right ventricle.
Chapter 2 Radiology of the Heart 37




Normal heart


Figure 2-16. Cardiac silhouette changes associated with vessel and chamber enlargement in the dorsoventral radiographic
projection. Aa, Aortic arch; PaS, main pulmonary artery; LAa, left atrial auricular appendage; LV, left ventricle; RV, right ventricle;
RA, right atrium.

4 RA

3 LV
2 Abdomen

f0170 Trachea CVC

Figure 2-17. Schematic representation of radiographic signs associated with right- heart enlargement in the lateral projection.
(1) Dorsal lifting of apex from sternum. (2) Increased sternal contact of cranial cardiac margin. (3) Disproportionate enlargement
of the cranial portion of the cardiac silhouette when empirically divided into its right and left chambers. (4) Elevation of the tra-
chea as it courses dorsally over the right atrium. RA, Right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; CVC, caudal
vena cava.

DV projection (Figure 2-16): Cardiomyopathy

Enlargement of the cardiac margin at 9 to 11 Right atrial neoplasia (e.g., hemangiosarcoma)
Enlargement can be dramatic in severe cases Differential Diagnosis s0270
(especially in the cat) and can be easily mis- Cranial mediastinal mass u0140
taken for pulmonary hilar mass lesion. Heart base neoplasia (most common in brachyce-
phalic breeds)
s0260 Causes of Right Atrial Enlargement Tracheobronchial lymphadenopathy
u0130 Right-heart failure Superimposition of the aortic arch or main pul-
Tricuspid insufficiency monary artery
38 Section I Diagnosis of Heart Disease

Right cranial or middle lobar pulmonary alveolar Cardiomyopathy

consolidation or mass lesion Cor pulmonale
s0280 Right ventricular enlargement
Congenital heart disease: pulmonic stenosis,
s0290 Radiographic Signs patent ductus arteriosus (PDA), ventricular sep-
u0150 Lateral projections (see Figure 2-15) tal defects, tetralogy of Fallot, tricuspid valve
Increased sternal contact of cranial cardiac dysplasia
Left Atrial Enlargement s0310
Elevation of the cardiac apex from the ster-
num Radiographic Signs s0320
Rounding of the conformation of the entire car- Lateral projection (see Figure 2-15) u0170
diac silhouette; increased cardiac width Dorsal elevation of the caudal portion of tra-
Disproportionate enlargement of the cranial chea and carina
portion of the cardiac silhouette when empiri- Disproportionate dorsal elevation of the main-
cally divided into its right and left chambers stem bronchi (the two will no longer be super-
(Figure 2-17) imposed; the left bronchus will appear more
Dorsal elevation of the caudal vena cava dorsal than the right bronchus)
DV projection (see Figure 2-16) Enlargement and straightening of the cau-
Cardiac silhouette enlargement at the 6 to 11 dodorsal portion of the cardiac silhouette
oclock position with almost a right-angle margin confor
Given the enlargement and rounded conformation mation (Figure 2-18); straightening of the
of the right margin, the left margin in comparison caudal margin of the heart and loss of the
assumes a more straightened conformation; an caudal waist (determined by the atrioven-
overall reverse-D conformational appearance tricular junction)
of the cardiac silhouette results DV projection (see Figure 2-16)
Shift of cardiac apex to the left The dog
Enlargement of the atrial auricular append-
s0300 Causes of Right Ventricular Enlargement age, which now produces a noticeable focal
u0160 Secondary to left-heart failure bulge enlargement at the 2 to 3 oclock po-
Tricuspid insufficiency sition (see Figures 2-13 and 2-16)


3 5



Figure 2-18. Schematic representation of radiographic signs associated with left- heart enlargement in the lateral projection.
(1) Rounding and widening of the cardiac apex conformation. (2) Straightening and increased vertical axis of the caudal cardiac
margin. (3) Left atrial enlargement with characteristic right-angular caudodorsal margin conformation. (4) Dorsal elevation of the
intrathoracic portion of the trachea, carina, and mainstem bronchi. The angle between the thoracic spine axis and the trachea is
diminished to the point of becoming parallel. (5) Separation of normally superimposed caudal mainstem bronchi. Left more dorsal
in position than the right. RA, Right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Chapter 2 Radiology of the Heart 39

A double opacity of the atrial body

s0380 Enlargement of the aortic arch and aorta
over the caudal aspect of the cardiac
s0390 silhouette; the body of the left atrium su- Radiographic Signs
u0220 perimposed over the caudal cardiac silhou- Lateral projection (see Figure 2-15)
ette producesaradiolucent mach line, Widening of the dorsal aspect of the cardiac
a radiographic edge effect caused by an silhouette
acute change in soft tissue thickness (see Enlargement of the craniodorsal cardiac
Figure 2-13) margin
The cat DV projection (see Figure 2-16)
Enlargement if the cardiac margin at the 2 to Widening and increased cranial extensions of the
3 oclock position of the silhouette cardiac margin between the 11 and 1 oclock
s0330 Causes of Left Atrial Enlargement
u0180 Mitral insufficiency Causes of Aortic Arch Enlargement s0400
Cardiomyopathy PDA; enlargement more abaxial (1 oclock) u0230
Congenital heart disease; mitral valve dyspla- Aortic stenosis with poststenotic enlargement of
sia, PDA, ventricular septal defects, atrial septal the aortic arch; enlargement more axial and cra-
defects nial (11 oclock)
Left ventricular failure Aortic aneurysm (very rare)

s0340 Differential Diagnosis Differential Diagnosis s0410

u0190 Hilar lymphadenopathy Normal variation in some dogs u0240
Pulmonary mass adjacent to hilus Very common variant in older cats with lazy
heart conformation; very prominent on the DV
s0350 Left Ventricular Enlargement
s0360 Radiographic Signs Cranial mediastinal mass
u0200 Lateral projection (see Figure 2-15) Thymus, or the sail-sign in young dogs
Loss of the caudal waist Cranial mediastinal fat in obese brachycephalic
Caudal cardiac margin straighter and more ver- dogs
tical than normal
Enlargement of the pulmonary artery s0420
Dorsal elevation of the intrathoracic portion
of the trachea, carina, and mainstem bronchi; Radiographic Signs s0430
the angle between the thoracic spine axis and Lateral projection (see Figure 2-15) u0250
trachea is diminished to the point of becoming Protrusion of the craniodorsal heart border
parallel DV projection (see Figure 2-16)
Disproportionate enlargement of the caudal Lateral bulge of the cardiac margin at 1 to 2
portion of the cardiac silhouette when em- oclock position
pirically divided into its right and left cardiac Radiographically defined as the pulmonary ar-
chambers (see Figure 2-18) tery segment (PAS)
DV projection (see Figure 2-16)
Rounding and enlargement of left ventricular Causes of Pulmonary Artery Segment s0440
margin Enlargement
Rounding and broadening of the cardiac apex Dirofilariasis u0260
conformation Pulmonary thrombosis and thromboembolism
Shift of the cardiac apex to the right Cor pulmonale
Congenital disease: pulmonic stenosis, PDA, sep-
s0370 Causes of Left Ventricular Enlargement tal defects both ventricular and atrial with left-to-
u0210 Mitral insufficiency right shunting
Congenital heart disease: PDA, aortic stenosis, Differential Diagnosis s0450
ventricular septal defects Previous dirofilariasis infection and treatment u0270
High-output cardiac disease: fluid overload, Rotational (oblique) positional artifact (usually
chronic anemia, peripheral arteriovenous fistula, on VD projection) most commonly experienced
obesity, chronic renal disease, hyperthyroidism with deep-chested conformation dogs
40 Section I Diagnosis of Heart Disease

Evaluation of the Radiographic Diagnosis s0460
Pulmonary Circulation of Heart Failure
p0220 The radiographic diagnosis of heart failure is de-
Undercirculation s0470
pendent upon recognition of imbalances in the
Radiographic Signs blood and fluid distribution within the body. This s0480
Lung field more radiolucent than normal owing circulatory imbalance is the result of diminished u0280
to lack of pulmonary vascular volume cardiac output into the pulmonary or systemic
Hyperinflation due to hypoxemia or ventilation/ vascular systems or reduced acceptance of blood
perfusion mismatch by the failing ventricle (hypertrophy), or both. De-
Pulmonary arteries smaller than normal; may be pending on which side of the heart is most severely
smaller in size when compared with correspond- affected, blood is shifted from the systemic to the
ing pulmonary veins pulmonary circulation (left-heart failure) or from
the pulmonary to the systemic circulation (right-
s0490 Causes of Pulmonary Undercirculation heart failure).
u0290 Congenital disease: pulmonic stenosis, te-
Right-heart failure s0560
tralogy of Fallot, reverse PDA (right-to-left
shunting) Physiologic Phenomenon s0570
In right-heart failure, an inadequate right ven- u0340
s0500 Differential Diagnosis tricular output into the pulmonary arteries ex-
u0300 Emphysema, chronic obstructive pulmonary ists concurrently with a reduced acceptance of
disease blood from the systemic veins. The blood vol-
Hyperinflation ume and pressure in the splanchnic and systemic
Pneumothorax veins are elevated. The venous congestion causes
Overexposure hepatomegaly.
Pulmonary thromboembolism With further progression of right-heart failure,
Hypovolemia, shock (the heart will also be a progression of systemic hypertension leads to
smaller than normal) increased amounts of fluid, solutes, and protein
Hypoadrenocorticism (Addisons disease); the escaping from the capillary beds of the major
heart may also be smaller than normal organs. The lymphatic circulation is overtaxed,
and fluid exudes into the serosal cavities, pro-
s0510 Overcirculation
ducing ascites, pleural, and even pericardial
s0520 Radiographic Signs effusions.
u0310 Both the pulmonary arteries and the veins are The extracardiac radiographic signs of progres-
enlarged sively worsening right-heart failure are hepato-
Arteries are frequently larger than the veins megaly, ascites, and then pleural effusion.
Pulmonary thoracic opacity is increased because
of larger vascular volume Radiographic Signs s0580
Right-sided cardiomegaly (see Figures 2-15 u0350
s0530 Causes of Pulmonary Overcirculation through 2-17). Patients with concentric cardiac
u0320 Dirofilariasis (arteries are larger than correspond- hypertrophy (e.g., pulmonic stenosis), thin-
ing veins) walled cardiomyopathy, or acute arrhythmias
PDA: both arteries and veins enlarged often may not have dramatic radiographic cardio-
Left-to-right shunts (ventricular and atrial septal megaly. Thus, subtle cardiac silhouette changes
defects): both arteries and veins enlarged in both the DV and the lateral projections must
Congestive heart failure: veins may be larger than be considered significant with supportive clinical
arteries if mainly left sided; both arteries and evidence of cardiac disease.
veins enlarged with concurrent left- and right- Hepatomegaly: rounded liver margin, which ex-
sided failure tends caudal to last rib; displacement of stomach
Fluid overload caudally and to the left
Ascites: abdominal distention; diffuse loss of
s0540 Differential Diagnosis intra-abdominal detail
u0330 Underexposure Pleural effusion
Expiratory phase of respiration Generalized increase in thoracic opacity
Chapter 2 Radiology of the Heart 41

Visualization of interlobar pleural fissures (see Engorgement and distention of the pulmonary
Figures 2-4 and 2-5, A) veins, especially in the hilar area as they enter
Obliteration of cardiac silhouette definition the left atrium. On the DV view these are iden-
(best demonstrated on the DV projection) (see tified as the more axial of the caudal vascula-
Figure 2-5, B) ture (see Figure 2-12).
Separation of pulmonary visceral pleural mar- The diameter of the pulmonary veins is greater
gin away from thoracic wall (see Figures 2-4 than that of their corresponding pulmonary ar-
and 2-5) teries (best seen on the lateral projection with
cranial lobar vessels) (see Figure 2-10).
s0590 Causes of Pleural Effusion Secondary to Right- The radiopacity of the lung parenchyma distal
Heart Failure and peripheral to the hilus is unchanged.
u0360 Decompensated mitral and tricuspid insufficiency Interstitial edema
Decompensated pulmonic stenosis, tetralogy of Diffuse increased radiopacity of the lung fields
Fallot owing to a hazy interstitial opacity is apparent.
Dirofilariasis (caval syndrome) The margins of the pulmonary veins and arter-
Pericardial effusion with tamponade ies are indistinct owing to perivascular edema.
Restrictive pericarditis As the lung parenchyma surrounding the pul-
monary vasculature fills with fluid, the normal
s0600 Differential Diagnosis pulmonary radiographic contrast between gas
u0370 Pleuritis (air-filled lung) and soft tissue (blood-filled
Chylothorax vessels) is lost. Thus, the pulmonary vascu-
Hemothorax laturebecomes indistinct and begins to dis
Pyothorax appearin the surrounding, fluid-filled lung
Hypoproteinemia parenchyma.
Neoplasia (pleural, mediastinal, cardiac, pulmo- In some patients, fluid accumulates around ma-
nary, primary, or metastatic) jor bronchi, producing prominent peribronchial
s0610 Left-heart failure
Alveolar edema
s0620 Physiologic Phenomenon Radiographic signs
u0380 In left-heart failure, inadequate left ven Fluid enters the alveolar air spaces and
tricular output into the aorta occurs, and a peripheral bronchioles, causing a coales-
diminished acceptance of blood from the pul- cent fluffy alveolar infiltrate. Air broncho
monary veins entering the left atrium results. grams(black tubes in a white radiopaque
This causes pulmonary venous congestion background) and air alveolograms (lung
and leakage of fluid into the pulmonary in- parenchyma with the radiopacity of liver
terstitium, with progression to flooding of the containing no vascular markings) are pres-
alveoli. ent. In the cat, cardiogenic alveolar consoli-
Clinically, this evolves as a progression of physi- dations can appear as a very well margined,
ologic events: pulmonary venous congestion, in- cloudlike conformation area of increased
terstitial pulmonary edema, alveolar edema, and pulmonary radiopacity.
lung consolidation. The margins of the pulmonary vessels are
usually completely obscured (see Figure 2-3,
s0630 Radiographic Signs B). The alveolar infiltrate is of greatest opac-
u0390 Left-sided cardiomegaly (see Figure 2-18). Pa- ity in the perihilar area, fading peripherally.
tients with concentric cardiac hypertrophy (e.g., In the dog, alveolar edema can be asymmet-
aortic stenosis), thin-walled cardiomyopathy rical, with the right lung fields more severely
(large- and giant-breed dogs), or acute arrhyth- affected than the left (best seen on the DV
mias often may not have dramatic radiographic projection).
cardiomegaly. Thus, subtle cardiac silhouette Differential diagnosis for pulmonary edema
changes in both the DV and lateral projections Neurogenic: electrocution, head trauma, post
as well as noncardiac changes (pulmonary vas- seizure, encephalitis, brain neoplasm
cular changes, pulmonary edema, etc.) must be Hyperdynamic (excessive negative intratho-
evaluated. racic pressures): choking, strangulation, up-
Pulmonary venous congestion per airway obstructions
42 Section I Diagnosis of Heart Disease

Trachea CVC


3 Abdomen

Pericardial Normal cardiac Pericardial

f0190 effusion silhouette effusion
Figure 2-19. Schematic representation of radiographic signs associated with pericardial effusion. (1) Dorsal elevation of the
intrathoracic portion of the trachea, carina, and mainstem bronchi. The angle between the thoracic spine axis and the trachea is
diminished to the point of becoming parallel. (2) Convex enlargement of the caudodorsal cardiac margin without a right-angle
conformation characteristic for left atrial enlargement. (3) Increased sternal contact of cranial margin. (4) Dorsal elevation and
enlargement of the caudal vena cava (CVC). The cardiac silhouette takes on a smoothly contoured circular conformation with
obliteration of normal cardiac contour.

Fluid overload: overhydration Dorsal elevation of the trachea (similar to left-

Toxicity side enlargement)
Systemic shock Hepatomegaly, ascites, and pleural effusion second-
Hypersensitization ary to cardiac tamponade (see Figures 2-4 and 2-5)
Increased bronchial markings in some cases
s0650 Summary of Radiographic
Pleural effusion
In the dog, this can occur only in very progres-
p0230 sive or severe forms of left-heart failure; this The clinician must be armed with both potential
usually indicates early concurrent left- and radiographic parameters and a clinically derived
right-heart failure. differential diagnostic list for cardiac disease
In the cat, pleural effusion is very common before the radiographic image can begin to pro-
with only left-heart failure; this can be sepa- vide useful information. Table 2-2 summarizes the
rated from right-heart failure by the absence of radiographic signs associated with congenital and
accompanying hepatomegaly and ascites. acquired heart diseases. Awareness of noncardiac
and artifactual conditions that can present with the
same radiographic signs is also paramount to a cor-
s0640 Radiographic Diagnosis of rect diagnosis.
Pericardial Effusion
u0400 Generalized enlargement of cardiac silhouette in
s0660 Introduction to Digital
a basketball conformation, with elimination of
all normal cardiac margin contours on all views
p0240 Increased sternal contact of the cranial margin Digital radiography is a relatively new technology
and convex bulging of the caudal margin, without that is becoming common place in veterinary medi-
the angular conformation and straightening char- cine. It is been used in human medicine for over 20
acteristic for left atrial and ventricular enlarge- years and has been thoroughly tested and proven.
ments (Figure 2-19) There are many advantages to digital radiography
Elevation and enlargement of the caudal vena beyond the excellent image quality (Figure 2-20)
cava which include:
TABLE 2-2 Summary of Radiographic Signs of Congenital and Acquired Cardiac Disease

Lesion RA RV LA LV Aorta MPAs PAb PV VC Failure/Side Failure/Type

Congenital defects
Patent ductus arteriosus N In In In In In In In N/In Left Volume
Pulmonic stenosis In In N/De N/De N In N/De N/De In Right Pressure
Aortic stenosis N N/In N/In In In N N N/In N Left Pressure
Ventricular septal defect N In In In N N/In In In N/In Left Volume
Tetralogy of Fallot N/In In N/De N/De N De/N/In De De N Right Pressure
Atrial septal defect In In N/In N N N/In N/In N/In N/In Left Volume
Acquired heart disease
Mital insufficiency N N/In In In N N N In N Left Fluid
Tricuspid insufficiency In In N N N N N N In Right Fluid
Aortic insufficiency N N In In N/In N N In N Left Fluid
Hypertrophic cardiomyopathy In In In In N N N/In N/In N/In Left>Right Myocardial
Dilated cardiomyopathy In In In In N N N/In N/In N/In Right>Left Myocardial
Pericardial effusion In In In In N N N/De N/De In Right Tamponade

RA, Right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; MPAs, main pulmonary artery segement; PAb, pulmonary artery branches; PV, Pulmonary vein; VC, caudal vena cava;
In, enlarged or increased; De, smaller or decreased; N, normal.
Chapter 2 Radiology of the Heart
44 Section I Diagnosis of Heart Disease

Figure 2-20. Right lateral view of the thorax taken with a flat panel detector system (DR). Note that all structures (bone, lung,
pulmonary vessels, spine, etc) are visible in the same image. There are no areas of overexposure or underexposure.

Other devices such as film scanners and digital

cameras can be used to digitize conventional
x-ray film that allows the image to be stored on a
computer. Once the image is acquired and stored
it can be manipulated by the user to taste.
There are financial savings over time including:
No cost for radiology disposable (film, chemi-
No expense for processor maintenance, film
jackets and storage space
Perhaps the most significant means of recoup-
ing revenue pertains to the fact there will be a
significant reduction in the number of retakes
because there should be little to no need to re-
take images due to under or overexposure.
Flat panel technology (also known as digital
f0210 radiography [DR] or direct digital radiography
Figure 2-21. Flat panel detector (DR plate) made by Can-
[DDR] [Figure 2-21]) is the most expensive form
on (CXDI-50G). This plate is mounted out of sight under of digital radiography; however, this technol-
the x-ray table top in the location of the Bucky tray. The plate ogy results in the highest quality image. These
converts x-ray photon energy to an electrical pulse which is systems consist of a DR plate that is physically
then interfaced with an acquisition station computer.
mounted in the area of the Bucky tray under the
x-ray table top. The plate is then electronically
interfaced to both the x-ray machine and a dedi-
u0410 No lost films cated computer (acquisition station). Of the three
No film degradation over time forms of digital radiography, DR systems are ex-
The ability to view images on any networked tremely forgiving as far as technique (kVp and
computer at your clinic or home mAs settings) (Figure 2-22). This in turn simpli-
The ability to easily send images to specialists fies a typical technique chart to essentially three
for consultation or four settings (small, medium, large and extra
There are several types of digital acquisition sys- large) no matter if you are imaging bone, tho-
tems, including flat panel radiology, computed rax, or abdomen. Another advantage of DR sys-
radiography, and charge-coupled device systems. tems include extremely quick image time (3 to 8
Chapter 2 Radiology of the Heart 45

Figure 2-22. Technique independence. These three exposures were made with different mAs settings and identical kVp (90). A,
1.8 mAs. B, 2.5 mAs. C, 5.0 mAs. Note that all three exposures appear similar and are diagnostic. The computer software corrects
for under or overexposure automatically. This decreased the number of retakes and increases productivity. On the other hand, if
image A is magnified, it will appear much grainier than the other images.
46 Section I Diagnosis of Heart Disease

seconds before the image is seen on a computer

monitor) which allows the user to either save or
delete the image immediately if it is not satisfac-
tory (rotated, crooked, etc).
Computed radiography (CR) systems use im-
aging plates that resemble traditional x-ray
cassettes. The major difference is that the in-
tensifying screen and film within the cassette is
replaced by a flexible phosphor plate that has
the ability to store a latent image. These storage
phosphor plates operate similarly to the screen
inside a conventional cassette in that they emit
light (scintillate) in response to incident x-ray en-
ergy. However, unlike an x-ray screen, a storage
phosphor plate retains a portion of the energy as
a latent image, which is extracted (read out) by
a CR reader. In general, the image quality from a
CR system is very high (similar to that of DR);
however, CR is typically less forgiving as far as
technique (compared to DR) which necessitates
a more complicated technique chart. The image
time for most CR systems range from about 55 to
90 seconds. CR systems are less expensive than
DR systems, however.
Charge-coupled device systems consist of a phos- f0230
phor storage plate mounted under the x-ray table Figure 2-23. Dedicated x-ray film scanner (Vidar Sierra). An
top that is in turn interfaced with a small light x-ray film is fed into the machine, and it is converted to a
sensitive chip (CCD chip) similar to that found in digital image that can be stored on a computer.

digital cameras and video cameras. These CCD

chips are commonly about 2 cm in size and may of significant grey scale data. Because of this
have thousands of individual light sensitive ele- fact, the use of film scanners and digital cameras
ments on them. Because of the small size of the are not recommended as a means of sending im-
chips, the aerial image (14 17, etc.) must be ages for consultation (teleradiology).
minified down to the size of the CCD chip. This
is usually accomplished using a series of mirrors
and lenses, which unfortunately results in a sig-
nificant loss (90%) of the photon data. This loss
of data can often make the resultant image appear b0030 Key Points
grainy or pixilated on the computer monitor Digital Radiography (DR) is extremely fast,
which is accentuated if the image is electroni- is technique independent, has the highest
cally magnified. On the other hand, CCD systems image quality but is the most expensive
have fast image time (similar to DR systems) and method.
are less expensive than DR systems. Because Computed Radiography (CR) is slower, is
of the nature of these systems, they are usually somewhere between conventional film-
sold as a complete system that includes the x-ray screen technology and DR as far as reliance
machine. on x-ray technique, has high image quality,
Dedicated x-ray film scanners (Figure 2-23) and and is moderately expensive.
digital cameras are not forms of digital radiogra- Charged Coupled Devices (CCD) systems
are fast, are similar to CR systems as far as
phy. Both of these methods only reproduce the
technical factors, have the poorest image
traditional hard copy radiograph, and in gen- quality, and are the least expensive.
eral do a poor job of image reproduction. Even Film scanners and digital cameras are not
expensive multi-megapixel digital cameras now forms of digital radiography and have a lim-
available do a poor job of converting an analog ited role.
xray image into a digital format without the loss
Chapter 2 Radiology of the Heart 47

for free) and they do not need to have specific

Introduction to s0670
GE software to view the images. DICOM allows
the practicing veterinarian to send non-lossy,
Teleradiology (telemedicine) offers the practi- high-quality images that incorporate patient data p0250
tioner quick access to board certified special- directly to any radiologist of their choosing. Al-
ists for case consultation. Once the radiographic though DICOM compliance initially met with
images are in a digital format, they can be sent resistance (mostly from vendors), it has become
to any specialist for review via the World Wide common place in veterinary medicine and will
Web. There are several methods of accomplish- continue to flourish.
ing this including using dedicated teleradiology
companies, emailing images directly to special- Frequently Asked Questions b0040
ists, or by using DICOM.
At this time, there are four or five companies in A Weimaraner dog is being anesthetized. Because of u0420
the United States that cater to veterinary telemed- a murmur and mild coughing episodes, the heart and
especially lung fields are of interest. The DV radio-
icine. In general, these companies provide the graph is not too light, and not too dark. This judgment
necessary software that allows the veterinarian is determined by the:
to upload digital images to the companys server 1. Inability to see the bony column details (very
and they in turn send those images to affiliated white), but a light (white) appearance of the lung
radiologists, internists, etc. The referring practice fields to increase detail visualization there.
pays a fee to the teleradiology company which 2. Ability to see the outline of the heart clearly
in turn pays the specialists to read their images. against the lungs.
3. Ability to see the thoracic vertebrae in the area
The disadvantage of this type of service is that where they overlap the cardiac silhouette.
the referring veterinarian often pays a premium 4. The appearance of the lungs as a dark air densi-
fee (more than they would pay if they could send ty, and full visualization of the bony structures.
the images directly to the specialist), they may The most correct answer is #3. This indicates
not have any or little input on exactly which spe- the appropriate technique. The first option indi-
cialist their images are sent to and they may have cates that this is too light a technique. This is com-
little ability to directly communicate with that mon where the technique has not been adjusted in
obese patients. In #2, seeing the outline of the heart
specialist. clearly against the lungs is not necessarily associ-
Submission of images via standard email can be ated with technique, but may be due to pathology in
simple, but it is not recommended. Because of the area. The #4 answer is burning through the soft
the very large image size of digital radiographs tissues and is not appropriate for heart and lung stud-
(a 14 17 radiograph of the thorax can be 14 ies.
megabytes of information) these images must be A new digital radiography system has just been in-
compressed or saved in a lossy format (such as stalled. The practice has opted for the flat panel tech-
nology. It does not appear that the image is different
jpg) before emailing, thus making the transmit- even when thin, obese or barrel shaped dogs are im-
ted image of poor quality. Also, in the authors aged using the same settings. This means:
experience, these images are often submitted 1. Further staff training is needed.
with a lack of necessary patient information and 2. This is normalonly four basic settings will be
history. needed with digital radiography, and that is why
DICOM (Digital Image Communication in Med- we chose the system!
icine) is a proven and world wide recognized 3. The chart needs to be evolved further, because
something must be wrong if the same setting
method of transmitting high-quality, lossless, dig- works for a large range of animals.
ital radiographs (and other medical images such 4. The equipment is working better than prom-
as ultrasound) from one place to another. DICOM ised.
images are embedded with very specific informa- Answer #2 is most correct. Answer #1 is not probably
tion regarding patient data as well as the type an issue because this is the most forgiving of the im-
of system that the images were acquired on and aging systems, digital or traditional.
this information cannot be altered. Also, DICOM Answer #3 is not relevant because only three or
four settings will capture all dog breeds and body
allows transmission of images without the need condition scores. Answer #4 is normal for this system.
for proprietary software that is vendor specific. Though most expensive, this digital radiography sys-
For example, if you have a GE brand ultrasound tem is known to be the most forgiving and is known
machine, the images can be read by any radiolo- to produce the highest quality images.
gist with a DICOM viewer (which can be found
48 Section I Diagnosis of Heart Disease

s0680 Suggested Readings

The thoracic radiographs for this patient are not
easily interpreted so the plan is to: Animal Insides. http://www.animalinsides.com (accessed
1. Take another view and use foam supports to help October, 2006).
stabilize the body in a fully vertical position, to Buchanan JW, Bucheler J: Vertebral scale system to mea-
ensure sternum and spine are superimposed sure canine heart size in radiographs. J Am Vet Med
which gives a better image. This still does not Assoc 206:194-199, 1995.
provide a clear answer, so no significant find- Bushberg JT, Seibert JA, Leidholdt EM, et al: The essen-
ings is placed on the medical record, assuming tial physics of medical imaging, Philadelphia, 2002,
that the standard of care has been met due to Lippincott, Williams & Wilkins.
acquisition of the best possible radiographs. Ettinger SJ, Suter PF: Canine cardiology. Philadelphia,
2. Follow the steps in answer #1 and send a jpg to 1970, WB Saunders.
the telemedicine group for a radiologist opinion. Kittleson MD, Kienle RD: Small animal cardiovascular
3. Follow the steps in answer #1 and send a DI- medicine. St Louis, 1998, Mosby.
COM image to the telemedicine group for a Lord PF, Suter PF: Radiology. In Fox PR, Sisson D, Moi-
radiologists opinion. use NS, eds: Textbook of canine and feline cardiol-
Answer #3 is the best option as a lossless format, ogy. ed 2, Philadelphia, 1999, WB Saunders.
and an expert opinion will provide best practices Matton JS: Digital radiography, Vet Comp Orthop Trau-
here. Answer #2 is going to degrade the imageif
matol, 19:123-132, 2006.
an important detail is lost during image compression,
Owens JM: Radiographic interpretation for the small ani-
it could compromise patient care. #1 is a good first
mal clinician, St Louis, 1982, Ralston Purina Co.
step, but if the attending clinician does not have a
confident interpretation, then use of a specialist will
provide the gold standard for care. Generalist prac-
titioners cannot be the master of all trades, and with
the ability to transmit high-quality images of reason-
able size, questionable interpretations for radiographs
should always be referred for a specialist evaluation
via telemedicine.
Chapter 3

Larry P. Tilley and Francis W. K. Smith, Jr.

s tatus of the patient. An electrocardiogram should

be recorded in animals with significant heart
Electrocardiography in clinical practice is the disease.
recording at the body surface of electrical fields gen The electrocardiogram is also used to monitor
erated by the heart. Specific waveforms represent efficacy of antiarrhythmic therapy and to deter
stages of myocardial depolarization and repolar mine whether arrhythmias may have developed
ization. The electrocardiogram is a basic and valu secondary to cardiac medications (e.g., digoxin).
able diagnostic test in veterinary medicine and is Significant arrhythmias may also occur in ani
relatively easy to acquire. The electrocardiogram is mals with systemic disease, including those dis
the initial test of choice in the diagnosis of cardiac eases associated with electrolyte abnormalities
arrhythmias and may also yield information regard (hyperkalemia, hyponatremia, hypercalcemia, and
ing chamber dilation and hypertrophy. hypocalcemia), neoplasia (particularly splenic
neoplasia), gastric dilatation-volvulus, and sepsis.

Indications and Role of

Assessment of Chamber
The Electrocardiogram
Enlargement Patterns
in Clinical Practice
Changes in waveforms may provide indirect evi
Documentation of Cardiac Arrhythmias
dence of cardiac chamber enlargement. The electro
An electrocardiogram should be recorded when cardiogram may be normal, however, in cases with
an arrhythmia is detected during physical exami chamber enlargement. Right ventricular hypertro
nation. This may include bradycardia, tachycar phy most consistently results in waveform changes.
dia, or irregularity in rhythm that is not secondary As heart disease progresses, waveform changes
to respiratory sinus arrhythmia. may indicate progressive chamber enlargement.
Animals presenting with a history of syncope or Thoracic radiography and, ideally, echocardiog
episodic weakness may have cardiac arrhythmias, raphy, should be performed for definitive assess
and an electrocardiogram is indicated in these ment of chamber enlargement.
cases. Arrhythmias in such cases may be tran
sienta normal electrocardiogram does not rule
Miscellaneous Indications
out transient arrhythmias. In some cases, long-
for Electrocardiography
term electrocardiographic monitoring (Holter
monitor or cardiac event recorder) is warranted. The electrocardiogram may provide evidence of
Arrhythmias often accompany significant heart pericardial effusion (electrical alternans, low-am
disease and may significantly affect the clinical plitude complexes).
50 Section I Diagnosis of Heart Disease

Electrocardiographic abnormalities are often pres A positive electrode is placed on the left side of the
ent with hypothyroidism and hyperthyroidism. chest, over the heart, and the negative electrode is
A pronounced sinus arrhythmia may be present placed in the area of the right shoulder or neck.
in animals with elevated vagal tone (often seen Esophageal ECG electrode lead for surgical mon
with diseases affecting the respiratory tract, cen itoring (Figure 3-3.) This technique is very use
tral nervous system, and gastrointestinal tract). ful as complexes recorded are increased in size,
providing an increased accuracy for diagnosing
an arrhythmia during surgery.
Principles of Hand-held, wireless ECG and ECG real time
Electrocardiography computer display represents new technology for
recording electrocardiograms (Figures 3-4 and
Surface Electrodes are Placed in a
Designated Fashion to Obtain Standard
Electrocardiographic Leads
Recording The
A lead consists of the electrical activity mea
sured between a positive electrode and a negative
electrode. The electrocardiogram should be recorded in an
Electrical impulses with a net direction toward area as quiet and as free of distraction as possible.
the positive electrode will generate a positive Noises from clinical activity and other animals
waveform or deflection. Electrical impulses with may significantly affect rate and rhythm. Any
a net direction away from the positive electrode use of electrically operated equipment, such as
will generate a negative waveform or deflection. clippers, may cause interference and should be
Electrical impulses with a net direction perpen minimized during the electrocardiogram. In some
dicular to the positive electrode will not generate cases, fluorescent lighting may result in electrical
a waveform or deflection (isoelectric). interference.
Standard electrocardiographic lead systems are The patient should ideally be placed in right lat
used to create several angles of assessment. A sin eral recumbency.
gle lead would provide information on only one Electrocardiographic reference values were
dimension of the current (e.g., left vs. right). Two obtained from animals in right lateral recumbency.
leads would allow two-dimensional information Limbs should be held perpendicular to the
(e.g., left vs. right and cranial vs. caudal). As many body. Each pair of limbs should be held paral
as 12 leads may be acquired simultaneously. lel, and limbs should not be allowed to contact
one another.
The animal should be held as still as possible
Standard Lead Systems
during the electrocardiogram. When possible,
The standard leads are I, II, III, aVR, aVL, and aVF panting should be prevented.
(Figure 3-1, Box 3-1). Placement of electrodes to When dyspnea or other factors prevent stan
generate each lead is illustrated in Figure 3-2. dard positioning, the electrocardiogram may be
Leads I, II, and III are bipolar limb leads. These recorded while the animal is standing, or, less
are termed bipolar because the electrocardiogram ideally, sitting.
is recorded from two specific electrodes. Electrode placement
Leads aVR, aVL, and aVF are augmented unipolar Alligator clips or adhesive electrodes may be
leads. To generate these, two electrodes are elec used. To reduce discomfort, teeth of alligator
trically connected (as a negative electrode) and clips should be blunted and the spring should
compared with the single electrode (positive). be relaxed.
Precordial chest leads are obtained using an explor Limb electrodes are placed either distal or prox
ing unipolar positive electrode at specific locations imal to the elbow (caudal surface) and over the
on the chest. These leads may provide additional stifle. Electrodes placed proximal to the elbow
information or supportive evidence of cardiac cham may increase respiratory artifact.
ber enlargement. They are also useful in evaluating Each electrode should be wetted with 70 % iso
for the P wave when limb leads are equivocal. propyl alcohol to ensure electrical contact.
The base-apex lead is often used in equine Recording the electrocardiogram
electrocardiography and may also be used in Approximately three to four complete complexes
small-animal practice for rhythm assessment. should be recorded from each lead at 50mm/s.
Chapter 3 Electrocardiography 51

Figure 3-1. The limb leads (I, II, III, aVR, aVL, aVF) surround the heart in the frontal plane as shown in the top part of the
figure (feline). The circled limb lead names indicate the direction of electrical activity if the QRS is positive in that lead. The
mean electrical axis in this canine ECG (bottom part of the figure) is +90. Lead I is isoelectric. The lead perpendicular to lead I
is aVF (see axis chart on top). Lead aVF is positive, making the axis +90. If lead aVF had been negative, the axis would have
been90. (From Tilley LP: Essentials of canine and feline electrocardiography. ed 3, Malvern, Penn: 1992, Lea & Febiger.)

A lead II rhythm strip should then be recorded

at 25mm/s or 50mm/s.
Cardiac Conduction and
Genesis of Waveforms
The function of the cardiac conduction system
Key Point is to coordinate the contraction and relaxation of
The 1 mV standardization marker should be re the four cardiac chambers (Figures 3-6 and 3-7).
corded at the onset of the electrocardiogram For each cardiac cycle, the initial impulse originates
and any time the sensitivity is changed. in the sinoatrial (SA) node located in the wall of the
right atrium near the entrance of the cranial vena
52 Section I Diagnosis of Heart Disease

Box 3-1 Lead Systems Used in Canine and

prominent QRS complex and causes ventricular
Feline Electrocardiography contraction.
The Q wave represents initial depolarization
Bipolar limb leads of the interventricular septum and is defined
I: Right thoracic limb () compared with left tho as the first negative deflection following the
racic limb (+) P wave and occurring before the R wave. A
II: Right thoracic limb () compared with left pelvic Q wave may not be identified in all animals.
limb (+) The R wave represents depolarization of the
III: Left thoracic limb () compared with left pelvic
ventricular myocardium from the endocardial
limb (+)
surface to the epicardial surface. The R wave is
Augmented unipolar limb leads the first positive deflection following the P wave
aVR: Right thoracic limb (+) compared with average
and is usually the most prominent waveform.
voltage of left thoracic limb and left pelvic limb ()
aVL: Left thoracic limb (+) compared with average The S wave represents depolarization of the
voltage of right thoracic limb and left pelvic limb () basal sections of the ventricular posterior wall
aVF: Left pelvic limb (+) compared with average voltage and interventricular septum. The S wave is
of right thoracic limb and left thoracic limb () defined as the first negative deflection following
Unipolar precordial chest leads plus exploring the R wave in the QRS complex.
electrode Ventricular repolarization quickly follows ven
CV5RL (rV2): Right fifth intercostal space near the tricular depolarization and results in the T wave.
sternum The delay in repolarization results in the ST seg
CV6LL (V2): Left sixth intercostal space near the sternum ment on the surface electrocardiogram.
CV6LU (V4): Left sixth intercostal space near the
costochondral junction
V10: Over the dorsal process of the seventh thoracic Evaluation of The
vertebra Electrocardiogram
Base-apex bipolar lead
Record in lead I position on ECG machine with leads The electrocardiogram should be evaluated from
placed as follows left to right.
LA electrode over left sixth intercostal space at Areas of artifact should be identified and avoided
costosternal junction in the evaluation.
RA electrode over spine of right scapula near the Calculate the heart rate.
vertebra Determine the number of R waves (or R-R inter
vals) within 3 seconds and multiply by 20 to obtain
beats per minute (bpm) (for an electrocardiogram
cava. This impulse is rapidly propagated through recorded at 50mm/s, vertical timing marks above
the atrial myocardium, resulting in depolarization the gridlines occur every 1.5 seconds).
of the atria. Depolarization of the atria results in the If the rhythm is regular, the heart rate may be
P wave and atrial contraction. The initial SA nodal derived by determining the number of small boxes
impulse is small and does not produce an electro in one R-R interval and dividing 3000 by that
cardiographic change on the bodys surface. number (for paper speed of 25mm/s, use 1500).
Immediately after atrial depolarization, the im The method is also useful for determining the
pulse travels through the atrioventricular (AV) rate of paroxysmal ventricular tachycardia and
node, located near the base of the right atrium. other arrhythmias lasting less than 3 seconds.
Conduction is slow here, which allows atrial con Obtain measurements for the waveforms and
traction to be completed before ventricular depo intervals (Figure 3-8).
larization occurs. As the impulse travels through P wave height and width
the AV node, there is no electrocardiographic ac Duration of PR interval
tivity on the bodys surfacerather the PR inter Duration of QRS complex and height of R wave
val is generated. Duration of QT segment
Upon leaving the AV node, conduction velocity Determine the approximate mean electrical axis
increases significantly, and the impulse is rapidly (MEA)
spread through the bundle of His, bundle branches, The MEA refers to the direction of the net
and Purkinje system. This results in rapid and nearly ventricular depolarization and refers solely
simultaneous depolarization of the ventricles. to the QRS complex. If there is significant
Depolarization of the ventricles results in the right ventricular hypertrophy, then the MEA
Chapter 3 Electrocardiography 53

Figure 3-2. A, Three bipolar standard leads. By means of a switch incorporated in the instrument, the galvanometer can be
connected across any pair of several electrodes. Each pair of electrodes is called a lead. The leads illustrated here are identified as
I, II, and III. B, Augmented unipolar limb leads aVR, aVL, and aVF. (From Tilley LP: Essentials of canine and feline electrocardio
graphy: interpretation and treatment, ed 3, Malvern, Penn, 1992, Lea & Febiger.)

will shift to the right. Because the left ven The MEA may be determined using the six stan
tricle is normally the dominant ventricle, the dard leads and the Bailey axis system (see Figure
normal MEA is to the left. A degree system is 3-1). If there is a lead with isoelectric QRS com
usedif the MEA is directly to the left, then it plexes, then the MEA equates to the lead on the
is said to be 0 degrees; if the MEA is directly Bailey axis perpendicular to the isoelectric lead.
downward, then it is 90 degrees, and if it is The MEA may also be determined by plotting
directly to the right, then it is 180 degrees. The the net amplitude of a lead I QRS complex (hori
MEA of the normal dog is 40 to 100 degrees. zontal axis) and the net amplitude of a lead aVF
For the cat, the MEA is more variable, ranging QRS (vertical axis). The intersection will provide
from 0 to 160 degrees. the vector equal to the MEA (see Figure 3-1).
54 Section I Diagnosis of Heart Disease

Figure 3-3. Esophageal ECG electrode and temperature probe positioned for surgical monitoring. This technique is very useful as
complexes recorded are increased in size, providing an increased accuracy for diagnosing an arrhythmia during surgery.

Evaluation of Waveforms
P Wave
Atrial enlargement patterns (Figure 3-9)
The P wave is generated by atrial depolarization.
Atrial enlargement may result in an increase in
width or height of the P waves recorded in leadII.
Enlargement of the right atrium may result in an
increased P wave height. This is referred to as P-
pulmonale. The height of the P wave should not
exceed 0.4 mV (dog) or 0.2 mV (cat). Chronic pul
monary disease may result in P-pulmonale in the
absence of heart disease.
Figure 3-4. Hand-held, wireless ECG and ECG real time Enlargement of the left atrium may result in
computer display. (Courtesy Vmed Technology, Redmond, an increased P wave width or duration. This
Wash. www.vmedtech.com.) is referred to as P-mitrale. The duration of the
P wave should not exceed 0.04 second (dog or
cat). Left atrial enlargement may also result in
The MEA may be approximated by inspecting notching of the P wave.
leads I and aVF. Presence or absence of P waves
If the net direction of the lead I QRS is posi There is no minimum height or duration forthe P
tive, then the MEA is to the left. If the net wave. In some cases, P waves maybeindistinct.
deflection of the lead I QRS is negative, then In this situation, carefully evaluate all leads for P
the MEA is to the right. wave activity. If P waves cannot be discerned in
If the net direction of the lead aVF QRS is pos any of the limb leads, evaluation of chest leads is
itive, then the MEA is downward or caudal. If recommended.
the net deflection of the lead aVF QRS is nega P waves may be absent in several arrhythmias,
tive, then the MEA is upward or cranial. including atrial fibrillation and atrial standstill.
The approximate angle can be estimated by P waves may be superimposed on other wave
examining the relative amplitudes of leads I forms in ventricular tachycardia and supraven
and aVF. tricular tachycardia (SVT).
Determine the rhythm. Variation of P wave height is a normal finding
Compare patient values with reference values in the dog and a manifestation of alterations in
(Table 3-1). vagal tone.
Chapter 3 Electrocardiography 55

Figure 3-5. Wireless ECG printout report from laptop computer software system in Figure 3-4. (Courtesy Vmed Technology,
Redmond, Wash. www.vmedtech.com.)

A significantly shortened PR interval may occur

when an accessory pathway allows conduction to
bypass the AV node.
posterior Prolongation of the PR interval represents first
A-V fascicle degree AV block.
Variation of the PR interval may occur with alter
ations in vagal tone or secondary to the presence
anterior of ectopic beats causing dissociation of atrial and
Bundle ventricular activity.
of His
QRS Complex
The QRS complex is generated by ventricu
Right Purkinje
bundle fibers lar depolarization (left ventricle, interventri
branch cularseptum, and right ventricle). Ventricular
enlargement may result in changes in the QRS
Figure 3-6. Anatomy of the cardiac conduction system. S-A,
Sinoatrial; A-V, atrioventricular. (Modified from Tilley LP: Es
sentials of canine and feline electrocardiography: interpretation Left ventricular enlargement pattern
and treatment, ed 2, Philadelphia, 1985, Lea & Febiger.) Increased amplitude of the R wave
Amplitude of R wave greater than 3.0 mV
PR Interval (2.5 mV in small-breed dogs) in leads II,
The PR interval reflects the slowed conduction aVF, and the precordial chest leads CV6LU,
through the AV node. The normal PR interval is CV6LL and CV5RL
0.06 to 0.13 second for dogs and 0.05 to 0.09 Amplitude of R wave greater than 1.5 mV
second for cats. in lead I
56 Section I Diagnosis of Heart Disease




Positive RBB
electrode P


Figure 3-7. Sequence of electrical impulse conduction and cardiac chamber activation as it relates to the electrocardiogram.
(Modified from Tilley LP: Essentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Philadelphia, 1992,
Lea & Febiger.)

Figure 3-8. Close-up of a normal feline lead II P-QRS-T complex with labels and intervals. Measurements for amplitude (mil
livolts) are indicated by positive (+) and negative () movement; time intervals (hundredths of a second) are indicated from left
to right. Paper speed, 50 mm/s; sensitivity 1 cm=1 mV. (From Tilley LP: Essentials of canine and feline electrocardiography:
interpretation and treatment, ed 2, Philadelphia, 1985, Lea & Febiger.)
Chapter 3 Electrocardiography 57

Table 3-1 Normal Canine and Feline ECG Values*

Canine Feline
Heart rate (HR) Puppy: 70-220 bpm 120-240 bpm
Toy breeds: 70-180 bpm
Standard: 70-160 bpm
Giant breeds: 60-140 bpm
Rhythm Sinus rhythm Sinus rhythm
Sinus arrhythmia
Wandering pacemaker
P wave
Height Maximum: 0.4 mV Maximum: 0.2 mV
Width Maximum: 0.04 s (Giant breeds 0.05 s) Maximum: 0.04 s
PR interval 0.06-0.13 s 0.05-0.09 s
Height Large breeds: 3.0 mV maximum Maximum: 0.9 mV
Small breeds: 2.5 mV maximum
Width Large breeds: 0.06 s maximum Maximum: 0.04 s
Small breeds: 0.05 s maximum
ST segment
Depression No more than 0.2 mV None
Elevation No more than 0.15 mV None
QT interval 0.15-0.25 s at normal HR 0.12-0.18 s at normal HR
T waves May be positive, negative, or biphasic usually positive and<0.3 mV
Amplitude range0.05-1.0 mV in
any lead
Not more than of R wave
Electrical axis +40 to + 100 0160
Chest leads
CV5RL (rV2) T positive; R<3.0 mV
CV6LL (v2) S<0.8 mV; R<3.0 mV R<1.0 mV
CV6LU (V4) S<0.7 mV; R<3.0 mV R<1.0 mV
V10 QRS negative; T negative except in T negative. R wave/Q wave<1

*Measurements are made in lead II unless otherwise stated.
Not valid for thin, deep-chested dogs under 2 years old.

Sum of R wave amplitudes in leads I and R wave/Q wave>1.0 in lead V10

aVF greater than 4.0 mV QRS duration greater than 0.06 second (large
Cat dogs), 0.05 second (small dogs), or 0.04 second
Amplitude of R wave greater than 0.9 mV (cats)
in lead II ST slurring or coving
Amplitude of R wave greater than 1.0 mV Shift in the MEA to the left (less than 40
in CV6LU and CV6LL degrees for dog, less than 0 degrees for cat)
58 Section I Diagnosis of Heart Disease

Right ventricular enlargement pattern (Figure S wave in lead I>0.05 mV

3-10) S wave in lead II>0.35 mV
Increased amplitude of S waves S wave in lead CV6LL>0.8 mV
Dog S wave in lead CV6LU>0.7 mV
Presence of S waves in leads I, II, III, and Cat
aVF Presence of S waves in leads I, II, III, and
Prominent S waves in CV6LU and CV6LL
T wave positive in lead V10 (except
W-shaped QRS complex in V10 (dog)
R:S ratio<0.87 in CV6LU
Shift in the MEA to the right (more than
100 degrees for the dog or more than 160
degrees for the cat)
Widening of the QRS complexes may occur with
left ventricular enlargement, right or left bundle
branch block (LBBB), and complexes of ven
tricular origin (ventricular premature complexes
[VPCs] or ventricular escape complexes).
Electrical alternans (Figure 3-11, A)
In electrical alternans, there is a pattern of
regular variation in the amplitude of normal
electrocardiographic complexes (excluding
ventricular ectopy). This is usually mani
B fested by an alteration in R wave height,
although variation in other waveforms
may be seen. The amplitude may change
significantly with every complex and alter
nate short-tall.
Electrical alternans is most often associated
with pericardial effusion. A severe pleural ef
Figure 3-9. A, Biatrial enlargement in a small-breed dog
with a collapsed trachea and compensated mitral regurgita
fusion may cause electrical alternans.
tion. The P wave is 0.5 mV tall (P pulmonale) and 0.05 sec SVT may result in an electrical alternans
wide (P mitrale). B, Left atrial enlargement in a geriatric, small- pattern.
breed dog with chronic acquired valvular disease (mitral in Low-amplitude QRS complexes
sufficiency). P waves are wide (0.075 second), notched, and
equivocally tall. (From Fox PR, Sisson D, Moise NS, eds: Text The minimum height for the normal R wave in
book of Canine and Feline Cardiology. Philadelphia, 1999, WB the dog is 0.05 mV to 1.0 mV.

Figure 3-10. Severe right ventricular enlargement in a dog with pulmonic stenosis. There is a right axis deviation of approxi
mately 110 degrees. Note the deep S waves in leads I, II, III, aVF, and CvsLU. The T wave is positive in V10. (From Tilley LP: Es
sentials of canine and feline electrocardiography: interpretation and treatment, ed 3, Philadelphia, 1992, Lea & Febiger.)

Chapter 3 Electrocardiography

Figure 3-11. A, Electrocardiogramelectrical alternans. B, ElectrocardiogramST segment elevation. C, ElectrocardiogramST segment depression.
Section I

Diagnosis of Heart Disease

Figure 3-11, contd. D, Electrocardiogramnormal sinus arrhythmia. E, Electrocardiogramsinus arrest. F, Electrocardiogramatrial premature complexes.

Figure 3-11, contd. G, Electrocardiogramatrial tachycardia. H, Electrocardiogramatrial fibrillation.

Chapter 3 Electrocardiography
62 Section I Diagnosis of Heart Disease

Low-amplitude R waves may occur when Box 3-2 Classification of Cardiac

transmission of the cardiac electrical impulse Arrhythmias
to the skin is hindered. This may occur with
pericardial effusion, pleural effusion, obesity, Normal sinus impulse formation
or subcutaneous edema. Pneumothorax and Normal sinus rhythm
pulmonary edema may also decrease R wave Sinus arrhythmia
height. Wandering sinus pacemaker
Hypothyroidism may result in low-amplitude R Disturbances of sinus impulse formation
Sinus arrest
waves (usually with accompanying slow rate).
Sinus bradycardia
Sinus tachycardia
ST Segment Disturbances of supraventricular impulse formation
ST segment elevation (Figure 3-11, B) Atrial premature complexes
Elevation of the ST segment greater than Atrial tachycardia
0.15 mV in leads II, III, or aVF is abnormal in Atrial flutter
the dog. Any ST segment elevation in the cat is Atrial fibrillation
Atrioventricular junctional rhythm
Disturbances of ventricular impulse formation
ST segment elevation may be caused by myo Ventricular premature complexes
cardial hypoxia, transmural myocardial infarc Ventricular tachycardia
tion, pericardial effusion, see pericarditis. In Ventricular asystole
cats, digoxin toxicity may cause ST segment Ventricular fibrillation
elevation. Disturbances of impulse conduction
ST segment depression (Figure 3-11, C) Sinoatrial block
Persistent atrial standstill (silent atrium)
Depression of the ST segment greater than 0.2
Atrial standstill (hyperkalemia)
mV in leads II, III or aVF is abnormal in the Ventricular pre-excitation
dog. Any ST segment depression in the cat is First-degree AV block
abnormal. Second-degree AV block
ST segment depression may be caused by myo Complete AV block (third degree)
cardial hypoxia, hyperkalemia, hypokalemia, Bundle branch blocks
subendocardial myocardial infarction, or di Disturbances of both impulse formation and impulse
goxin toxicity.
Sick sinus syndrome
Pseudodepression due to prominent Ta waves Ventricular pre-excitation and the Wolff-Parkin
(atrial repolarization) caused by atrial disease or son-White (WPW) syndrome
tachycardia also causes ST segment depression. Atrial premature complexes with aberrant ventric
Miscellaneous ST segment changes ular conduction
ST segment changes may occur secondary to Escape rhythms
bundle branch blocks, myocardial hypertro Junctional escape rhythms
Ventricular escape rhythms (idioventricular rhythm)
phy, or VPCs. The changes in the ST seg
ment are in the opposite direction from the
main QRS deflection.
different sympathetic neurons that may or may
Key Point not be activated together. Corrections of the QT
Baseline artifact may mimic changes with the interval (QTc) for heart rate appear to be appli
ST segment. cable under circumstances, such as exercise.
Within the past two decades, the overall ven
tricular repolarization and its relationship to the
QT Interval QTc interval has led to studies for using the QTc
The normal QT interval is 0.15 to 0.25 second (dog) interval as a prognostic marker of ventricular
and 0.12 to 0.18 second (cat). The QT interval tends tachyarrhythmias and death. Class IA or class
to increase with slow heart rates and decrease with III antiarrhythmic drugs, such as quinidine and
rapid rates. In general, the QT interval should be sotalol, are known to prolong myocardial repolar
less than half of the preceding R-R interval. ization. This may either provide a protective effect
The length of the QT interval is chiefly determined against arrhythmias or lead to an increased occur
by an interplay of autonomic influences. Heart rence of QTc interval-related arrhythmias, includ
rate and QT interval are governed separately by ing torsade de pointes ventricular tachycardia.
Chapter 3 Electrocardiography 63

Torsades de pointes (turning about a point) is a not exceed one-fourth the height of the R wave,
rare arrhythmia in the dog. It is a form of poly one-fourth the height of the Q wave (if Q wave is
morphic ventricular tachycardia or flutter in greater than R wave), or 0.5 mV to 1.0 mV in any
which the amplitude of the complexes increases lead.
and decreases in size so that they appear to twist The T wave should be positive in CV5RL in dogs
around the baseline. Human patients with tors 2 months of age and should be negative in V10,
ades de pointes are at risk for sudden death. except in the Chihuahua.
Prominent T waves may occur with myocardial
Possible Formulas for Corrected QT intervals. hypoxia, interventricular conduction distur
Many formulas and methods for correcting the QT bances, ventricular enlargement, and in some ani
interval for the effects of heart rate, including log mals with heart disease and bradycardia.
arithmic, hyperbolic, and exponential functions, Prominent and peaked T waves are associated
but they also have limitations. These limitations with hyperkalemia.
result from both physiological and computational Small, biphasic T waves may occur with
problems. The Bazetts formula, for example, hypokalemia.
predicts an ever-increasing increment in the Nonspecific T wave changes may occur with
QT interval as the heart rate slows and an ever- metabolic disturbances (hypoglycemia, anemia,
decreasing increment as the rate rises, both of which shock, fever), drug toxicity (digoxin, quinidine,
are physiologically improbable. In addition, all procainamide), and neurologic disease.
these formulas do not account for the effects of T wave alternans has been reported second
autonomic tone on the QT interval independent ary to hypocalcemia, increased circulating cat
of the effects on rate. They also do not account for echolamines, and sudden increases in sympathetic
the relatively slow adaptation of repolarization to tone.
changes in rate. Fridericias formula (QT divided
by the cube root of the R-R interval) is a modi
fication of Bazetts formula. This modification is Arrhythmias and
important, because Bazetts formula will over Conduction Disturbances
correct for rates higher than 60 bpm. Van de Wa An arrhythmia (or dysrhythmia) refers to an
ter formula (study was done in dogs) involves irregularity in the cardiac rhythm. In general, an
regression analysis yielding the following equa arrhythmia denotes an abnormality of the car
tion: QTc=Van de Water formula=QT87(60/ diac rhythm, although in the dog the term normal
HR1). Recent publications have recommended sinus arrhythmia is used to describe the normal
the use of the log-log formula for correcting the variation in heart rate associated with respiration
QT interval for heart rate (Linear regression with (see Box 3-2).
logcHR as the covariate: QT=a + b (logcHR); Arrhythmias may be classified according to
a & b are constants). their origin.
Prolongation of the QT interval may occur with Supraventricular arrhythmias arise from the
interventricular conduction disturbances that atria or AV node.
are associated with prolongation of the QRS Ventricular arrhythmias arise from the
complexes, bradycardia, ethylene glycol toxic ventricles.
ity, strenuous activity, or CNS disturbances. QT Arrhythmias may be classified according to
prolongation has been reported with many drugs their rates.
and electrolyte imbalances. These include hypo Arrhythmias with slow rates are referred to as
kalemia, hypocalcemia, quinidine, procainamide, bradyarrhythmias.
bretylium, tricyclic antidepressants and many Arrhythmias with rapid rates are referred to
anesthetics. as tachyarrhythmias.
Shortening of the QT interval may occur with Arrhythmias may be classified according to
hypercalcemia, hyperkalemia, or digoxin therapy. their regularity.
Fibrillation is an irregular, chaotic rhythm.
Tachycardia is a regular (non irregular) rhythm.
T Wave
Examples: Atrial fibrillation is an irregular,
The T wave is quite variable in the dog and cat. chaotic arrhythmia originating from the atria;
In most leads, the T wave may be positive, nega ventricular tachycardia is a regular arrhythmia
tive or biphasic. The height of the T wave should originating from the ventricles.
64 Section I Diagnosis of Heart Disease

There are several pathophysiologic causes of Check for pauses in the rhythmperiods of
arrhythmias. inactivity greater than two R-R intervals.
Abnormal automaticity of normal pacemaker Check for P waves occurring prematurely
cells (occurring earlier than expected)distinguish
Shift of the pacemaker from the SA node to from normal sinus arrhythmia, where P wave
other areas of the heart rate increases during inspiration. Premature
Conduction blocks that terminate or slow nor P waves will noticeably break the rhythm. Pre
mal conduction through the heart mature P waves indicate the presence of atrial
Abnormal pathways of impulse conduction premature complexes (APCs).
through the heart Check for QRS complexes occurring prema
Spontaneous impulse formation in any area of turely. These may occur without preceding
the heart P wave, may be superimposed on P wave,
Systemic approach to arrhythmia recognition and or may follow P wave with shortened PR
evaluation interval. Premature QRS complexes indicate
Any lead may be used for arrhythmia evalua presence of VPCs.
tionlead II is generally used as waveforms
are usually best defined in this lead. A signifi
cant duration of artifact-free lead II should be
Key Point
carefully evaluated.
Determine if P waves are present. Examine all Remember, a ventricular premature complex
leadsP waves may be small or isoelectric in is premature. A ventricular complex occurring
several leads. You must distinguish baseline after a pause is not prematureit is a ven
tricular escape complex.
motion (artifact) from P waves. P waves are
generally consistent in size and distance from
associated QRS complex. The presence of
P waves indicates a sinus (originating from SA
node) rhythm. Evaluation of PR interval
D etermine if an atrial (P wave) and ven PR interval may vary slightly with changes in
tricular (QRS complex) association exists. vagal tonethis would also result in a sinus
There should be a P wave for every QRS arrhythmia.
complex. If there are a greater number of P Progressive prolongation of the PR interval
waves or QRS complexes, then an arrhyth signals first degree AV block.
mia exists. P waves without associated QRS complexes
P waves should slightly precede QRS are usually indicative of second degree AV
complexes. block
If P waves follow the QRS complex, then AV Shortened PR interval may be seen with
dissociation exists, and the rhythm is ventric increased sympathetic tone and pre-excitation
ular or junctional rather than sinus. syndromes (presence of accessory pathway
There should be a QRS complex following bypassing AV node).
each P wave. If not, then a conduction distur Evaluation of QRS complexes
bance is present. Height of R wave and duration of QRS complex
Determine the regularity of the rhythm. Presence of prominent S waves
Normal sinus rhythminsignificant (less Morphology of QRS complexes should not
than 10%) variation in the P-P or R-R vary significantly. Variation may be caused by:
intervals VPCs or ventricular escape complexes
Normal sinus arrhythmiasignificant (more Fusion beatssimultaneous occurrence of
than 10%) variation in the P-P or R-R VPC and normal QRS
intervals Electrical alternans
A pattern of irregularity is usually noted Intermittent bundle branch block
the heart rate increases during inspiration Artifact
and decreases during expiration in a cycli Premature QRS complexes suggest VPCs;
cal pattern. QRS complexes without P waves and oc
This may be referred to as a respiratory curring after a pause suggest ventricular
sinus arrhythmia. escape complexes.
Chapter 3 Electrocardiography 65

Note morphology of any premature com Key Point

plexesAPCs have a QRS of normal morphol
ogy; VPCs have a QRS that is significantly Sinus arrhythmia is NOT expected in the cat,
different from the normal QRS. but is normal, and the result of variations in
vagal tone in dogs.

Key Point
Disturbances of Sinus
QRS complexes should not vary in their mor
phology in a normal animal.
Impulse Formation
Sinus Arrest
When the SA node fails to discharge as expected,
Normal Rhythms a pause in the rhythm will occur. The duration
of the pause is at least twice the preceding R-R
Normal Sinus Rhythm interval. When severe, pause duration may be 5
Normal rhythm in the dog and cat to 12 seconds (Figure 3-11, E).
P wave for every QRS complex, regular rhythm For survival, the pause is ended by a ventricular
Rate between 60 bpm and 180 bpm for the dog, escape complex, junctional escape complex, or
depending on size of dog and degree of anxiousness normal complex.
Rate between 140 bpm and 240 bpm for the cat, Causes include fibrosis of the SA nodal tis
depending on degree of anxiousness sue, greatly increased vagal stimulation, drug
Rate and rhythm dependent on SA nodal dis influences (digoxin, beta blockers), and rarely
charge. This is highly influenced by changes in neoplasia.
autonomic tone. An elevated sympathetic tone If severe and frequent, intermittent weakness or
will increase rate of SA nodal discharge; an ele syncope may occur.
vated parasympathetic (vagal) tone will decrease
rate of SA nodal discharge. Sinus Bradycardia
A sinus rhythm with an abnormally slow rate
Normal Sinus Arrhythmia May be physiologicduring sleep, the heart rate
Normal in the dog, generally abnormal in the cat of many dogs drops to 30 to 40 bpm. Calm ani
A pattern of irregularity is presentthe heart mals or athletic animals at rest may have a physi
rateincreases during inspiration and decreases ologic sinus bradycardia.
during expiration in a cyclical pattern (Figure Elevated vagal tone may result in a sinus bradycardia.
3-11, D). Drug-inducedanesthetics and sedatives, di
Irregularity is secondary to fluctuations in vagal goxin, calcium channel blockers, beta blockers
tone associated with the respiratory cycle. Pathologichypothermia, hypothyroidism, sick
When respiratory effort is increased (brachyce sinus syndrome (SSS)
phalic breeds, animals with respiratory disease), Specific therapy for sinus bradycardia is not
fluctuations in vagal tone may be dramatic, pro warranted unless clinical signs (weakness,
ducing a pronounced sinus arrhythmia. reduced cardiac output) have developed as a
Normal sinus arrhythmia is a rhythm of high result of the arrhythmia.
vagal tone and low sympathetic tonethis situ
ation is rare in dogs with congestive heart failure. Sinus Tachycardia
The presence of a sinus arrhythmia in a dog with A sinus rhythm with an abnormally rapid rate
severe cough is more supportive of primary respira May be physiologicassociated with exercise,
tory disease rather than congestive heart failure. stress, anxiousness, pain
Drug-inducedatropine or glycopyrrolate,
Wandering Sinus Pacemaker methylxanthines (theophylline), excessive thyroid
The origin of SA nodal discharge may change as supplementation, catecholamines (epinephrine,
a consequence of alterations in vagal tone. This dobutamine)
is noted on the electrocardiogram as a cyclical Pathologicfever, shock, hyperthyroidism, ane
change in the height of the P wave. At times, the P mia, hypoxia, and congestive heart failure
wave may become isoelectric and not detectable. Specific therapy for sinus tachycardia is usually
Often associated with normal sinus arrhythmia or indicated for rate control in congestive heart fail
pronounced sinus arrhythmia. ure patients.
66 Section I Diagnosis of Heart Disease

Key Point May be clinically significant depending on rate,

frequency of runs, and length of runs
The underlying cause of the sinus tachycardia
should be identified and addressed if necessary.
Atrial Flutter
An uncommon arrhythmia characterized by
a rapid atrial rate (greater than 250 bpm) and
Disturbances of altered atrial depolarization resulting in bidirec
Supraventricular tional saw-toothed atrial complexes (F waves).
Impulse Formation Ventricular rate varies depending on refractori
ness of AV node.
Atrial Premature Complexes Usually a result of severe structural heart disease
An APC is an abnormal beat occurring prema Clinical significance depends on ventricu
turely and originating in atrial tissue lar rate. If excessive, then cardiac output is
Electrocardiographic features Figure 3-11, F reduced.
Presence or absence of ectopic P wave
P wave is usually of normal morphology Atrial Fibrillation
Ectopic P wave may be superimposed on pre A common arrhythmia in the dog characterized
ceding T wave. by lack of P waves, rapid ventricular rate, and
Premature QRS with identical or nearly iden irregularity of ventricular depolarizations. In atrial
tical appearance to normal QRS fibrillation, there are numerous sites of ectopic
A compensatory pause may follow the APC. atrial depolarization and varying AV nodal
If the APC occurs when the ventricles are refractoriness (Figure 3-11, H). Atrial fibrillation
refractory, then an isolated ectopic P wave is uncommon in the cat.
will be notedit is nonconducted owing to Baseline may be flat or may exhibit fine fibrilla
the refractoriness of the ventricles. tion potentials.
Causes generally include any disease associ Causes include
ated with atrial enlargement, such as degenera Structural heart disease (advanced degenerative
tive valve disease, congenital heart disease, or valve disease, dilated cardiomyopathy, atrial
cardiomyopathy. Other causes include hypoxia, neoplasia, congenital heart disease)
atrial neoplasia, and chronic obstructive pulmo Lone atrial fibrillationoccurs in large- to
nary disease. giant-breed dogs without structural heart disease
Therapy is not generally warranted for infre May occur as a complication of noncardiac
quent APCs. Antiarrhythmic therapy may be disease, such as gastric dilatation-volvulus or
needed if APCs are frequent and thought to other disorders altering vagal tone
be compromising cardiac output, or if there is May be drug-induced, for example, digoxin
a concern of impending atrial tachycardia or Clinical significance depends on ventricular rate
atrial fibrillation. in most cases. With atrial fibrillation there is also
loss of atrial contraction (atrial kick), which may
Atrial Tachycardia reduce ventricular performance. If the rate is not
A paroxysmal tachycardia originating from controlled, then lone atrial fibrillation may cause
atrial tissue ( other than SA node) myocardial deterioration and secondary dilated
Electrocardiographic features (Figure 3-11, G) cardiomyopathy.
Rapid ratefrom 200 to 350 bpm
Usually a regular rhythm. If originating from Junctional Premature Complexes
multiple atrial sites, then an irregular rhythm A junctional premature complex is an abnormal
may occur. beat occurring prematurely and originating in the
P waves may be difficult to discern. QRS AV nodal area.
complexes are generally normal but may Electrocardiographic characteristics include
widen, or electrical alternans may develop. abnormal-appearing P wave (often inverted), which
Sudden onset and sudden termination of may precede QRS, be superimposed on QRS,
arrhythmia or follow QRS complexes. The QRS complex is
May occur as a reentrant arrhythmia within usually unaffected.
the AV node Causes are the same as for APCs.
Causes are the same as for APCs. Clinical significance is the same as APCs.
Chapter 3 Electrocardiography 67

Atrioventricular Junctional Tachycardia node reaches the AV node by way of internodal

A paroxysmal or sustained rhythm originating fibers. Hyperkalemia also slows the rate of SA
from AV nodal tissue nodal discharge and affects ventricular depolar
Electrocardiographic features ization and repolarization.
Rate is greater than 60 bpm (inherent rate of Electrocardiographic characteristics of persistent
AV nodal tissue is approximately 40 bpm to 60 atrial standstill
bpm) Absence of P waves
A regular rhythm Heart rate usually slow (<60 bpm)
Abnormal appearing P wave (often inverted in Rhythm regular with supraventricular-appear
lead II), which may precede QRS, be superim ing QRS complexes
posed on QRS, or follow QRS complexes Heart rate does not increase with atropine ad
QRS complexes may be normal or may be wid ministration
ened secondary to aberrant conduction. Electrocardiographic characteristics of atrial
Causes include digoxin toxicity and structural standstill due to hyperkalemia (Figure 3-12, A)
heart disease As serum potassium increases, P wave ampli
May be clinically significant depending on ven tude diminishes. Absence of P waves occurs
tricular rate when the potassium approaches 8.0 mEq/L.
Slow ventricular ratethe rhythm is termed
Supraventricular Tachycardia sinoventricular, and the rate is approximately
SVT refers to a rapid arrhythmia originating from 20 to 40 bpm.
supraventricular tissue, but in which the exact As serum potassium increases, T wave ampli
site of origin cannot be determined. Atrial tachy tude increases and becomes peaked.
cardia and AV junctional tachycardia are often QRS duration progressively increases and R
indistinguishable, so the term SVT may be more wave height decreases as serum potassium lev
precise in these cases. els increase.
Heart rate may increase slightly with atropine
Key Point
Causes of hyperkalemia include hypoadre
AV junctional tachycardia may be difficult to nocorticism, anuric or oliguric renal failure,
distinguish from atrial tachycardia uncontrolled diabetic ketoacidosis, metabolic
acidosis, urethral obstruction, rupture of the
urinary bladder.
Disturbances of Impulse
Sinus Block Key Point
The SA node discharges normally, but the Atrial standstill due to hyperkalemia is usually
impulse is blocked by neighboring tissue. life threatening.
Produces a pause equal to twice the preceding
R-R interval, with immediate restoration of rhythm
Causes are the same as for sinus arrest Ventricular Pre-Excitation Syndrome
Usually not clinically significant In these syndromes, an abnormal accessory path
way exists, which bypasses the AV node. This
Atrial Standstill results in a shortening or loss of the PR interval due
Atrial standstill is characterized by an absence of P to premature activation of the ventricles. With an
waves and can be temporary in nature or persistent. accessory pathway, there are two electrical connec
The most common cause of temporary atrial stand tions between the atria and the ventricles, and both
still is hyperkalemia. Persistent atrial standstill is due may simultaneously be relaying impulses. There
to an atrial muscular dystrophy, most commonly also exists the potential for reentry as the impulse
occurring in English Springer Spaniels. may leave the atria through one pathway and
In atrial standstill due to hyperkalemia, SA immediately reenter through the other. The accessory
nodal discharge occurs, but atrial depolarization pathway may connect the atria to the distal AV node,
is blocked by the effects of hyperkalemia. As bundle of His, or directly to ventricular tissue.
there is no atrial depolarization, P waves are Electrocardiographic features (Table 3-2 and
absent. The impulse originating from the SA Figure 3-13)

Section I

Diagnosis of Heart Disease

Figure 3-12. A, Electrocardiogramatrial standstill. B, Electrocardiogramfirst-degree AV block. C, Electrocardiogramsecond-degree AV block.


Chapter 3 Electrocardiography

Figure 3-12, contd. D, Electrocardiogramthird-degree AV block. E, Electrocardiogramright bundle branch block. F, Electrocardiogramunifocal ventricular premature
Section I

Diagnosis of Heart Disease

Figure 3-12, contd. G, Electrocardiogrammultiform ventricular premature complexes. H, Electrocardiogramrun of ventricular premature complexes.
Chapter 3 Electrocardiography 71

Table 3-2 Summary of Pre-Excitation Syndrome

Cardiac Sequence Mechanism ECG

Sinus impulse Normal

Atrial depolarization Normal Normal P wave
Relatively rapid conduction,
AV node accessory pathways Short PR interval
skirting the A-V nodal system
Early ventricular depolarization One ventricle activated early Initial QRS slurred (delta
wave) ( widened QRS)
Retrograde conduction from Atrial re-entry impulse Tendency to supraventricu
ventricles to atria lar paroxysmal arrhythmias
Late ventricular depolarization Fusion between normal and Delay, often with altered
anomalous ventricular activation direction, of terminal QRS

Isolated first degree AV block is not clinically

significant but may be an early indicator of pro
gressive AV nodal dysfunction.

Second-Degree Atrioventricular Block

There is intermittent blockage of conduction
through the AV node.
Following discharge of the SA node and atrial
depolarization, there is no associated ventricular
Figure 3-13. Ventricular pre-excitation in a dog. A short
P-R interval and a widened QRS complex with slurring or
notching (arrow) of the upstroke (delta wave) are present. Electrocardiographic features include absence of
(From Fox PR, Sisson D, Moise NS, eds: Textbook of canine QRS-T complexes following P wave (see Figure
and feline cardiology, St Louis, 1999, Elsevier.) 3-12, C).
In Mobitz type I (Wenckebach) block, there is
progressive prolongation of the PR interval, fol
lowed by occurrence of second degree AV block.
A shortened PR interval In Mobitz type II block, there is second degree
If the accessory pathway terminates in ven AV block without preceding prolongation of
tricular tissue, then initial slurring of the QRS the PR interval.
complex (delta wave) occurs. A pattern of block may exista 2:1 AV block
Paroxysmal reentrant tachycardia in some cases would refer to the presence of two P waves for
Causes include congenital anomalies, feline every QRS complex.
hypertrophic cardiomyopathy, and other struc Advanced or high-grade AV block consists of
tural heart diseases. more than two consecutive blocked atrial de
Clinical significance depends on the frequency polarizations.
and severity of secondary tachycardia resulting Causes are identical to those of first-degree AV
from the accessory pathway. block.
High-grade AV block may reduce cardiac output
First-Degree Atrioventricular Block and result in clinical signs.
Conduction through the AV node is delayed.
Produces prolongation of the PR interval (more
than 0.13 second for the dog, more than 0.09 sec Key Point
ond for the cat) (see Figure 3-12, B). Second-degree block may progress to com
Causes include fibrosis of the AV node, vagal plete AV block. This is more common with
stimulation, and drug-induced (digoxin) and Mobitz type II AV block.
electrolyte imbalance.
72 Section I Diagnosis of Heart Disease

Third-Degree Atrioventricular Block The presence of an LBBB does not impair car
(Complete Heart Block) diac performance directly, but is a marker of sig
All conduction through the AV node is blocked. nificant heart disease.
Atrial and ventricular depolarizations are no lon
ger coordinated and occur independently of one Key Point
another. Ventricular depolarization is initiated by Complete heart block will occur if right bun
discharge of a ventricular escape focus. dle branch block (RBBB) develops in an ani
Electrocardiographic features (see Figure 3-12, D) mal with LBBB.
There is no association between P waves and
QRS-T complexes.
P waves are of normal morphology and usually Left Anterior Fascicular Block
occur at a normal rate. There is a block in the left anterior fascicle of the
QRS complexes are of ventricular origin left bundle branch slowing depolarization of the
morphology. left ventricle.
Ventricular rate is typically 30 to 50 bpm. Electrocardiographic features
Causes include fibrosis of the AV node, drug-in QRS duration is within normal limits
duced (digoxin), infiltrative disease, Rickettsial Left axis deviation (dog less than 40 degrees,
myocarditis, hyperkalemia. cat less than 0 degrees)
Usually associated with clinical signs of weak Small Q wave and tall R wave in leads I and
ness or collapse. Complete AV block warrants aVL (small Q wave not consistent)
implantation of a permanent pacemaker in most Deep S waves in leads II, III, and aVF
cases. (exceeding R wave)
Associated with feline hypertrophic cardiomy
Left Bundle Branch Block opathy, other diseases associated with left ven
A conduction delay or block in both the left pos tricular hypertrophy, hyperkalemia, ischemia,
terior and the left anterior fascicles of the left bun and post-cardiac surgery
dle. A supraventricular impulse activates the right
ventricle first through the right bundle branch. Key Point
Left ventricular depolarization is delayed.
Electrocardiographic features (Figure 3-14) Left anterior fascicular block does not directly
impair cardiac function, but if present, then
Prolongation of QRS duration (>0.08 second
one should look for underlying etiologies.
for the dog;>0.06 second for the cat)
QRS wide and positive in leads I, II, III, and aVF
Unlike VPCs, the QRS complex is associated
with a preceding P wave. Right Bundle Branch Block
May be difficult to distinguish from left ven There is block of the right bundle branch, delay
tricular enlargement pattern ing depolarization of the right ventricle.
Causes include structural heart disease (car Electrocardiographic features (Figure 3-12, E)
diomyopathy, congenital anomalies, neoplasia, QRS duration increased
trauma, fibrosis) Prominent S waves in leads I, II, III, and aVF

Figure 3-14. Intermittent left bundle branch block in a dog. The QRS complexes are wider and taller than normal in the fourth,
fifth, and sixth complexes. (From Fox PR, Sisson D, Moise NS, eds: Textbook of canine and feline cardiology, St Louis, 1999,
Chapter 3 Electrocardiography 73

Right axis shift When every other complex is a VPC, ven

Associated with structural heart disease, Chagas tricular bigeminy exists.
disease, heartworm disease, acute pulmonary When every third complex is a VPC, ventric
thromboembolism, hypokalemia. ular trigeminy exists.
R-on-T phenomenon occurs when the VPC
occurs immediately following a normal beat
Key Point
within the T wave. This may predispose to
As in the case of LAFB, RBBB does not signifi the development of ventricular tachycardia.
cantly impair cardiac function, but one should Causes are numerous and include structural heart
look for underlying etiologies. disease, familial in young German Shepherds,
arrhythmogenic right ventricular cardiomyopathy
(boxer cardiomyopathy), hypoxia, anemia, ure
Disturbances of Ventricular mia, gastric dilatation-volvulus, splenic torsion
Impulse Formation and splenic neoplasia, pancreatitis, myocarditis,
Ventricular Premature Complexes and drug induced (digoxin, anesthesia).
An abnormal beat originating in the ventricles Clinical significance depends on the frequency
and occurring earlier than expected in relation to of VPCs, pattern of ectopy, and cause of the
the existing rhythm. A compensatory pause often arrhythmia.
follows a VPC. Isolated VPCs usually pose no significant
Unifocal VPCs occur from one ventricular site problems but may signal the presence of pro
and have identical morphologies (see Figure 3- gressive disease and potential for more serious
12, F). arrhythmia.
Multifocal VPCs usually occur from more Runs of VPCs do suggest the potential for ven
than one ventricular site and have differing tricular tachycardia and possibly ventricular
morphologies. Electrophysiologic studies fibrillation.
have demonstrated that a single ventricular
site may produce VPCs of differing morphol
ogythis is due to altered conduction of the Key Point
VPCs rather than multiple ectopic sites. It is The finding of isolated VPCs in a young to
more precise, therefore, to use the term mul middle-aged Doberman Pinscher or Boxer is
tiform rather than multifocal (see Figure 3- highly suggestive of occult dilated cardiomy
12, G). opathy or arrhythmogenic right ventricular
When the VPC does not alter the under cardiomyopathy respectively.
lyingnormal rhythm, it is said to be
When normal ventricular depolarization is Ventricular Tachycardia
interrupted by a VPC, a fusion beat occursthis Runs of VPCs occurring in succession at a rate of
is essentially the electrocardiographic merging usually greater than 100 bpm. The inherent dis
of a normal QRS and VPC. charge rate of the ventricle is approximately 40
Electrocardiographic features (Figures 3-12, to 50 bpm (seen with complete heart block). In
F to H) normal animals, this is overdriven by the sinus
As the site of depolarization is ventricular, rhythm. An accelerated idioventricular rhythm re
there is no AV association. P waves are not fers to a ventricular rhythm at a rate of 60 to 100
associated with the QRS complexes of the bpm. Ventricular tachycardia may be sustained or
VPCs. paroxysmal.
QRS complexes wide and bizarre, consistent Electrocardiographic features (Figure 3-15, A)
with ventricular origin P waves not associated with QRS complexes
T wave polarity often reversed QRS complexes wide and bizarre, consistent
Compensatory pause following VPC is typical. with ventricular origin
Patterns of VPCs Regular rhythm, as contrasted with atrial fibril
Two consecutive VPCs are referred to as a lation and RBBB
couplet Causes are the same as for VPCs.
Three or more consecutive VPCs is a salvo or Ventricular tachycardia indicates significant
run (see Figure 3-12, H). heart disease or systemic disease. Cardiac
74 Section I Diagnosis of Heart Disease

output may be significantly impaired, and Atrial Premature Complexes with Aberrant
the arrhythmia predisposes to ventricular Conduction
fibrillation. When the impulse of an APC encounters an area of
refractoriness (AV node, bundle of His, or ventricu
Ventricular Fibrillation lar myocardium), it may terminate or continue with
Completely irregular, chaotic variable fibril aberrant conduction. The latter may result in a wide
lation potentials, indicating lack of organized and bizarre QRS configuration resembling a beat of
ventricular depolarization and impending ventricular origin.
death Most often occurs at slow heart rates
Electrocardiographic features (Figure 3-15, B) QRS may take the form of RBBB.
There is no evidence of organized cardiac
depolarization (absence of P-QRS-T waves)
Wavy, undulating baseline Escape Rhythms
Coarse ventricular fibrillation is character Junctional Escape Beat
ized by large wavelets. When not activated by atrial depolarization, the
Fine ventricular fibrillation is characterized junctional AV nodal area may spontaneously dis
by small wavelets. charge. This impulse results in ventricular depo
larization in a normal fashion. Junctional escape
Key Point beats may occur when there is a significant pause
in the sinus rhythm.
Ventricular fibrillation indicates cardiopul Electrocardiographic features
monary arrest, and immediate restoration of Inverted P wave, occurring before, during, or
rhythm is required to preserve life.
just after QRS complex
Normal or relatively normal QRS complex
Ventricular Asystole Occurs after significant pause in sinus rhythm
Lack of any significant ventricular electrical activity Clinical significancethis complex is adaptive
Electrocardiogram demonstrates flat baseline and helps to maintain cardiac output in the face
occasional ventricular escape complexes may of a slow rate or sinus arrest.
A terminal rhythm requiring immediate restora
Key Point
tion of rhythm to preserve life
Junctional escape beats should not be sup
Disturbances of Both
Impulse Formation and Junctional Rhythm
Impulse Conduction Succession of junctional escape beats in absence
Sick Sinus Syndrome of adequate sinus node function
SSS is a progressive heart disease charac Rate of junctional escape rhythm is typically
terized by a variety of arrhythmias, including 40 to 60 bpm.
sinusbradycardia, sinus arrest, paroxysmal This rhythm is adaptive and should not be sup
atrial tachycardia (bradycardia-tachycardia pressed. Correction of the cause of sinus node
syndrome), intermittent AV nodal block, and dysfunction is warranted.
lack of ventricular escape complexes (Figure
3-15, C). Ventricular Escape Beat
Breeds predisposed include Miniature Schnau When not activated by atrial depolarization, a
zers, Cocker Spaniels, Dachshunds, Pugs, West ventricular focus may spontaneously discharge.
Highland White Terriers. SSS is most common in This impulse results in an abnormal ventricular
older female dogs. depolarization, but contraction is not affected.
The cause is unknown but likely involves idio Ventricular escape beats may occur when there is
pathic degeneration of the conduction system. a significant pause in the sinus rhythm and lack of
Most cases are presented with a history of inter junctional escape complexes.
mittent weakness and collapse. Electrocardiographic features
Medical therapy may be successful in some cases; Ventricular escape beat occurs following a
many require pacemaker implantation. pause in the rhythm

Chapter 3 Electrocardiography

Figure 3-15. A, Electrocardiogramventricular tachycardia. B, Electrocardiogramventricular fibrillation. C, Electrocardiogramsick sinus syndrome.

76 Section I Diagnosis of Heart Disease

QRS wide and bizarre, consistent with ventric Ventricular parasystole focus is located within
ular origin ventricular myocardium and produces regularly
Clinical significancethis complex is adaptive spaced QRS complexes. When the focus dis
and helps to maintain cardiac output in the face charges during the ventricles refractory period,
of a slow rate or sinus arrest. a QRS will not be created.

Ventricular Escape Rhythm Ashmans Phenomenon

Succession of ventricular escape beats in absence Tendency of premature supraventricular beats
of adequate sinus node function to have aberrant ventricular conduction when a
Rate of ventricular escape rhythm is typically 30 short cycle follows a long one.
to 40 bpm.
This rhythm is adaptive and should not be sup
pressed. Correction of the cause of sinus node
Key Point
dysfunction is warranted.
The beats generated by the pacemaker are
Key Point not of normal morphologythis is expected.
These ventricular escape beats should not be

Miscellaneous Frequently Asked Questions

Artificial Pacemaker If a veterinarian auscults an abnormality that comes
A permanent pacemaker is used to control brady and goes, and the ECG does not show an arrhythmia,
arrhythmias that caused clinical signs and were then what should be done?
unresponsive to medical therapy. Repeat ECGs may be required to pick up changes in
Transvenous implantation with an endocardial lead heart activity occurring only in a paroxysmal pattern.
is the preferred means and is much less invasive than In some cases, a Holter monitor must be used for a
abdominal surgery and epicardial lead implantation. 24-hour recording so that the pattern and frequency
of abnormality can be properly tracked.
Most pacemakers used in dogs are set at 100 bpm.
Electrocardiographic features Interference is occurring on an ECG tracing; it
If the sinus node is functioning and the heart appears to be 60 cycle (small waveforms) and is not
improved when the fluorescent bulbs and all electri-
rate is greater than 100 bpm (or discharge rate
cal equipment in the room are turned off. What could
of pacemaker), then there will be no electrocar cause this ongoing interference?
diographic changes. Sometimes, interference may travel through the walls
Once the heart rate decreases below the pace from the adjacent room and close proximity to power
makers minimum rate, a pacing spike will supply in the wall could also send off interference.
appear followed by a wide and bizarre QRS Electrical supply to the facility must be properly
(ventricular origin of impulse). grounded and so if the problem persists when all of
those factors have been controlled, then an electrician
should examine the electrical system of the building.
Key Point We must do a surgery that requires an unusual posi-
Ashmans aberrance may mimic a VPC. tion for the dog. Will abnormal relative and absolute
position of the clips interfere with our routine intra-
operative monitoring?
Position is not critical for routine intra-operative
Parasystole electrocardiography, as opposed to position required
In parasystole, there is an independent fo for a primary ECG with multiple leads for diagnostic
cus discharging spontaneously. There is an purposes, and so a useful capture can be done in spite
entrance block, so the focus is not overdriven by of unorthodox limb or animal position. Any position
for the recording will still always give an analysis
the normal cardiac impulse. The parasystolic fo
of an arrhythmia and/or conduction abnormality.
cus will discharge at a regular rate and may cause It is important to watch that the extreme position
complete depolarization of the atria or ventricles. ing required will not lead to the lead wires or clips
Atrial parasystole focus is located within atrial touching a metal surgical table since that can cause
myocardium and produces small P waves, usu interference.
ally unassociated with QRS complexes.
Chapter 3 Electrocardiography 77

Suggested Readings Miller MS, Tilley LP, Detweiler DK: Cardiac electro
physiology. In Dukes physiology of domestic ani
Davis AS, Middleton, BJ: Relationship between QT mals, ed 11, Ithaca, NY, 1993, Cornell.
interval and heart rate in Alderley Park beagles, Redfern WS, Carlsson L, Davis AS, Lynch WG, Mac
Record, 145:248-250, 1999. Kenzie I, et al: Relationships between preclinical
Detweiler DK: The dog electrocardiogram: a critical cardiac electrophysiology, clinical QT interval prolon
review. In MacFarlane, PW, Lawrie, TDV, eds: Com gation and torsade de pointes for a broad range of
prehensive electrocardiography: theory and practice drugs: evidence for a provisional safety margin in
in health and disease, New York, 1998, Pergamon drug development. Cardiovasc Res, 58, 32-45, 2003.
Press. Smith, FWK, Tilley, LP, Miller, MS: Disorders of cardiac
Ettinger SJ Le Bobinnec G, Cote E: Electrocardiography. rhythm. In Brichard, SJ, Sherding, RG, eds: Manual
In Ettinger SJ, Feldman EC, eds: Textbook of Vet of small animal practice, ed 3, St Louis, 2007, WB
erinary internal medicine, ed 5, St Louis, 2000, WB Saunders.
Saunders. Smith FWK, Tilley, LP, Miller, MS. Electrocardiography.
Finley MR, Lillich JD, Gilmour RF, Freeman LC: In Brichard, SJ, Sherding, RG, eds: Manual
Structural and functional basis for the long QT syndrome: of small animal practice, ed 3, St Louis, 2007,
relevance to veterinary patients. J Vet Med 17:473-488, WB Saunders.
2003. Tilley LP: Essentials of canine and feline electrocardio
Kittleson MD: Electrocardiography. In Kittleson MD, graphy, ed 3, Ames, Iowa, 1992, Blackwell.
Kienle RD, eds: Small animal cardiovascular medi Tilley LP, Miller MS, Smith FW, Jr: canine and feline
cine, St Louis, 1998, Mosby. cardiac arrhythmias: self-assessment. Ames, Iowa,
Miller MS, Tilley LP, Smith FWK Jr, Fox PR, Electro 1993, Blackwell.
cardiography. In Fox PR, Sisson D, Moise NS, eds:
Textbook of canine and feline cardiology, St Louis,
1999, Elsevier.
Chapter 4

Echocardiography and Doppler

Virginia Luis Fuentes

Introduction that obtained with 2D, so that the frame is updated

Echocardiography has become the most important thousands of time per second rather than the 40 to
diagnostic technique for the diagnosis of canine and 200 times per second obtained with 2D.
feline heart disease. The interaction between ultra-
high-frequency sound waves and the heart allows Applications
the depiction of cardiac morphology, information on Time-dependent measurements (chamber dimen-
the movement of myocardium and valves, and blood sions, wall motion)
flow within the heart. Echocardiography is comple-
mentary to physical examination, radiography and
Doppler Echocardiography
electrocardiography (ECG) and has replaced invasive
techniques such as cardiac catheterization for all but a Doppler echocardiography uses the Doppler princi
few specific indications. ple: the frequency of a reflected sound wave depends
on the direction and velocity of the reflector and the
transmitted frequency (producing a Doppler shift).
Types of Imaging If the transmitted ultrasound frequency and the
velocity of sound in soft tissue and blood are
Two-Dimensional Echocardiography
known, then the velocity of red blood cells can be
A sector-shaped beam of ultrasound waves is calculated.
reflected by the interfaces of cardiac tissue to
provide a two-dimensional (2D) cross-sectional Key Point
(tomographic) image (Figure 4-1). The angle of the incident ultrasound beam is
critical: the ultrasound beam must be parallel with
Applications flow (or less than 20 from the direction of flow)
Demonstrating cardiac morphology or the velocity will be underestimated.
Increasingly important in quantification of cham-
ber dimensions (as machines become capable of There are several modes of Doppler echocardiography:
faster frame rates) Spectral Doppler, where the velocity of blood
flow is calculated in a region of interest selected
by moving a cursor (Figure 4-3)
M-Mode Echocardiography
Color Doppler, where the blood flow is coded in
M-mode uses a single narrow beam of ultrasound, red (toward the transducer) or blue (away from
but displays the resulting echoes as a distance-time the transducer) and superimposed on the black-
graph (Figure 4-2). The time resolution is superior to and-white 2D image (Figure 4-4)
Chapter 4 Echocardiography and Doppler Ultrasound 79

Figure 4-1. Right parasternal echocardiographic views. A, Long-axis four-chamber view optimized for left ventricular inlet.
B, Long-axis view optimized for left ventricular outflow tract. C, Short-axis view at the papillary muscle level.
80 Section I Diagnosis of Heart Disease

Figure 4-1. contd. D, Short-axis view at chordal level. E, Short-axis view at mitral valve level. F, Short-axis view at the heart base,
optimized for left atrium and aortic valve.
Chapter 4 Echocardiography and Doppler Ultrasound 81

Figure 4-1. contd. G, Short-axis view at the heart base, optimized for pulmonary artery. LA, Left atrium; LV, left ventricle; RA,
right atrium; RV, right ventricle; Ao, aorta; R, right coronary sinus of Valsalva; L, left coronary sinus of Valsalva; NC, noncoronary
sinus of Valsalva; PA, pulmonary artery; rPA, right pulmonary artery.

Tissue Doppler imaging (TDI), where the velocity times as a receiver or transmitter of ultrasound
of myocardial motion is displayed (Figure 4-5, E) waves, allowing the interrogation of blood flow
velocities within a specific region of interest.
This region of interest is represented as a sample
Spectral Doppler Echocardiography
volume on the cursor.
A graph of blood flow velocity against time Pulsed wave Doppler has limitations in the maxi-
is shown, usually with a simultaneous ECG mum velocities that it can display without ambigu-
display. ity: high velocities result in aliasing, where blood
Blood flow velocities toward the transducer are flow will be displayed as both positive and negative
displayed as positive (above the baseline), and velocities (i.e., signal wraps around the baseline).
blood flow velocities away from the transducer The velocity at which aliasing will occur depends
are displayed as negative (below the baseline). on the Nyquist limit (half the pulse repetition
The Doppler shift can also be represented by an frequency), with higher velocities without alias-
audible sound, because the shift in frequency is ing achieved at lower transducer frequencies, and
usually quite small and within the audible range reduced depth from the transducer.
(around 10 kHz), so that most machines will
show a visual spectral display with a simultane- Continuous Wave Doppler
ous audible signal. In contrast, with continuous wave (CW) Doppler,
Spectral Doppler is usually recorded with guid- ultrasound waves can be transmitted and received
ance from two-dimensional echocardiographic simultaneously. This allows much higher veloci-
images (2D-Doppler, or Duplex Doppler). This ties to be displayed, but it is not possible to draw
allows a cursor to be superimposed over a 2D any conclusions about the depth along the cursor
image, showing the angle of interrogation of the from where these velocities are originating (i.e.,
Doppler beam in two dimensions. there is range ambiguity).
Spectral Doppler can be further subdivided into
pulsed wave, continuous wave, and high-pulse High-Pulse Repetition Frequency Doppler
repetition frequency. High-Pulse repetition frequency Doppler is a form
of pulsed Doppler that shares some similarities
Pulsed Wave Doppler with CW Doppler. Frequent pulses of ultrasound
The ultrasound waves are transmitted as pulses waves are produced so that a number of sample
of waves, with the transducer acting at different volumes will be superimposed on the 2D image.
82 Section I Diagnosis of Heart Disease

Figure 4-2. M-mode echocardiograms of the left heart at the mitral valve chordal level (note that the 2D image is moved to the
left of the screen to allow correct placement of the cursor) (A); mitral valve leaflet level (B); aortic valve level.
Chapter 4 Echocardiography and Doppler Ultrasound 83

Figure 4-2. contd. (C). IVS, Interventricular septum; LV, left ventricle; LVFW, left ventricular free wall; RV, right ventricle;
Ao, aorta; LA, left atrium; LAur, left auricle.

This not only allows the display of higher veloci- indices, because they may be less influenced by
ties without aliasing, but also increases the num- loading conditions.
ber of possible sites from which the velocities are
being recorded. Applications
Doppler echocardiography is most often used to
Color Flow Doppler characterize abnormal direction or velocity of
Color flow Doppler represents the velocity and blood flow, or to indicate the origin of turbulent
direction of blood flow in color, superimposed blood flow. This is invaluable in valve disease or
on a black-and-white 2D image. In effect, the congenital heart disease, but Doppler echocardiog-
color is displayed within a very large sample vol- raphy may also be used to estimate flow volumes,
ume superimposed on the 2D image. Blood flow to assess systolic and diastolic function, and to ob-
away from the transducer is shown in blue, and tain information about intracardiac pressures.
blood flow toward the transducer is displayed in Abnormal blood flow direction may be noted
red (BART: blue away, red toward). Disturbed with conditions such as valvular insufficiency.
or turbulent flow may be displayed in green or Abnormal blood flow velocity may be a clinically
yellow. Aliasing may also occur in color flow useful finding, as the velocity of blood flow across
Doppler. an orifice is chiefly determined by the difference
in pressure. If there is a large difference in the
Tissue Doppler Imaging pressures in the chambers on each side of a valve,
More sophisticated machines may include fa- then the velocity of flow across the valve will be
cilities for recording the velocity of myocardial high. For example, during systole the pressure in
motion. The signals reflected by the moving the left ventricleisvery high, and the pressure
myocardium are high amplitude, but low veloc- in the left atrium is very low. If the mitral valve
ity. These myocardial velocities can be displayed is incompetent and regurgitation occurs, then
in spectral format, as a color display, or as color the velocity of the regurgitant jet traveling from
M-mode. It is believed that TDI indices may have the left ventricle to the left atrium will be very
advantages over conventional echocardiographic high, reflecting the large difference in pressures.
84 Section I Diagnosis of Heart Disease

Chapter 4 Echocardiography and Doppler Ultrasound 85

Figure 4-3. Doppler echocardiographic studies. A, Mitral inflow obtained from the
left caudal parasternal (apical) four-chamber view, with the cursor placed parallel with
mitral inflow, and a small sample volume placed at the tips of the mitral valve leaflets
when the mitral valve is open. The typical spectral Doppler waveform of mitral inflow
displays an early diastolic (E) wave and an atrial contraction (A) wave of filling. B, Aortic
flow obtained from the left caudal parasternal (apical) five-chamber view, showing
left ventricular outflow tract and placement of pulsed wave sample volume in ascend-
ing aorta. The typical spectral Doppler waveform of aortic flow is displayed. C, Aortic
flow obtained from the subcostal view, showing continuous wave cursor positioned
in ascending aorta. The typical spectral Doppler waveform of aortic flow is displayed.
D, Tricuspid valve flow obtained the left cranial parasternal view optimized for right
ventricular inflow. The pulsed wave sample volume is placed at the tricuspid leaflet tips,
with the probe in a cranial position. The spectral waveform is similar to that of mitral
inflow, although sometimes an additional systolic forward flow wave is recorded. E,
Pulmonary artery flow from the right parasternal short-axis view optimized for right
ventricular outflow (left panel) with the pulsed wave sample volume positioned in the
main pulmonary artery, and from the left cranial parasternal view optimized for the
pulmonary artery (middle panel). The typical spectral Doppler waveform of pulmonary
artery flow is displayed. LA, Left atrium; LV, left ventricle; RA, right atrium; RV, right
ventricle; CdCV, caudal vena cava; Ao, aorta; RVOT, right ventricular outflow tract; PA,
pulmonary artery.
86 Section I Diagnosis of Heart Disease



Figure 4-4. Color flow echocardiographic studies of mitral regurgitation. A, Mild mitral regurgitation. The color jet occu-
pies<20% of the left atrial area. B, Moderate mitral regurgitation. The color mitral regurgitation jet occupies 20% to 40% of
the left atrial area. C, Severe mitral regurgitation. The color jet occupies>40% of the left atrial area (the jet is rebounding from
the dorsal LA wall in red), the vena contracta is wide, and a proximal flow convergence region can be seen. D, Right parasternal
long-axis view of a dog with severe mitral regurgitation, showing a large vena contracta width (black arrow). E, Left apical view of
a dog with severe mitral regurgitation, showing a large proximal flow convergence region. The white arrows indicate the borders
of the hemisphere where aliasing is occurring. The larger the hemispheres diameter for a particular aliasing velocity (in this case
69 cm/s), the more severe the mitral insufficiency.

onversely, for much of diastole, the pressure

C flow will be present when a murmur is audible,
in the left atrium is only slightly higher than the making Doppler echocardiography particularly
pressure in the left ventricle, so the velocity of useful in conditions where a murmur is present.
the early filling (E) wave is fairly low. This ve- Estimation of flow volumes is possible using
locity information can therefore be used to derive Doppler echocardiography combined with 2D
information about intracardiac pressures. measurements. Flow is the product of cross-sec-
Turbulent blood flow is relatively uncommon in tional area multiplied by the area under the spec-
the normal heart, but when present, is most likely tral Doppler curve (velocity time integral).
to occur where velocity is highest (i.e., within Assessment of pressure gradients is possible
the aorta). Even in a normal heart, vigorous using the modified Bernoulli equation, where
ejection into the aorta can sometimes result in [4 (blood flow velocity) 2 ] gives the difference
signal aliasing on color Doppler. Blood flow will in pressure across a valve or between chambers.
be turbulent whenever velocity is high, and val- Diastolic dysfunction can also be assessed withDop-
vular insufficiency or stenosis almost inevitably pler echocardiography, although many measurements
results in turbulent blood flow. Turbulent blood are influenced by loading conditions. Evaluation of
flow may be displayed in a different color (green/ transmitral and pulmonary venous flow in conjunc-
yellow) or color distribution (mosaic pattern); tion with TDI indices can suggest abnormal left ven-
this is termed variance. In most cases, turbulent tricular (LV) relaxation and filling pressures.
Chapter 4 Echocardiography and Doppler Ultrasound 87


Figure 4-5. Echocardiographic evaluation of ventricular diastolic function. A, Normal transmitral flow pattern demonstrating an
early filling wave (E) with higher velocity than the atrial contraction wave (A). B, Delayed relaxation transmitral flow pattern dem-
onstrating reduced amplitude and prolonged duration of the E wave. C, Pseudonormal transmitral flow pattern demonstrating a
normal E:A velocity ratio, but this is the result of the combined effects of delayed relaxation, increased LA pressures and increased
LV stiffness. D, Restrictive transmitral flow pattern. High LA pressures result in increased E wave amplitude despite delayed relax-
ation. Decreased LV compliance (sometimes with atrial systolic dysfunction) results in a diminished A wave. E, Pulsed wave tissue
Doppler (TDI) image of mitral annulus velocity, displaying a systolic wave (S), early diastolic wave (E) and atrial wave (A).

Echocardiographic a lthough this will also be affected by the choice of

Technique transducer. High-end machines may have additional
options such as TDI or even 3D echocardiography.
Echocardiographic Machines Transducers
Echo machines are becoming increasingly afford Linear scanners are unsuitable for echocardiog-
able for many practices. Almost all machines have raphy because of the limited acoustic window
appropriate software for cardiac measurements and available between ribs.
will be capable of 2D and M-mode imaging. Many Sector probes produce a fan-shaped arc of ultra-
machines will also have Doppler capabilities, with sound waves, and so they will provide a wide im-
spectral and CW as well as color Doppler. Im- age of the far field from a small acoustic window.
age quality remains the most important feature, These are ideal for cardiac applications.
88 Section I Diagnosis of Heart Disease

Types of sector probes include: Sedation

Mechanical transducers, where the crystal is The ideal is to echo patients without sedation,
oscillated back and forth to produce the arc- but a sedated patient may be better than a rest-
shaped ultrasound beam. These are more com- less one, because it can be impossible to obtain
mon with basic machines. the necessary images without adequate patient
Curvilinear probes are similar to linear probes, cooperation. A reasonable compromise for most
but have a rounded surface. They tend to canine and feline patients is a combination of
produce good images when the footprint is low-dose acepromazine and an opiate. This may
placed between ribs, but rib shadows are a have a mild effect on some blood flow velocities,
problem when they are rotated through 90. but is less likely to affect cardiac dimensions
Phased array transducers are also available and and will not affect lesions. General anesthesia
have an array of crystals that are electronically and alpha-2 agonists will affect systolic func-
fired in sequence to produce the fan-shaped tion and may affect ventricular dimensions.
wavefront. They are more expensive, but they
have better beam focusing. Electrocardiography
Some commercially available transducers have An ECG should be obtained simultaneously.
a wide frequency bandwidth that allows a single ECGs allow a much longer time period of screen-
probe to operate at more than one frequency, for ing for arrhythmias than would be normally
example, 2.5 and 3.5 MHz, or 5 and 7.5 MHz. practicable with an ECG machine and a paper
Higher-end machines may have harmonic imag trace. An ECG also allows accurate timing of
ing, which results in a better signal to noise measurements. Adhesive ECG electrodes are
ratio. more comfortable than traditional alligator clips
and can be attached with tape or bandage, and
electrical contact can be maintained by using ad-
Key Point
ditional alcohol, if necessary.
Low-frequency transducers have high pen-
etrating power but poor resolution. They pro-
duce better Doppler signals. Echocardiographic Views
High-frequency transducers have low
penetrating power but high resolution. The Two-Dimensional Imaging
higher the frequency, the better the imaging
(providing the tissue can be penetrated and
It is worthwhile to adopt a consistent technique
signal strength is adequate). so that the same views are obtained in the same
sequence with each study. Some views may be
more difficult to obtain in some patients. The
most commonly used imaging planes are obtained
The Echo Table with the transducer on the right side of the chest
The majority of echocardiographers position (right parasternal views; see Figure 4-1). Views
animals in lateral recumbency and approach obtained from the left apical windows (caudal
from underneath, with the probe on the de- and cranial left parasternal views; see Figure 4-3)
pendent chest wall. This minimizes air artifact are mainly used for Doppler echocardiography
in the lung tissue between the probe and the applications, but as with radiography, it is helpful
heart. The ideal table will have a wedge-shaped to confirm lesions in more than one view.
cut-out rather than a circular hole, and should
be covered with a comfortable but hygienic
Doppler Imaging
Most Doppler recordings can be made from the
Patient Preparation
left parasternal views, with the subcostal view
Clipping preferred for aortic velocities. Color Doppler
Most dogs will need to be clipped for echo used in the right parasternal views can be used for
cardiography. In some short-coated breeds and screening for mitral and aortic insufficiency. The
cats, good acoustic contact may be obtained with features of blood flow across each valve are listed
liberal use of alcohol and acoustic gel (but check in the following sections. Normal values for blood
first that the transducer used is not damaged by flow velocity are derived from several studies (See
alcohol). reference list) and are summarized below.
Chapter 4 Echocardiography and Doppler Ultrasound 89

wave is sometimes recorded corresponding to

Pulmonary Artery Flow
vena caval inflow.
Recorded from the right parasternal short-axis
view or the left cranial parasternal position (see
Figure 4-3, E). Both should be recorded, in an
attempt to record the highest velocity. A large
sample volume should be used to minimize Echocardiography is ideally suited to identifica-
aliasing. tion of structural lesions, but quantitative assess-
There is usually one single systolic envelope, ment of cardiac dimensions and function is also
away from the transducer, with peak veloci- important. Echocardiography allows quantifica-
ties<1.5 m/s. tion of chamber dimensions, systolic and diastolic
There may be some positive flow (toward the performance, valve function and hemodynamic
transducer) during diastole associated with pul- estimates (e.g., intracardiac pressures).
monic insufficiency. A small amount of pulmonic
insufficiency is common in healthy dogs and is
Chamber Dimensions
usually considered a normal finding.
LV diameter
LV wall thickness
Aortic Flow
Left atrial (LA) and aortic dimensions
Recorded from the left caudal parasternal (apical)
5 chamber (see Figure 4-3, B) or from the sub-
Left Ventricular Diameter
costal position (see Figure 4-3, C). The subcostal
view usually allows the best alignment with flow. LV diameter is typically measured from M-mode
A large sample volume should be used to mini- images (see Figures 4-2, A, and 4-6, A).
mize aliasing.
There should be one single systolic envelope, M Mode Measurement Technique
away from the transducer, with peak veloci- Measure from leading edge to leading edge
ties<1.7 m/s (left caudal parasternal view) Diastolic measurements made at onset of QRS
or<2.0 m/s (subcostal). (LVDd)
Systolic measurements made at peak excursion
Mitral inflow
Average several beats, particularly if the rhythm
Recorded from the apical four- or two-chamber is irregular
view (see Figure 4-3, A). As small a sample
volume as possible should be used, with the Problems with Left Ventricular Dimension
sample volume placed at the leaflet tips during Measurements
diastole. Poor alignment may result in diameter inaccuracies
Two peaks of flow are generally recorded, cor- Difficulties in establishing normal values for a
responding to early passive filling at the start of widely varying canine population
diastole (the E wave: 0.5 to 1.0 m/s) and filling One suggestion is to divide every measurement by
across the mitral valve during atrial contraction the aortic diameter in the same animalthis should
(the A wave: 0.3 to 0.6 m/s). normalize for body size, although normal refer-
ence ranges derived for specific breeds are the ideal.
Tricuspid Inflow
Index of Sphericity
Tricuspid flow is recorded one or two intercos-
tal spaces cranial to the position for mitral inflow One solution to the problem of identifying LV
(see Figure 4-3, D). As small a sample volume as dilation (eccentric hypertrophy) in a wide range
possible should be used. of breeds is to measure the long axis from a 2D
Two peaks of flow are recorded, corresponding to image and divide by the M-mode LV diameter,
early passive filling at the start of diastole (the E as LV dilation usually results in a more spherical
wave: 0.3 to 0.9 m/s) and filling across the tricus- chamber (due to a bigger increase in diameter
pid valve during atrial contraction (the A wave: than length). The LV length: diameter ratio should
0.3 to 0.6 m/s). In addition, a systolic forward be>1.65.
90 Section I Diagnosis of Heart Disease

Left Ventricular Wall Thickness Left Ventricular Fractional Shortening

This is more important in cats than in dogs, as LV fractional shortening (FS%) is the most
detection of LV hypertrophy is an important commonly used echo index of systolic function
clinical goal in feline myocardial disease. In cats, (Figure 4-8, A).
M-mode imaging planes may miss localized ar- Calculated using the following formula:
eas of hypertrophy, or erroneously include papil- FS% = [(LVDd LVDs) / LVDd ] 100
lary muscles, so that wall thickness may be best FS% will increase with improved contractility,
measured from 2D images. 2D echocardiography increased preload, or decreased afterload, and
has the advantage of allowing measurements ir- only assesses shortening in the minor axis
respective of the location of hypertrophy. dimension.
Normal reported mean values range from 25% to
Key Point 39% or 40%. Note that individual normal dogs
Measurements must be made at end-diastole, may have values less than 25%.
when the walls are at their thinnest. There is a
risk of overestimating wall thickness from 2D
E Point to Septal Separation
images with machines with slow frame rates.
E point to septal separation (EPSS) may be
increased with reduced systolic function. It is
Left Atrial Diameter
unreliable in the presence of mitral stenosis or
LA size can be estimated from M-mode, 2D short aortic regurgitation.
axis, or 2D long axis. Measured from an M-mode recording at the
mitral valve level as the distance between the
M-Mode Measurements septum and peak opening of the anterior mitral
The aortic diameter is measured in diastole (Ao), valve leaflet (see Figure 4-6, B).
and the LA diameter is measured in systole. The Normal reported mean values range from 5 mm
LA:Ao ratio should be approximately 1.0, but in to 8 mm in giant breeds.
many dogs alignment is difficult, so that the left
auricle is measured rather than the left atrium. In
End-Systolic Volume Index
cats, the cursor is more likely to cross the main body
of the LA rather than the auricle, so that M-mode End-systolic volume index (ESVI) should be mea-
measurements may more accurately reflect LA size sured from 2D images, not from indices derived
than in dogs (see Figures 4-2, C, and 4-6, C). from M-mode such as with the Teichholz formula
Endocardial borders of left ventricle are traced
Two-Dimensional Measurements in a right parasternal long-axis or left caudal
Short axis: the LA:Ao ratio should be<1.6. Mea- parasternal view, and an area-length formula or
surements are usually made in diastole. There can modified Simpsons rule are generally used to
be problems avoiding pulmonary veins, and the LA calculate LV volumes (see Figure 4-8, B).
size may vary throughout diastole (Figure 4-7, A). ESVI is end-systolic volume divided by body
Long axis: the LA:Ao ratio should be<2.5, surface area
where the aortic diameter is measured from a Normal ESVI is often quoted as 30 ml/m2,
right parasternal long-axis view at the valve level although this value has been extrapolated from
during systole (Figure 4-1, B, and 4-7, B). human reference ranges and relationship with
In cats, there is no need to normalize the LA bodyweight may not be linear.
diameter to the aortic diameter; absolute diameter
should be<1.6 cm (note, however, that this is a
Ejection Fraction
technically difficult view to achieve in cats).
Calculation of LV volumes allows calculation of
ejection fraction (EF%).
Systolic Function
EF% = [(end-diastolic volume end-systolic
Many different echocardiographic measurements
volume) / end-diastolic volume] 100
can be made to assess systolic performance, but
virtually all are affected by loading conditions. Normal EF% in dogs is 50% to 65%
Chapter 4 Echocardiography and Doppler Ultrasound 91

Systolic Time Intervals Mitral Insufficiency

The ratio of pre-ejection period (PEP) and LV 2D echocardiography should be used to deter-
ejection time (LVET) is another global index mine whether the underlying cause of mitral in-
of systolic function, and can be measured from sufficiency is structural valve disease or whether
the spectral Doppler aortic velocity waveform the mitral regurgitation is functional (i.e., second-
(see Figure 4-8, C). Normal PEP/LVET should ary to diseases such as dilated cardiomyopathy
be<0.40. [DCM]). Functional mitral regurgitation often
results in a central jet, whereas the jet is often
eccentric or multiple with myxomatous valve
Diastolic Function
Diastolic function is complex: clinically rel- Mitral insufficiency can be graded as mild,
evant aspects of diastolic function include LV moderate, or severe (see Figure 4-4, A through
relaxation, LV compliance, LA pressures, LA C). The grade of mitral regurgitation can be as-
systolic function and heart rate and rhythm. sumed to be severe when the following criteria
Clearly, no single echocardiographic measure- are present:
ment will provide a complete overview of dia- Large regurgitant jet area compared with LA area
stolic function. However, a range of Doppler Increased width of the vena contracta (see
measurements can be used to give a composite Figure 4-4, D)
assessment of diastolic function or highlight Presence of large proximal flow convergence
specific aspects, and Doppler echocardiog- region (see Figure 4-4, E)
raphy has become the technique of choice High-intensity CW spectral Doppler signal
for evaluation of diastolic function in human Increased mitral E wave velocity
patients. Chamber remodeling (dilated left atrium or left
Similar principles apply to tricuspid regurgitation.
Transmitral Flow
Transmitral flow reflects the instantaneous
Aortic Insufficiency
pressure gradient across the mitral valve.
There is a progressive change in the ventric- Less common than mitral insufficiency, aortic in-
ular filling pattern with advancing disease sufficiency is considered severe when the following
across a range of underlying cardiac diseases criteria are present:
(see Figure 4-5, A through D). The principal Large insufficiency jet size compared with LV area
difficulty with use of transmitral flow patterns Increased width of vena contracta
is the confounding effect of a pseudonor- Rapid deceleration of aortic insufficiency spec-
mal phase, where the transmitral flow pattern tral Doppler signal
is similar to that seen in the normal animal.
Transmitral flow patterns should therefore be
Aortic and Pulmonic Stenosis
interpreted in the context of other clinical and
echocardiographic findings. Pulmonary ve- The severity of aortic or pulmonic stenosis is
nous flow patterns and Doppler tissue imaging generally assessed in terms of the magnitude of
of mitral annular velocities (see Figure 4-5, E) the pressure gradient across the stenosis.
have been used to distinguish pseudonormal
filling from normal. Assessment of Pressure Gradients
Pressure gradients (PGs) across a valve or be-
tween chambers can be estimated by using the
Valve Function
modified Bernoulli equation (Figure 4-9).
Color Doppler can be used as a quick screen for PG (in mm Hg ) = 4 (V 2 )
valve function, but caution should be used in de-
termining severity of valvular regurgitation on where V=velocity of blood flow distal to the ori-
regurgitant jet size alone, or in relying on the fice (m/s). For example, if the velocity in the aorta
presence of turbulent signals to identify valvular is 5 m/s, then the pressure gradient can be estimated
stenosis. as 4 (52 ), or 4 25 = 100 mm Hg.
92 Section I Diagnosis of Heart Disease

Figure 4-6. M-mode measurements of the left heart and aorta. A, M-mode at chordal level, showing measurements at end-diastole
(onset of QRS) and end-systole (peak septal motion). Septal thickness in diastole (IVSd), left ventricular diameter in diastole (LVDd), left
ventricular free wall in diastole (LVFWd), septal thickness in systole (IVSs), left ventricular diameter in systole (LVDs), left ventricular free
wall in systole (LVFWs). B, M-mode measurements at mitral valve level, showing an increased E-point to septal separation (EPSS) of
15.6 mm. C, M-mode measurements at the atrial and aorta level showing measurement of left atrial (LA) and aortic (Ao) diameter.
Chapter 4 Echocardiography and Doppler Ultrasound 93

Figure 4-7. Measurement of the left atrial (LA) and aortic (Ao) diameters from the right parasternal short-axis view (A) and LA
diameter from the right long-axis view optimized for the left ventricular inlet (B).

Common Acquired Cardiac

Conditions Dilation of LA and LV
The LV systolic function usually appears hyper-
Degenerative (Myxomatous) Mitral Valve dynamic (see Figure 4-8, A)
Disease Tricuspid valve may also be affected, with pro-
Degenerative mitral valve disease (endocardiosis) lapse or flail leaflets sometimes seen
must be distinguished from mitral infectious en-
docarditis, although this generally occurs in dogs
with a different signalment and presenting signs,
as well as differing subtly in lesion morphology. Key Point
Infectious endocarditis usually does not
Two-Dimensional Changes result in mitral valve prolapse and is more
likely to result in oscillating focal vegeta-
Thickened, distorted mitral leaflets (Figure 4-10) tions than degenerative mitral valve dis-
The mitral valve motion is usually abnormal ease.
often with prolapse or flail with chordal rupture
94 Section I Diagnosis of Heart Disease

Figure 4-8. Echocardiographic evaluation of ventricular systolic function. A, M-mode of ventricular hypokinesis from a dog
with dilated cardiomyopathy (DCM) (left panel), normal ventricular motion from a healthy dog (middle panel), and ventricular
hyperkinesis from a dog with mitral regurgitation (MR) (right panel).

Dilated Cardiomyopathy
basis of a low fractional shortening value alone
Overt DCM is a relatively easy diagnosis to make, (especially in dogs of nonpredisposed breeds).
with global hypokinesis of a dilated heart in the Dilation of LA and LV
absence of any other lesions (Figure 4-11). Occult  Dilation of RA and RV
DCM may be more difficult, and caution is required LV hypokinesis ( FS%, EF%)
in diagnosing DCM in asymptomatic dogs on the  EPSS
Chapter 4 Echocardiography and Doppler Ultrasound 95

Figure 4-8. Contd. B, Measurement of left ventricular volume from a right parasternal long-axis view. The endocardial borders are
traced, with the left ventricular length measured from a line drawn across the mitral annulus to the apex. LA, Left atrium; RA, right atri-
um; RV, right ventricle. C, Spectral Doppler aortic blood flow velocity, showing preejection period (PEP) and LV ejection time (LVET).

Hypertrophic Cardiomyopathy
Thrombus or spontaneous echocontrast (smoke)
Feline hypertrophic cardiomyopathy (HCM) is may be present in left auricle
very common, and a spectrum of disease exists.
Severe HCM is easy to diagnose (Figure 4-12),
Pericardial disease
but mild HCM may be very difficult (focal hy-
pertrophy may be the only recognizable feature Pericardial effusions can be identified as an
that distinguishes mild HCM from a normal heart echo-free space around the heart, although
with a functional murmur). they may be confused with pleural effusions.
Septal or free wall thickness in diastole>6.0 Tamponade may be suggested by collapse of
mm on 2D and/or M-mode the right atrial wall. The heart may be affected
LA may or may not be dilated (depending on by a number of different neoplasms which can
degree of hemodynamic compromise) result in pericardial effusions, and these may
Systolic anterior motion of the mitral valve often be best imaged while some pericardial fluid is
present (hypertrophic obstructive cardiomyopathy) present.
96 Section I Diagnosis of Heart Disease

Figure 4-9. CW spectral Doppler recording of high-velocity flow in pulmonary artery in a dog with severe pulmonic stenosis. The
measured peak velocity of 5.47 m/s corresponds with a pressure gradient of 119.8 mm Hg across the pulmonic valve.



Figure 4-10. Right parasternal long-axis view of dog with myxomatous mitral valve disease, showing thickened, distorted
mitral leaflets with prolapse of the anterior leaflet.
Chapter 4 Echocardiography and Doppler Ultrasound 97



Figure 4-11. Right parasternal long-axis view of a dog with dilated cardiomyopathy, showing a rounded LV with normal mitral
valve morphology (and no mitral valve prolapse).



Figure 4-12. Right parasternal long-axis view of a cat with hypertrophic cardiomyopathy, showing marked LV hypertrophy.

Chemodectomas generally involve the heart base to image at this site. They may also infiltrate
and may be imaged as homogeneous soft tissue other areas of the heart (such as the septum
densities encircling the aortic and pulmonary ar- and ventricular walls) where they may have
tery roots. They may be associated with pericar- an irregular echotexture compared with sur-
dial effusion. rounding myocardium. Right atrial hemangio-
Hemangiosarcomas frequently affect the right sarcomas are often associated with pericardial
atrium, although they can be very difficult effusions.
98 Section I Diagnosis of Heart Disease

Frequently Asked Questions Suggested ReadingS

1. How can you tell when the left ventricle is dilated Bonagura JD, et al: Doppler echocardiography I: pulsed
when there are no breed-specific normal reference and continuous wave studies, Vet Clin N Am Small
values? Anim Pract 28:1325, 1998.
A. A number of approaches can be used Boon JA: Manual of veterinary echocardiography, Balti-
when there are no breed-specific reference more, 1998, Williams & Wilkins.
intervals. Reference intervals based simply Brown DJ, Rush JE, MacGregor J, et al: M-mode echo-
on bodyweight are not reliable, because cardiographic ratio indices in normal dogs, cats, and
the relationship between LV dimensions horses: a novel quantitative method, J Vet Intern Med
and bodyweight is not linear. One solution 17:653, 2003.
has been to reference the LV diameter to Brown DJ, et al: M-mode echocardiographic ratio indices
another dimension, such as aortic diameter. in normal dogs, cats, and horses: a novel quantitative
An alternative solution is to look for signs of method, J Vet Intern Med 17:653, 2003.
chamber remodeling. A decrease in the index of Bussadori C, et al: Guidelines for the echocardiographic
sphericity to<1.65 would support a suspicion studies of suspected subaortic and pulmonic stenosis,
of LV dilation (eccentric hypertrophy). J Vet Cardiol 2:17, 2000.
2. How does one interpret a low value for fractional Dukes-McEwan J, Borgarelli M, Tidholm A, et al: Pro-
shortening in an otherwise healthy dog? posed guidelines for the diagnosis of canine idiopathic
dilated cardiomyopathy, J Vet Cardiol 5:7, 2003.
A. Caution should be used when making a Hansson K, Haggstrom J, Kvart C, et al: Left atrial to aor-
diagnosis of DCM in an asymptomatic dog tic root indices using two-dimensional and M-mode
based on a fractional shortening value<25%.
echocardiography in cavalier King Charles spaniels
Multiple other variables should be assessed,
with and without left atrial enlargement, Vet Radiol
including evidence of chamber dilation, any
Ultrasound 43:568, 2002.
increase in end-systolic volume index, whether
the EF% is also subnormal, and systolic time OGrady MR, Bonagura JD, Powers JD, et al: Quantita-
intervals (PEP/LVET). Guidelines have been tive cross-sectional echocardiography in the normal
proposed for a scoring scheme for diagnosis dog, Vet Radiol 27:34, 1986.
of DCM in asymptomatic dogs (see Dukes- Thomas WP, Gaber CE, Jacobs G, et al: Recommenda-
McEwan J, et al. in Suggested Readings). tions for standards in transthoracic two-dimensional
echocardiography in the dog and cat, J Vet Intern Med
3. Does an increased aortic blood flow velocity 7:247, 1993.
always indicate aortic stenosis? Yuill CDM, OGrady MR: Doppler-derived velocity of
A. A fixed LV outflow tract obstruction such as blood flow across the cardiac valves in the normal
subaortic stenosis will result in increased dog, Can J Vet Res 55:185, 1991.
blood flow velocity, with the velocity
correlating with the severity of obstruction.
The velocity recorded also depends on flow,
so with increased blood flow, the velocity will
be increased even without any decrease in LV
outflow tract diameter. An extreme example is
the increased aortic blood flow velocity often
recorded with patent ductus arteriosus, where
the left-to-right shunting across the ductus
leads to an increased volume of blood flowing
through the aortic valve, sometimes resulting
in dramatically elevated aortic velocities
(which return to normal after ductal ligation).
Other conditions with increased stroke volume
(e.g., anemia, bradycardias) may also result
in increased aortic blood flow velocity. A
diagnosis of subaortic stenosis is supported by
the presence of anatomic lesions imaged with
2D echocardiography.
Chapter 5

Special Diagnostic Techniques for

Evaluation of Cardiac Disease*
Meg M. Sleeper

Introduction Technique
Many special diagnostic techniques are available Continuous electrocardiographic monitoring re-
for evaluation of animals with cardiovascular dis- quires an ECG unit with an oscilloscope or light-
ease. Ambulatory electrocardiographic equipment emitting diode (LED) display.
is available through various services, continu- Use of a chest lead configuration with adhesive
ous in-hospital electrocardiographic monitoring electrode patches will minimize artifacts on the
equipment is widely available, and several large tracing while allowing the patient the most free-
diagnostic laboratories provide specialized clinical dom for mobility.
pathology services. Additionally, veterinary car- Clip two 2- to 3-cm square areas at the left apex
diology referral centers are increasingly available and the heart base (where the apex beat is pal-
for special diagnostic techniques such as cardiac pable on the left chest and at the heart base caudal
catheterization. to the right or left scapula).
Clean and de-fat the area with 70% isopropyl al-
cohol. Allow to dry.
Continuous In-Hospital Place the positive electrode patch at the left api-
Electrocardiographic cal site and the negative electrode at the heart
Monitoring base site. A ground electrode may be placed at
Continuous electrocardiographic monitoring is either site (Figure 5-1).
recommended for hospitalized patients at risk of Apply a light chest wrap to secure the electrodes
heart rate or rhythm disturbances. These patients and wires.
include: If a multiple-lead electrocardiographic (ECG) unit is
Patients with congestive heart failure being used, then use the left arm electrode for the pos-
Patients hospitalized with clinical signs (e.g., itive electrode, the right arm electrode for the nega-
syncope) secondary to arrhythmia tive electrode lead, and lead I for display/recording.
Patients with systemic disease that puts them at If the patient is recumbent and unlikely to move, leads
risk for arrhythmias (e.g., shock, sepsis, gastric attached directly to the patient limbs can be used.
dilation-volvulus, etc.) Depending on the unit available, the signal
is transmitted to the machine by cables or by
*John Karl Goodwin contributed to previous versions of this chapter. radiotelemetry.
100 Section I Diagnosis of Heart Disease

or neurologic disease, or is associated with primary

cardiac conduction system disease. If the bradycar-
dia is due to elevated vagal influence, then atropine
administration or exercise will result in its abolition.

Vagal Maneuver
The techniques listed below can be used for ele-
vating vagal tone. The patient should be restrained
and calm so that a good quality lead II ECG is
obtained prior to and during the technique.
Figure 5-1. Chest lead preparation in a Boxer. The
Ocular Pressure
negative lead should be placed in the upper patch behind
the scapula and the positive lead should be placed at the Moderately firm digital pressure is applied over
left apex (behind the elbow). This configuration can be used the closed eyelid to one or both eyes for a period
for in hospital continuous ECG monitoring or ambulatory of 5 to 10 seconds or until significant slowing of
the heart rate occurs.

Many ECG units will print out an ECG strip, which Carotid Body Massage
can be added to the permanent patient record. The carotid bodies are located in the area behind
the larynx. Apply moderate digital pressure around
the larynx while monitoring the ECG. Initiation of
a gag response or a cough yields similar results
Excessive patient motion may result in displace- and suggests adequate pressure has been applied.
ment of electrodes or motion artifact in the ECG.
Adhesive patches may occasionally result in con-
Inhibition of Vagal Tone
tact dermatitis.
Two techniques are possible for abolishing vagal
tone and are useful if the patient is suspected to have
a vagally mediated bradycardia. With either tech-
nique, it is important to first obtain a baseline ECG.
In some patients, the history or baseline ECG is sug- Postexercise Electrocardiography
gestive of pathologic arrhythmias, but a definitive Typically, strenuous leash running is used; how-
diagnosis is elusive. In these cases, vagal stimula- ever, the duration of exercise is not standardized.
tion or abolition may be informative. A provocative Evidence of exertion, such as panting, is sufficient
vagal maneuver will transiently elevate parasympa- to stop exercise and an immediate post-exercise
thetic tone. In normal animals, the technique typi- ECG is obtained. A delay of as little as 30 seconds
cally slows the heart rate or has no effect. However, may alter results, and heavy panting can result in
when there is sinoatrial or atrioventricular (AV) artifacts making the ECG difficult to interpret.
nodal dysfunction, or an abnormal sensitivity to
parasympathetic tone, transient sinus arrest or sig- Atropine Response Test
nificant AV block may occur. Similarly, a vagal ma- Atropine (0.04 mg/kg IV or IM) will result in
neuver may be diagnostic and/or therapeutic for an abolition of vagal influence. An ECG should be
ectopic supraventricular tachycardia. A sinus tachy- obtained 10 to 15 minutes after administration of
cardia typically slows over several seconds while an the drug for comparison with the baseline ECG.
ectopic supraventricular tachycardia may terminate
Clinical Utility
abruptly (see Frequently Asked Questions).
An ECG recorded immediately post exercise may Vagal Maneuver
demonstrate cardiac arrhythmias associated with in- Clinically useful in two scenarios:
creased sympathetic tone. Likewise, an atropine re- In the evaluation of dogs with a history of syn-
sponse test can be used to determine if a slow heart cope, a vagal maneuver may demonstrate sinus
rate is associated with elevated vagal tone, as can oc- arrest or AV block, suggestive of parasympathetic
cur with respiratory disease, gastrointestinal disease hypersensitivity or primary nodal disease.
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 101

In dogs with tachycardia, abrupt termination of the recording of the ECG increases the sensitivity of
arrhythmia with a vagal maneuver suggests an ec- arrhythmia detection. Major indications include:
topic supraventricular origin because ventricular Detection of transient arrhythmias associated
tachycardias are not usually sensitive to vagal tone; with syncope or periodic weakness.
however, lack of response is not helpful in differen- Screening of high-risk breeds for cardiomyopathy
tiating the origin of the tachycardia. The maneuver (e.g., Boxers, Doberman Pinschers).
can also be useful to differentiate sinus tachycardia Evaluation of frequency, severity, and significance
(no response or gradual slowing of heart rate) from of arrhythmias detected on in-hospital ECG.
pathologic ectopic supraventricular tachycardia (no Monitoring efficacy of antiarrhythmic therapy
responce or abrupt termination of tachycardia). (e.g., control of heart rate in patients with chronic
atrial fibrillation).
Postexercise Electrocardiography Determining the true incidence and type of ar-
This test can be performed in the evaluation of rhythmia in heart disease patients.
dogs with subaortic stenosis or occult cardio-
myopathy. In affected dogs, the combination of
exercise, myocardial disease and left ventricular
hypertrophy may result in electrocardiographic Modern Holter monitors use a high-fidelity digital
indicators of myocardial ischemia (i.e., ST seg- recorder to capture and store the cardiac electrical
ment depression or ventricular ectopy). Lack of re- activity for 24 hours. Some digital recorders are
sponse does not necessarily rule out heart disease. now capable of monitoring the patient for up to 7
In dogs with bradycardia, abolition of the arrhyth- days. Two to three simultaneous ECG chest leads
mia after exercise suggests a vagally mediated are typically recorded.
etiology. The increased availability of ambulatory Electrode sites are prepared by clipping, shaving,
ECG recordings has markedly reduced the use of cleaning and drying the chest.
post exercise ECGs in clinical practice. Adhesive patches are firmly adhered to the skin
(see Figure 5-1).
Atropine response test A chest wrap is essential for securing electrodes,
Sinus tachycardia with a heart rate greater than 135 wires and the recorder. A vest or harness can also
beats per minute suggests normal sinus node func- be used (Figure 5-2).
tion in the dog. Additionally, this response suggests Once the monitor has been applied, the animal re-
that medical management with vagolytic therapy turns home to resume normal activity. Very small
may be effective if the bradycardia is associated dogs and cats that find it cumbersome to ambu-
with clinical signs such as syncope or collapse and late with the monitor in place may respond better
implantation of a pacemaker is not possible. to hospitalization with cage restraint during the
24-hour recording session.
Key point
Provocative ECG techniques are easily per-
formed, relatively inexpensive, and can be
very helpful for diagnostic and therapeutic
purposes in animals with bradycardias and/or

(Holter Monitoring and
Cardiac Event Recording)
Routine in-hospital electrocardiography only pro-
vides a glimpse of the daily electrocardiographic
activity. Moreover, arrhythmia detection may be con- Figure 5-2. A vest can be placed over the light wrap, which
founded by iatrogenic changes in the autonomic ner- secures Holter or CER monitor electrodes in place. The vest has
vous system activity. A 24-hour ambulatory (Holter) pockets to hold the monitor and helps keep the device in place.
102 Section I Diagnosis of Heart Disease

Owners or caretakers should maintain a diary of Use of Cardiac Event Recorders

significant changes in activity, such as sleeping, The CER will not store an ECG unless the activa-
exercising, and so on. Any clinical signs such as tion button is pressed; therefore, the event must
syncopal events must be noted. be witnessed by the owner. If an event does not
At least 24 hours should be evaluated in order to occur during the time the unit is worn, then a de-
assess a full circadian cycle. finitive diagnosis is not possible.
At the conclusion of the recording period, the CERs may be rented from a commercial service
components are removed and the monitor is ana- or the patient may be referred to a specialty prac-
lyzed with the aid of automated computer-based tice offering this service.
software. Operator interaction and editing is es-
sential for diagnostically accurate results. Implantable Cardiac Event Recorders
Consultation with a veterinary cardiologist is Implantable loop recorders are available for those
recommended regarding the significance of unusual cases in which syncope is very rare and
arrhythmias found and the need for therapy. difficult to capture with a 7 day CER. These de-
Many normal dogs will have infrequent ven- vices are small enough to implant subcutaneously
tricular premature complexes and/or sinus in most dog or cat patients. They are capable of
pauses noted during a 24 hour period. Assess- monitoring the ECG for longer than 18 months, and
ment of arrhythmia significance and risk/ben- can be activated to store the ECG by a person ob-
efit ratio of anti-arrhythmic medications is serving an episode, or can be programmed to store
essential. the ECG if the heart rate is slower or faster than
the programmed limits (set at the time of implanta-
tion). The device is interrogated by a radiotelem-
Cardiac Event Recorders
etry device (similar to those used for pacemakers)
The cardiac event recorder (CER) is an ambulatory to determine if unobserved episodes occurred. The
microprocessor with a solid-state memory loop ca- devices are expensive; however, they can be very
pable of storing portions of ECG tracings when acti- helpful in cases with rare clinical signs.
vated. The CER is lightweight, activated by a person
witnessing an event (e.g., weakness or syncope) and Key point
can be worn by small dogs and cats without restrict- If syncope is very infrequent, then a CER is
ing activity. Unlike most 24 hour Holter monitors, much more likely to result in definitive diag-
which are worn for only 1 day, the CER can be worn nosis than a 24-hour Holter recording.
for up to a week, increasing the diagnostic yield in
animals with infrequent clinical signs.
CERs can be programmed to store up to five sep- Nonselective angiography
arate, one minute duration, single channel ECGs,
or fewer ECGs of longer duration.
Recording is activated by pressing the event but- Nonselective angiography is occasionally helpful
ton on the device. The CER utilizes a memory to identify congenital and/or acquired abnormali-
loop to store the ECG (most commonly 30 sec- ties of intracardiac or intravascular blood flow. Ab-
onds before activation to 30 seconds after activa- normalities of the right side of the heart (e.g., right
tion); however, these times may be changed as atrium, right ventricle, pulmonary arteries) are
indicated for the individual patient. most readily identified by this technique; however,
After one or more events, the CER is detached echocardiography and ultrasound have superseded
and the stored ECG is transmitted and down- the need for this technique at most facilities.
loaded to a receiving station for computer-based
analysis and interpretation.
Application Sedation or a light plane of anesthesia is usually
The CER uses two adhesive electrodes in a necessary.
base-apex configuration and is relatively easy to A large bore catheter (18 gauge or larger) is placed
apply. intravenously (preferably in the jugular vein).
A light chest wrap is used to secure the unit over The animal is placed in the most appropriate
the dorsum. As with Holter monitoring, the patient position for opacification of the structures of
may be discharged to resume routine activity. interest (i.e., lateral recumbency for most cardiac
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 103

defects, sternal recumbency to visualize pulmo- The standard cardiac catheterization procedure
nary arteries). for evaluation of congenital or acquired cardiac
A large bolus of contrast is rapidly injected intra- diseases typically includes measurement of intra-
venously. Typically, 1 ml of radiopaque contrast cardiac pressures, blood oximetry, and selective
per kg of body weight is used for the injection. angiocardiography. The most common indica-
Alternatively, the dose of iodine to be injected tion for cardiac catheterization is to ameliorate
can be calculated using 400 mg iodine/kg body congenital heart disease (e.g., pulmonic stenosis
weight as the desirable dose. or patent ductus arteriosus). For the purposes of
A fluoroscopy unit allows continuous assessment. diagnosis, advances in echocardiography have
If fluoroscopy is not available, radiographic expo- markedly reduced the need for routine cardiac
sures are obtained 2 to 8 seconds after the injection catheterization.
is initiated (depending on the structures of interest
and cardiovascular performance). Shorter times
should be used for evaluation of the right heart and
pulmonary arteries, longer times for evaluation of Anesthesia is usually required.
structures on the left side of the heart or animals Surgical preparation of the neck (carotid artery
with heart failure and slow circulation. or jugular vein) or inguinal area (femoral vein or
artery) is required.
Vascular access can be obtained by dissecting
Clinical Utility
down to the vessel or with a percutaneous cath-
Nonselective angiography is an alternative tech- eter introducer system using a modified Seldinger
nique primarily used to evaluate lesions that in- technique.
volve the right side of the heart, particularly when Catheter advancement to the chamber of interest
echocardiography or cardiac catheterization is ei- is performed under fluoroscopic or pressure wave
ther not an option or is inconclusive. form guidance (Figure 5-3).
Intravascular pressures are recorded from cham-
bers of interest. Pressures are typically recorded
Limitations, Risks, and Costs
before and after therapeutic interventions (e.g.,
Dilution of contrast material occurs as it moves balloon valvuloplasty) to assess procedure
through the circulation. Thus, nonselective angi- efficacy.
ography results in poor opacification of structures
that are very distal to the site of injection (e.g., Oximetry
left heart and systemic arteries). Blood samples are obtained from various cardiac
Timing of radiographs is difficult to predict and or great vessel locations to measure oxygen satu-
several attempts are often required unless fluoros- ration and to calculate shunt fraction in animals
copy is available. with congenital shunting defects.
Intravenous contrast agents may result in tran-
sient hypotension, cardiac arrhythmias, nephro- Angiocardiography
toxicity (especially in patients with pre-existing Radiopaque contrast material is injected
renal dysfunction), and allergic reactions. through the catheter(s) located at the appropri-
ate areas of interest, and the image is recorded
Key point on videotape, radiographic film, by cineangi-
Nonselective angiography is significantly ography or is digitally stored (Figure 5-4). Post
limited, particularly in the assessment of left processing can be performed on digital im-
heart structures. Echocardiography and/or ul- ages using digital subtraction techniques. The
trasound are preferred diagnostics. primary advantage over nonselective angio
graphy involves superior opacification of struc-
tures of interest.
Cardiac Catheterization Cardiac output may be determined using thermo-
dilution or indicator dye techniques.
Additional procedures such as balloon valvulo-
Generally, cardiac catheterization is defined as a plasty, patent ductus arteriosus coil occlusion,
combined angiographic and hemodynamic study endomyocardial biopsy, heartworm retrieval, and
undertaken for therapeutic or diagnostic purposes. cardiac pacing can be performed.
104 Section I Diagnosis of Heart Disease

Figure 5-3. Fluoroscopically obtained images of a balloon-tipped cardiac catheter being placed into the right heart. The cath-
eter is advanced to the heart via the jugular vein. The balloon on the tip of the catheter facilitates traversing the tricuspid valve
because it will tend to follow blood flow.
Contrast solutions can result in hemodynamic ab-
Clinical Utility
normalities. Patients with severe heart disease or
Angiocardiography is valuable to diagnose cases of renal disease are at a relatively higher risk.
complex heart disease and to guide therapeutic in- Infection, cardiac arrhythmias, air embolism,
terventions such as balloon valvuloplasty or patent vascular thromboembolism or perforation are
ductus arteriosus occlusion. The approach provides possible complications. With appropriate experi-
useful morphologic and physiologic information re- ence and case selection, mortality rate is low.
garding interventional responses to therapy.

Serologic Testing
Limitations, Risks, and Costs
Cardiac catheterization requires specialized
equipment and training and is typically limited to Animals with clinical signs suggestive of myo-
tertiary care facilities. cardial dysfunction resulting from infectious or
The technique can be time consuming. immune-mediated etiologies and animals at risk of
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 105

Cardiac Neurohormones
and Biomarkers
Cardiac Troponins
Cardiac troponin I and T are specific markers of
myocyte injury, ischemia, and necrosis. Cardiac
troponin I is more sensitive than cardiac troponin
T. Specific indications include cases of suspected
myocardial infarction, toxic myocardial disease
(e.g., secondary to doxorubicin), myocarditis, or
blunt myocardial trauma (e.g., vehicular injury).

A variety of human cardiac troponin I assays that
Figure 5-4. Selective aortogram demonstrating a patent cross-react with canine and feline cardiac tropo-
ductus arteriosus with radiographic contrast material crossing nin I are available, but standardization is lacking,
the ductus and entering the pulmonary artery (left to right making it difficult to compare results from dif-
ferent machines. Most cardiac troponin assays
accept either serum or heparinized or ethylenedi-
aminetetra acetic acid (EDTA) plasma. Some use
yocardial toxicity from chemotherapeutic agents
m whole blood. If testing is not performed within 12
are candidates. hours after collection, then the samples should be
Trypanosoma titer. Animals from Mexico, south- frozen until testing is done.
ern Texas, or other regions where Chagas disease
is endemic, with right-heart failure. Clinical Utility
Antinuclear antibody titer. Animals with heart Elevated cardiac troponin I has been demon-
failure or arrhythmias in addition to other clinical strated in a wide range of cardiac and extracar-
signs suggestive of immune-mediated disease. diac diseases. Concrete diagnostic, prognostic
Toxoplasmosis titer. Cats with myocardial dys- and therapeutic recommendations based on assay
function, fever, pneumonia, neurologic disease, results are not yet available; however, cardiac tro-
chorioretinitis or other signs compatible with ponin I results may give useful supportive infor-
toxoplasmosis. mation to the electrocardiographic, radiographic,
and echocardiographic findings in some patients.
Serial testing of individual patients is more likely
to be useful than one measurement at a single
Serum or plasma should be submitted to a labora- point in time.
tory that has the appropriate facilities to perform
the indicated serologic testing. Limitations
Since cardiac troponin I can be elevated with both
cardiac and extracardiac disease, the test does not
Clinical Utility
appear to be a useful screening tool for cardiac
In selected cases, these tests can be very useful in disease.
establishing an etiologic agent and in monitoring
patients at risk for myocardial toxicity. Results
must be interpreted in concert with the patients Natriuretic Peptides (Atrial
clinical signs. And B-Type)
Limitations, Risks, and Costs
Atrial natriuretic peptide (ANP) and B-type natriuretic
These tests are only limited by correct interpre- peptide (BNP) are produced by myocardial tissue in
tation. Otherwise, there are no particular risks. response to increased pressure and wall stress and are
Costs are dependent on the laboratory. markers for cardiac dysfunction and heart failure.
106 Section I Diagnosis of Heart Disease

Figure 5-5. Simultaneous lead I, II, and III ECG showing the effect of a vagal maneuver on a supraventricular tachycardia (atrial
fibrillation in this example). Note the dramatic slowing of the heart rate which results in clearer demonstration of the hallmarks of
atrial fibrillation (irregularly irregular rhythm, lack of P waves and fibrillation waves). 50 mm/sec; 10 mm/mV.

Technique Limitations, Risks, and Costs

Mature ANP and BNP have short half-lives, Natriuretic testing in veterinary medicine is a
and clinical assays that target prohormones relatively recent phenomenon and caution should
(proANP and NT-proBNP) are more useful. De- be exercised when using new diagnostic tests
pending on the assay being used, heparinized or until they are more fully validated. Further stud-
EDTA plasma or serum is submitted to the ap- ies are necessary to better characterize the util-
propriate laboratory. Samples should be centri- ity of these tests for prognostic and therapeutic
fuged and separated after collection. If analysis monitoring.
is delayed more than a day, samples should be
Newer Cardiac Imaging
Clinical utility Techniques
These assays have the potential to differenti- Although these techniques are not widely avail-
ate between cardiac and extracardiac causes of able, familiarity with their potential applications
dyspnea, allow prognostication, and monitor is helpful for identifying referral candidates.
response to cardiac disease therapy. The follow- Computed tomography and magnetic resonance
ing guidelines have been established for canine imaging are useful adjunctive techniques that are
proANP (Vetsign proANP, Guildhay Ltd, UK): less invasive than angiocardiography, and may be
proANP > 1700 fmol/ml is consistent with con- advantageous over echocardiography for certain
gestive heart failure; proANP < 1350 fmol/ml is diseases such as cardiac neoplasia and pericar-
considered normal; proANP 1351 to 1700 fmol/ml dial disease. Nuclear scintigraphy is particularly
is suggestive for heart failure, but results are useful for quantitative assessment of intracardiac
notconclusive. In dogs presenting to emergency shunts.
services with dyspnea, EDTA plasma proANP
concentrations >1350 fmol/ml were consistent
with dyspnea due to congestive heart failure (as
Computed Tomography
opposed to dyspnea caused by primary respiratory
disease). The following guidelines appear use- An x-ray technique that displays cross-sectional
ful for canine NT-proBNP (Canine CardioCare, images of the body.
Veterinary Diagnostics Institute, Irvine, CA): NT- Assessment of cardiac function and precise defi-
proBNP > 450 pmol/L is consistent with heart nition of intracardiac anatomy requires either
disease (but not necessarily congestive heart fail- electrocardiographic gating or a millisecond
ure), NT-proBNP > 1000 pmol/L accompanied computed tomography (CT) scanner.
by clinical signs of dyspnea is consistent with An intravenous injection of iodinated contrast is
congestive heart failure. used to define the blood pool.
Chapter 5 Special Diagnostic Techniques for Evaluation of Cardiac Disease 107

the blood pool. A scintillation (gamma) camera

Magnetic Resonance Imaging
interfaced with a computer analyzes and stores
A high natural contrast exists between blood and the data.
cardiovascular structures; therefore, contrast me- The direction and severity of congenital intra-
dium is not required to discriminate the blood cardiac shunts can be determined. Regional dis-
pool. tribution of myocardial perfusion can also be
Physiologic gating of the imaging sequence is visualized.
necessary for cardiac imaging.
Magnetic resonance images give useful informa-
tion on cardiovascular morphology, function, and
tissue character. The required technical expertise and expense of
equipment limit their use in general veterinary
Nuclear Cardiology
Gamma rayemitting radiopharmaceuticals (ra-
dionuclides) are injected intravenously and are
Suggested Readings
either extracted by the myocardium or remain in Daniel MD, Bright JM: Nuclear imaging, computed to-
mography, and magnetic resonance imaging of the
heart. In Fox PR, Sisson DD, Moise NS, eds: Text-
Frequently Asked Questions book of canine and feline cardiology, Philadelphia,
1999, WB Saunders.
How is a vagal maneuver helpful when assessing a Kittleson MD: Syncope. In Kittleson MD, Kienle RD,
dog with a suspected supraventricular tachycardia? eds: Small animal cardiovascular medicine, St Louis,
An effective vagal maneuver will transiently increase 1999, Mosby.
vagal tone. The technique can be helpful to differen- Miller MS, Calvert CA: Special methods for analyzing
tiate between sinus tachycardia, as during a normal arrhythmias. In Tilley LP, ed: Essentials of canine
physiologic response to pain, fever, and so on, and
and feline electrocardiography, ed 3, Malvern, Penn,
a pathologic ectopic supraventricular tachycardia
1992, Lea & Febiger.
(SVT), such as paroxysmal atrial tachycardia. A grad-
Rush JE: Syncope and episodic weakness. In Fox PR,
ual slowing of the heart rate (over several seconds)
suggests the focus is sinus because the sinus node Sisson DD, Moise NS, eds: Textbook of canine and
accelerates and decelerates gradually. An abrupt ces- feline cardiology, Philadelphia, 1999, WB Saunders.
sation of the tachycardia is suggestive of a pathologic Thomas WP, Sisson D: Cardiac catheterization and angio
focus (ie., SVT). Lack of response to a vagal maneuver graphy. In Fox PR, Sisson DD, Moise NS, eds: Text-
can occur with either condition and is nondiagnostic. book of canine and feline cardiology, Philadelphia,
Occasionally an SVT will respond to a vagal maneu- 1999, WB Saunders.
ver with slowed AV nodal conduction resulting in
second degree AV block with an underlying rapid
P-wave rate.

Cardiovascular Disease

6. Acquired Valvular Disease 11. Pericardial Disorders and Cardiac

Jonathan A. Abbott Tumors
Anthony H. Tobias and Elizabeth A. McNiel
7. Canine Cardiomyopathy
Mark A. Oyama 12. Congenital Heart Disease
Keith N. Strickland
8. Feline Cardiomyopathy
Richard D. Kienle 13. Cardiovascular Effects of Systemic
9. Cor Pulmonale and Pulmonary
Francis W. K. Smith, Jr., Donald
P. Schrope, and Carl D. Sammarco
Lynelle R. Johnson
14. Systemic Hypertension
10. Heartworm Disease
Rosemary A. Henik and Scott A. Brown
Clay A. Calvert and Justin David Thomason
Chapter 6

Acquired Valvular Disease

Jonathan A. Abbott

Introduction Prevalence and Incidence

s0010 s0030

Acquired primary valvular disease in dogs and cats Degenerative MVD is the most common car-
p0010 u0010

generally is degenerative or less commonly, infec- diac disease in the dog; it is an acquired disease,
tive. Other pathologic processes, such as neoplasia, and the prevalence is greatest in the geriatric
rarely affect the cardiac valves. Myxomatous de- population.
generation of the mitral valve is the most common Clinical evidence of degenerative valvular dis-
cardiac disease in the dog. Mitral valve incompe- ease is detected in approximately 30% of dogs
tence due to valvular degeneration can result in pro- aged 13 years and older.
gressive cardiac enlargement and, in some cases, MVD is a progressive disease, and subtle changes
congestive heart failure (CHF). Clinical signs, par- in valve structure precede the development of
ticularly cough due to compression of the mainstem clinically evident valvular dysfunction. Conse-
bronchi by an enlarged left atrium, may precede the quently, the prevalence of MVD detected by post-
development of CHF. The clinical consequences of mortem examination is higher than that reported
degenerative valvular disease are observed primar- in clinical studies.
ily in elderly, small-breed dogs. Postmortem evidence of advanced degenerative
Infective endocarditis (IE) is an uncommon form valvular disease was found in 58% of dogs older

of acquired valvular disease that is observed oc- than 9 years; when mild degenerative changes
casionally in dogs and rarely in cats. Middle-aged are included, the postmortem prevalence exceeds
medium- and large-breed dogs are affected most of- 90% in dogs older than 13 years.
ten. The clinical signs of IE relate to sepsis, throm- MVD may affect any breed of dog, but clinical
boembolism, and CHF. consequences of MVD are observed most often
in small-breed dogs. Miniature Poodles, Pomera-
nians, Yorkshire Terriers, Chihuahuas, and other
Degenerative Mitral Valve

small dogs are commonly affected. The prevalence

of MVD in Cavalier King Charles Spaniels is par-
Based on its clinical and pathologic features, nu- ticularly high, and in dogs of this breed, the disease

merous designations for degenerative mitral value is sometimes clinically evident at a young age.
disease (MVD) have been proposed. The terms Male dogs are affected somewhat more often than
myxomatous valvular degeneration, myxomatous females.
transformation, mucoid degeneration, endocardio- Degenerative valvular disease is uncommon in
sis, chronic valvular disease, and degenerative val- cats, and when it occurs it seldom results in clin-
vular disease all refer to the same disorder. ical consequences.
Chapter 6 Acquired Valvular Disease 111

Key Point


Degenerative MVD is the most common The cause of MVD is unknown.


cardiac disease in the dog; it is an acquired

MVD is often observed in chondrodysplastic dog
disease, and the prevalence is greatest in the
geriatric population. breeds. Because MVD has been associated with
concurrent disorders such as bronchomalacia and
intervertebral disc disease, it has been suggested

that MVD is but one expression of a systemic

connective tissue disease.
Grossly, MVD is characterized by nodular distor- Recent evidence suggests a possible role for the

tion of the valve leaflets as well as by thicken- vasoactive peptide endothelin in the pathogenesis
ing and, sometimes, lengthening of the chordae of MVD. Relative to mitral valve tissue obtained
tendineae. The appearance of a small number from healthy young dogs, degenerative mitral
of nodules at the free edge of the valve leaflet is leaflets had a greater density of endothelin recep-
the initial pathology. As the disease progresses, tors. Furthermore, the density of endothelin re-
these nodules increase in number and size and co- ceptors was related to the severity of MVD.
alesce. In severe cases, the leaflets are contracted, Because distinct breed predispositions are recog-
and the free edge of the leaflet rolls inward to- nized, it is likely that there is a genetic predis-
ward the ventricular endocardium (Figure 6-1). position for the development of MVD. Available
When severe, these abnormalities prevent coapta- evidence suggests that the tendency to develop
tion of the valve leaflets, resulting in mitral valve MVD is not subject to simple Mendelian inheri-
incompetence. tance but rather is a polygenic trait.
MVD is histologically characterized by the In Cavalier King Charles Spaniels, parental sta-
deposition of mucopolysaccharides primarily tus with respect to age and murmur intensity is
within the spongiosa layer of the valve leaflet. an important determinant of the prevalence of
Fibrosis of the valve is also present, but is not murmurs in 5-year-old offspring. Based on this,
the dominant histologic feature. Inflammatory it appears that the age at which MVD develops is
infiltrates are absent; MVD is a sterile, degen- inherited.
erative disease that bears no known relationship
Key Point

to endocarditis.
The cause of MVD is not known but genetic

factors are likely important.

Key Point
The prevalence of endocarditis is no greater

in dogs affected by MVD than in other dogs.

The mitral valve apparatus consists of the mitral

valve leaflets, the fibrous valve annulus, the chor-

dae tendineae, and the left ventricular papillary
The two mitral leaflets are known as the septal
(anterior) and the caudal (posterior) leaflets. In
health, the mitral leaflets are thin, translucent
structures that are tethered to the left ventricular
papillary muscles by the chordae tendineae. The
two left ventricular papillary muscles arise from
the caudal (free) wall of the left ventricle. The
basilar attachment of the mitral leaflets is to the
fibrous left atrioventricular valve ring, known as

the mitral annulus.

Figure 6-1. A specimen that demonstrates the gross features The initiation of valve closure is a passive pro-
of severe mitral valve degeneration. The mitral valve leaflets cess; in early systole, when left ventricular pres-
are abnormally thick and nodular. (The author acknowledges
sure exceeds left atrial pressure, the mitral valve
the Department of Veterinary Pathology, Western College of
Veterinary Medicine, University of Saskatchewan, Saskatoon, leaflets are forced into apposition. In normal
SK, Canada S7N 5B4, for providing this photograph.) individuals, the tethering effect of the chordae
112 Section II Cardiovascular Disease

tendineae prevents prolapse, or bowing, of the Due to maladaptive neuroendocrine responses

leaflets into the left atrium. associated with heart failure, cardiac dysfunc-
Coaptation of the normal mitral leaflets is tion tends to be progressive. Because of this, the
complete, and there is little or no regurgitation elimination of congestive signs does not signify
through the valve orifice. The normal mitral resolution of the heart failure state. When the
valve ensures that the entirety of the left ventric- disorder responsible cannot be definitively cor-
ular stroke volume is ejected through the aorta. rected, heart failure is a terminal syndrome.
When the mitral valve is incompetent, a fraction The imposition of a chronic volume load on the
of the left ventricular stroke volume is ejected heart can result in deterioration of systolic myo-
through the mitral valve regurgitant orifice into cardial function, a state sometimes known as
the left atrium. cardiomyopathy of overload. In general, MR is
Mitral valve regurgitation (MR) may be mild and relatively well tolerated by the myocardium be-
have minimal consequences, or it can be severe. cause the left atrium represents a low-pressure
The severity of MR is determined principally reservoir into which the ventricle can eject blood.
by the size of the regurgitant orifice and the re- In fact, dogs that develop CHF due to MR often
lationship between left atrial and left ventricular do so at a time when systolic myocardial function
systolic pressure. Potentially, both of these deter- (contractility) is, based on echocardiographic in-
minants can be pharmacologically manipulated dices, normal or only mildly diminished.
by administration of vasodilators. MR may remain clinically silent until it is advanced.
MR increases left atrial pressure which poten- When CHF results from MR, clinical signs may in-
tially results in left atrial dilation. When the mi- clude weakness, syncope, cough, and dyspnea.
tral valve leaks, the pulmonary venous return is Cough is a centrally mediated reflex, and most
augmented by the regurgitant volume; in conse- cough receptors are located in the large airways.
quence, the ventricle is filled in diastole not only The etiology of cough associated with MR in
by blood that has returned from the lungs, but small-breed dogs is probably multifactorial and
also by blood that has been regurgitated into the may result from any of the following:
atrium. Therefore, MR imposes a volume load on Pulmonary edema when fluid floods the alveoli
the left ventricle and the left atrium. Compression of the mainstem bronchi by an
High end-diastolic pressures and volumes result enlarged left atrium
in ventricular dilation and hypertrophy. Hyper- Reflexes mediated through stimulation of the
trophy of this type, in which the ratio of wall juxtapulmonary (J) receptors; these receptors
thickness and chamber size remains roughly un- are associated with the pulmonary capillaries
changed, is known as eccentric hypertrophy. and are sensitive to increases in pulmonary ve-
Severe MR may increase left ventricular filling nous pressure.
pressures. High filling pressures are reflected
backward, raising pulmonary vein pressure and Key Point

potentially initiating the development of pulmo-

It is important to recognize that cough can
nary edema.
be associated with MVD in the absence of
The syndrome of clinical signs and neuroendo- pulmonary edema. When this is the case, the
crine activation that results from cardiac dysfunc- cough is a sign of heart disease but not a sign
tion is known as heart failure. Because veterinary of heart failure; this distinction is important
patients cannot offer subjective observations because a diagnosis of CHF carries important
the perception of breathlessness during exertion prognostic and therapeutic implications.
for examplethe presence of congestive signs s0070

is generally used as an objective criterion for the

Clinical Presentation
CHF is the syndrome of clinical signs caused by
venous pressure elevations that result from car- History

diac dysfunction. Left-sided CHF is defined by MVD exhibits a broad spectrum of severity. In

the presence of cardiogenic pulmonary edema. most affected dogs, MVD does not cause clinical
Right-sided CHF refers to clinical signs that signs, and the disease is detected when a cardiac
result from systemic congestion; in dogs, asci- murmur is incidentally identified in patients pre-
tes is the most common manifestation of right- sented for routine health care or for management
sided CHF. of noncardiac disease.
Chapter 6 Acquired Valvular Disease 113

In cases in which MVD does become clinically

apparent, cough is usually the clinical sign that
is first observed by the dog owner. Coughing due
to bronchial compression is often dry and harsh.
When coughing is due to pulmonary edema or
congestion, other signs, such as exercise intol-
erance and tachypnea, are usually present. The
cough associated with pulmonary edema may be
moist and productive. The expectoration of pink
froth is sometimes observed in patients with ful-
minant pulmonary edema.
Occasionally, syncope is the clinical sign that is
seen first in dogs with MVD. Syncope is a tran-
sient loss of consciousness that is usually related
to a sudden and precipitous decline in cerebral
perfusion. MVD can be responsible for syncope
when cardiac enlargement predisposes to arrhyth- f0020

mias. Additionally, exertional syncope may result Figure 6-2. A phonocardiogram recorded from a 13-year-
old female spayed mixed-breed dog with a grade 4/6 systolic
when MR limits stroke volume so that cardiac murmur. The systolic murmur (sm) begins at the first heart
output does not adequately increase to meet the sound (S1), is evident throughout systole and obscures the
physiologic demands of exercise. Alternatively, second heart sound.
syncope on exercise or excitement or associated
with paroxysmal cough can result from sudden present when the murmur intensity is grade V/VI
onset of reflex-mediated bradycardia. or greater.
Other clinical signs related to reduced cardiac A high-frequency, mid-systolic click (Figure 6-3) is
performance, including tachypnea, exercise in- sometimes heard in older, small-breed dogs. These
tolerance, and abdominal distention caused by clicks may be associated with prolapse of the mitral
ascites, occasionally prompt owners of affected valve. In many dogs, clicks are a precursor of MR.
dogs to seek veterinary attention. Often, a soft systolic murmur of MR can also be
heard in patients that have systolic clicks.
Physical Findings When MR is severe, the third heart sound some-

The most notable feature of the physical ex- times is audible and results in an S3 gallop. Care

amination is a systolic murmur that is usu- must be taken to distinguish a mid-systolic click
ally heard best over the left cardiac apex. The from a gallop. In general, a systolic click is louder
murmur of MVD is indistinguishable from the than is the third heart sound, and in patients with
murmur caused by other disorders, such as IE MVD, a click typically is heard in association with
or dilated cardiomyopathy (DCM), which also findings that suggest mild MR. In contrast, an S3
can result in MR. Importantly, however, an ac- gallop usually reflects severe MR and generally
quired, left apical, systolic murmur in an older, is heard in patients with loud murmurs. Note that
small-breed dog is almost always due to MVD. S3 is sometimes audible in patients with DCM.
The intensity of the murmur depends on a num- However, DCM is typically a disorder of large
ber of factors, but severe MR usually causes and giant breed dogs.
a loud murmur. Severe MR associated with a The femoral arterial pulse is usually of normal
nonrestrictive regurgitant orifice can result in a strength when MR is present, but the pulse may
soft murmur but this is extremely uncommon in have a rapid rise. Very severe MR can be associ-
MVD. Phonocardiographically, the murmur of ated with diminished pulse strength.
MR typically has a plateau-shaped configura- Crackles may be heard in patients with pulmo-
tion meaning that the murmur has a similar in- nary edema. It should be recognized that the
tensity throughout systole; when the murmur is prevalence of primary respiratory diseases such
loud, the second heart sound may be obscured as chronic bronchitis in the patients most often
(Figure 6-2). affected by MVD is relatively high. Primary re-
An exaggerated apical impulse is often evident spiratory tract diseases can explain adventitious
on precordial palpation of patients with moderate pulmonary sounds, such as crackles, in the ab-
or severe MR. By definition, a precordial thrill is sence of pulmonary edema.
114 Section II Cardiovascular Disease


Figure 6-3. A phonocardiogram recorded from an 11-year-old male castrated Shih-Tzu. A mid-systolic click (click) is shown.

Abdominal palpation is usually normal in patients The presence of respiratory sinus arrhythmia (RSA)
with MVD, but hepatic enlargement or even asci- can also be of diagnostic value. Much of the mo-
tes may be present when there is severe tricuspid ment-to-moment heart rate variability observed in
valve disease, or when pulmonary hypertension healthy dogs is due to the effect of vagal discharge.
complicates the presentation of MVD. In patients with severe cardiac disease, there is little
vagal influence on heart rate and rhythm and as a
Key Point

result, RSA is not prominent. In contrast, sinus ar-

Patients with clinically evident MVD have car- rhythmia is often preserved or even accentuated
diac murmurs. The intensity of the murmur when primary respiratory tract disease is respon-
roughly parallels disease severity so that se- sible for clinical signs. The physical finding of RSA
vere MR usually results in a loud murmur. is virtually incompatible with a diagnosis of CHF.
Although exceptions occur, clinical signs are usu-
Patients with Mitral Regurgitation and ally related to respiratory tract disease in patients
concurrent respiratory tract disease that are overweight, have sinus arrhythmia and a

Primary diseases of the respiratory tract, such soft cardiac murmur.


as collapsing trachea and chronic bronchitis, are In contrast, the clinical signs of thin patients with
common in the patient group that is affected by loud murmurs and tachycardia are more likely to
MVD. In an individual patient, it can be difficult result from cardiac disease or CHF.
to determine whether cardiac disease or respira- Coughing in elderly, small-breed dogs that do not
tory disease bears the greatest responsibility for have cardiac murmurs is almost always due to
the development of clinical signs. Key Point

In general, patients that have severe MR are more


Primary respiratory tract disease is relatively

likely than patients with respiratory disease to
common in the patient group affected by
have poor body condition. MVD. The patient history and physical find-
Although loud murmurs of MR are sometimes ings are helpful in distinguishing clinical signs
clinically inconsequential, it is extremely uncom- caused by cardiac disease from signs caused
mon for soft murmurs to indicate severe MR with by respiratory disease.
cardiac enlargement.

primary respiratory tract disease (Table 6-1).

Chapter 6 Acquired Valvular Disease 115

Table 6-1 Guidelines for Clinical Assessment Diagnostic findings



of Elderly Small-Breed Dogs With

Cough and Cardiac Murmur* Thoracic radiography

In most cases, thoracic radiography is the most im-


Cardiac Respiratory portant element of the diagnostic approach to MVD.

Disease Disease
MVD is extremely common but progresses at a rate
Body Thin Obese that varies greatly among individuals. Many patients
condition with MVD are subclinical (asymptomatic) and
Cardiac Loud Often soft, occa- never develop clinical signs related to MR. Early in
murmur sionally loud the course of MVD, the cardiac silhouette is normal.
Heart rate Rapid Normal or slow If clinically consequential MR develops, then there
Rhythm Regular, unless Exaggerated is enlargement of the cardiac silhouette. It should be
pathologic arrhyth- respiratory ar- recognized that the ability of thoracic radiographs to
mias are present rhythmia may delineate specific cardiac chambers is limited. In gen-
be present eral, the left atrium can be assessed with the greatest
certainty. This is fortunate because, in the overwhelm-
*It is important to recognize that exceptions to these generali-
ties certainly occur. However, when a patient exhibits all of
ing majority of cases, left atrial enlargement precedes
the findings in the left-hand column, it is likely that cardiac the development of CHF. A diagnosis of left-sided
disease or, perhaps, congestive heart failure, is responsible CHF secondary to MVD rarely can be supported in
for the cough. It must be recognized that some patients have the absence of radiographic left atrial enlargement.
both respiratory tract disease and cardiac disease. Ultimately,
the distinction between respiratory tract disease and cardiac
Radiographic Appearance of Left Atrial

is made through diagnostic imaging; thoracic radiographs are

indispensable, and echocardiography often provides useful, Enlargement

complementary data. The left atrium is left of, and caudal to, the right
atrium. Radiographically, it occupies the cau-
dodorsal area of the cardiac silhouette in the lat-
Large-Breed Dogs with Mitral Valve Disease eral projection.
A syndrome of severe MR and concurrent myo- In the absence of left atrial enlargement, the cau-

cardial dysfunction is recognized in medium- and dal portion of the trachea curves ventrally over
large-breed dogs. The fact that this observation the caudal aspect of the cardiac silhouette.
was made relatively recently is probably explained When the left atrium is enlarged, the caudal border
by the increasing availability of echocardiog- of the cardiac silhouette straightens, and the trachea
raphy and not by a change in the epidemiology is forced dorsally to varying degrees. With marked
of MVD. Before widespread availability of this left atrial enlargement, the left mainstem bronchus
technology, large-breed dogs with heart failure is narrowed, and the trachea adopts a path that is

generally were assumed to have primary myocar- parallel to the thoracic vertebrae. Occasionally, se-
dial disease. vere left atrial enlargement has the appearance of a
For reasons that are not known but may relate to mass that splits the mainstem bronchi.
the geometry or pattern of contraction of inher- In the ventrodorsal projection, the left atrium is
ently larger ventricles, large-breed dogs with MR located near the center of the cardiac silhouette.
are more apt to develop echocardiographically When enlarged, the left atrium splits the mainstem
evident myocardial dysfunction than are small- bronchi to varying degrees. This is apparent in well-
breed dogs. penetrated radiographs and results in an appearance
The gross appearance of the valvular lesions in that is sometimes known as the crab sign or the
large dogs tends to be less impressive than it is in bowlegged cowboy (Figures 6-4 and 6-5).
small breed dogs. Additionally, in the ventrodorsal view, enlargement
Perhaps because myocardial dysfunction compli- of the left atrium may cause a bulge which repre-
cates MVD in large dogs more often than it does sents the atrial appendage at the 3 oclock position.
in small dogs, the prognosis may be worse than in
smaller dogs. Radiographic Findings of Pulmonary

Congestion and Edema

The radiographic finding of pulmonary venous

distention reflects increases in pulmonary venous

pressure. Pulmonary venous distention suggests
116 Section II Cardiovascular Disease

Figure 6-4. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from a 10-year-old mixed-breed dog with degen-

erative mitral valve disease. There is relatively mild but distinct left atrial enlargement, as evidenced by elevation of the trachea
and loss of the caudal waist in the lateral film.


Figure 6-5. A lateral thoracic radiograph obtained from a 14-year-old female spayed mixed-breed dog with severe mitral valve
incompetence due to degenerative disease. The left atrium is markedly enlarged, and the left mainstem bronchus is compressed.
Chapter 6 Acquired Valvular Disease 117


Figure 6-6. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from an 11-year-old female spayed Miniature
Poodle with degenerative mitral valve disease. The cardiac silhouette is markedly enlarged, and there is evidence of left atrial
enlargement. Pulmonary opacities compatible with edema are distributed throughout the lung; the edema is most noticeable in
the caudodorsal lung field.

pulmonary congestion and may precede the de- When tissue fluid weeps into the pulmonary
velopment of pulmonary edema. alveoli, it provides contrast with air-filled
A central, or perihilar, distribution often charac- structures such as the bronchi, resulting in air
terizes cardiogenic pulmonary edema in dogs. bronchograms. Alveolar pulmonary opacities
The development of interstitial pulmonary edema together with radiographic evidence of left atrial
precedes the appearance of alveolar edema. enlargement are diagnostic of left-sided CHF
Blurring of vascular detail in the presence of left atrial (Figure 6-6). The presence of alveolar pulmo-
enlargement and, sometimes, concurrent pulmonary nary edema indicates severe CHF that is almost
venous distention characterizes the radiographic ap- invariably associated with noticeable respiratory
pearance of interstitial pulmonary edema. distress.
118 Section II Cardiovascular Disease


Figure 6-7. A right parasternal short-axis echocardiographic image obtained from an 11-year-old male castrated Cocker Spaniel
with severe mitral valve regurgitation. The left atrium (LA) is markedly enlarged; the dimension of the body of the atrium is more
than twice the diameter of the aorta (Ao).


Figure 6-8. A right parasternal long-axis echocardiographic image obtained from a 15-year-old male castrated Cavalier King
Charles Spaniel with mitral regurgitation due to degenerative disease. The image was obtained during systole. The left atrium is
enlarged and there is distinct prolapse of the mitral valve leaflets. LV, Left ventricle; LA, left atrium.

Key Point the left atrium in systole is commonly observed

In most cases, thoracic radiography is the (Figure 6-8).
most important aspect of the diagnostic ap- The echogenicity of affected leaflets is gener-
proach to MVD. ally uniform and nodular thickening is diffuse. In
contrast, infective vegetations typically are local-
ized, may exhibit motion that is independent of
Echocardiography the valve leaflet and are more, or less, echogenic
Echocardiographic examination of patients with than the valve leaflet.

MVD demonstrates variable degrees of left atrial Often, the tricuspid leaflets are affected, although
(Figure 6-7) and left ventricular dilation. Hypertro- seldom as markedly as the mitral valve.
phy is usually adequate to preserve a near-normal Evaluation of myocardial function in patients
relationship between the diastolic luminal dimen- with MR is difficult. When MR is moder-
sion and wall thickness. ate or severe, loading conditions imposed on
The mitral leaflets may be noticeably thicker the left ventricle are altered and left ventricu-
than normal, and prolapse of the leaflets into lar performance is hyperdynamic (Figure 6-9)
Chapter 6 Acquired Valvular Disease 119



Figure 6-9. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from an 11-year-old female
spayed Cavalier King Charles Spaniel. Left ventricular dilation and hypertrophy are evident. Left ventricular systolic performance
is hyperdynamic; the fractional shortening is 46%.

provided myocardial function (contractility) is scaling, in which echocardiographic dimensions

preserved. are related to the cube root of body weight, and the
Ejection phase indices of systolic performance use of aorta-based ratio indices overcome some of
such as fractional shortening are elevated because the theoretical and practical limitations of compar-
these variables are highly load-dependent. When ing cardiac dimensions to body weight.
MR is present, impedance to ventricular empty- The end-systolic volume index calculated as
ing is reduced because the ventricle is able to LVIDs3/BSA, where LVIDs is the end-systolic
eject blood into the low-pressure reservoir of the left ventricular dimension and BSA is body sur-
left atrium. Additionally, end-diastolic ventricular face area has been used in the assessment of
stretch associated with MR increases the force of myocardial function in dogs with MR. An in-
contraction and contributes to the finding of hy- dex greater than 30 ml/m2 suggests myocardial
perdynamic ventricular performance. A normal dysfunction.
or subnormal fractional shortening in the setting Doppler echocardiography is used to evaluate ve-
of moderate or severe MR suggests systolic myo- locity, direction, and character of blood flow.
cardial dysfunction (Figures 6-10 and 6-11). Doppler evidence of disturbed flow within the
Because the end-systolic left ventricular dimen- left atrium during systole is noninvasive confir-
sion is determined by relatively few factors, it is mation of the presence of MR (see Figure 6-8).
likely a better index of myocardial function but, When stroke volume is severely affected by MR
because cardiac dimensions are related to body or systolic failure, reductions in aortic outflow
size, end-systolic left ventricular dimension has velocities may be apparent.
the disadvantage that it must be interpreted in the Assessment of the severity of MR can be evalu-
context of body weight or perhaps more appro- ated quantitatively or more often, semi-quantita-
priately, the cube root of body weight. Recently tively by Doppler echocardiography.
a method of echocardiographic mensuration in Quantitative methods include evaluation of the
which cardiac dimensions are indexed to aortic radius of color Doppler proximal flow conver-
diameter or the aortic diameter predicted based gence and the calculation of regurgitant fractions
on body weight was proposed. Both allometric through volumetric flow analysis; however, these

Figure 6-10. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from 12-year-old male cas-
trated Keeshond weighing 18 kg. There was Doppler evidence of severe mitral regurgitation due to degenerative valve disease. Left
ventricular systolic performance evaluated by fractional shortening is normal (38%) but the end-systolic left ventricular dimension is
markedly enlarged which provides evidence of systolic myocardial dysfunction. The cardiac rhythm is atrial fibrillation.


Figure 6-11. M-mode echocardiogram obtained at the level of the left ventricular papillary muscles from 12-year-old male
castrated Dalmatian. There was Doppler evidence of severe mitral regurgitation due to degenerative valve disease. Left ventricu-
lar systolic performance evaluated by fractional shortening is subnormal (22%) and the end-systolic left ventricular dimension
is markedly enlarged. These findings provide evidence of systolic myocardial dysfunction. An examination recorded three years
before this one had demonstrated mitral valve regurgitation and mildly hyperdynamic systolic performance. In the interim, the
end-diastolic and end-systolic left ventricular dimensions had enlarged. Large dogs are more apt to develop systolic myocardial
dysfunction as a consequence of mitral valve disease than are small dogs.
Chapter 6 Acquired Valvular Disease 121


Figure 6-12. A right parasternal long-axis echocardiographic image obtained from a 5-year-old female spayed Cavalier King
Charles spaniel with mitral regurgitation due to early onset degenerative disease. Color-flow Doppler mapping demonstrates mild
mitral valve regurgitation (MR). The color mosaic occupies less than 50% of the area of the left atrium and the jet is relatively
narrow at its origin (arrow). LV, left ventricle.

Figure 6-13. A right parasternal long-axis echocardiographic image obtained from a 12-year-old female spayed Whippet with
mitral regurgitation due to degenerative disease. Color-flow Doppler mapping demonstrates marked mitral valve regurgitation.
The color mosaic nearly fills the enlarged left atrium and more importantly with respect to evaluation of the severity of regurgita-
tion, the jet is very broad at its origin. LV, left ventricle.

methods are time consuming and have not found means of evaluating the severity of regurgita-
widespread clinical application. tion; a greater width indicates a larger orifice
The area of the color Doppler regurgitant jet and, more severe regurgitation (Figures 6-12 and
relative to that of the receiving chamber is one 6-13). The appearance of proximal flow conver-
means of semi-quantitatively evaluating the se- gencethe color Doppler appearance of accel-
verity of valvular regurgitation; however, many eration through the regurgitant orificesuggests
physiologic and technical factors influence the that MR is at least of moderate severity (Figure
size of the jet and this intuitively simple method 6-14).
has limitations. The width of the regurgitant jet The density of the regurgitant continuous wave
at its origin is another, perhaps more accurate, spectral Doppler signal is roughly proportional
122 Section II Cardiovascular Disease


Figure 6-14. A left parasternal apical echocardiographic image from a 13-year-old male castrated mixed-breed dog with mitral
regurgitation due to degenerative disease. Color-flow Doppler mapping demonstrates marked mitral valve regurgitation. The
region of proximal flow acceleration (arrow) is evident within the left ventricle (LV).

to the number of cells that move into the receiv- e chocardiography cannot provide a diagnosis of
ing chamber and is an alternative means of semi- CHF; it can only demonstrate that cardiac disease is
quantitatively evaluating regurgitant severity sufficiently severe that a diagnosis of CHF is plau-
(Figure 6-15). sible. Although the clinical signs associated with
Ultimately, it is important that the echocardio- MVD may have a sudden onset, the disease pro-
graphic assessment is clinically relevant: in vet- cess itself is chronic. Therefore, left atrial dilation
erinary patients in whom valvular repair is seldom and, usually, concurrent left ventricular dilation are
performed, the effect of valvular regurgitation might expected prior to the onset of clinical signs. Echo-
be of greater importance than its magnitude cardiographic evidence of MR in the absence of left
information regarding chamber size and myocardial atrial and left ventricular dilation is seldom of clini-
function is essential in placing Doppler findings in cal importance. In most cases, then, echocardiogra-
the appropriate clinical context. phy is not essential for the clinical management of
patients with MR. In patients with suspected MR,
Relative merits of radiography and echocardiography is likely to provide clinically

echocardiography in Mitral Valve Regurgitation useful information in the following scenarios:

It should be emphasized that MVD exhibits a broad When the cause of a cardiac murmur is uncertain
p0060 u0120

spectrum of severity. Often, the presence of MR (for example, patients in which the signalment is
is incidental to the presentation, and clinical signs atypical or there is the possibility that the murmur
such as cough are not the result of CHF or even is congenital)
heart disease, but, rather, result from primary re- When it is difficult to discern from thoracic radio-
spiratory disease. Therefore, in most cases, the graphs whether or not the left atrium is enlarged
thoracic radiograph provides the most useful diag- When sudden deterioration has occurred, and
nostic and prognostic information in patients with rupture of the chordae tendineae or left atrium is
MVD. Thoracic radiography not only provides an suspected
assessment of cardiac size but also allows visual- When it is important to evaluate systolic myocar-
ization of the pulmonary vessels and parenchyma. dial function
Thus, thoracic radiography provides an indirect When pulmonary hypertension is suspected
assessment of cardiac performance, and currently
it is the only widely available noninvasive route to
a diagnosis of CHF. Key Point
Echocardiography provides a noninvasive

Echocardiography is not essential to the man-

means by which to evaluate valvular structure, as- agement of most cases of MVD but often pro-
sess cardiac dimensions, evaluate left ventricular vides useful, noninvasively acquired, ancillary
systolic performance, and, with Doppler studies, information.
confirm the clinical diagnosis of MR. However,
Chapter 6 Acquired Valvular Disease 123


Figure 6-15. A, Pulsed wave Doppler echocardiogram obtained from a dog with mitral valve incompetence due to degenera-
tive mitral valve disease. The pulsed wave sample volume was placed within the left atrium; during systole there is a dense, aliasing
multifrequency signal. B, Continuous wave Doppler study of the left atrium of a dog with severe mitral valve incompetence due
to degenerative mitral valve disease. The signal is quite dense, suggesting severe regurgitation.
124 Section II Cardiovascular Disease

Electrocardiography Unfortunately, despite evidence that angiotensi-

Electrocardiography is useful primarily for the converting enzyme (ACE) inhibitors favorably

diagnosis of arrhythmias but also can provide in- affect prognosis in people with asymptomatic
direct evidence of chamber enlargement. ventricular dysfunction, only limited efficacy
The electrocardiogram is an insensitive gauge of of ACE inhibitors in subclinical MVD has been
cardiac chamber size. Nevertheless, it is likely demonstrated.
that findings such as P mitrale are relatively spe- The possibility that enalapril might delay the onset of
cific; that is, when P waves in the caudal fron- heart failure in subclinical MVD has been addressed

tal leads (i.e., II, III, and aVF) are wide, the left by two separate clinical trials. In both the Scandina-
atrium is usually enlarged (Figure 6-16). vian Veterinary Enalapril Prevention (SVEP) Trial
Arrhythmias can complicate the presentation of and the Veterinary Enalapril Trial to Prove Reduc-
MVD. Most often, arrhythmias in MVD take the tion in Onset of Heart Failure (VETPROOF), dogs
form of supraventricular tachyarrhythmias that with subclinical MR were randomized to receive
reflect atrial stretch. Atrial premature complexes placebo or enalapril. Neither trial demonstrated a
and paroxysms of atrial tachycardia are relatively statistically significant effect of enalapril on time
common in patients with MVD. Atrial fibrillation to development of CHF. Although the result of the
develops occasionally and generally indicates VetProof trial was not statistically significant
advanced disease with marked atrial dilation. with respect to the primary end point, the data did
Ventricular arrhythmias (ventricular premature show a tendency toward a favorable treatment ef-
complexes) may develop in association with left fect. Atrial enlargement was an inclusion criterion
ventricular dilation and myocardial fibrosis. for VETPROOF but not for SVEP; however, it is
worthy of consideration that both trials included

patients with relatively mild MR. Patients with

Subclinical (Asymptomatic) Mitral Valve mild and slowly progressive disease tend to expe-

Disease rience few events of interestdeath or occurrence

Definitive published evidence that medical ther- of heart failure, for exampleeven during rela-

apy slows the progression of subclinical (asymp- tively long periods of follow-up. The inclusion of
tomatic) MVD is lacking. mildly affected patients in a clinical trial might
A theoretical, ideal treatment for MVD could be mask a treatment effect that is evident only for
used to prevent or reverse myxomatous degenera- patients with severe disease. It is therefore possible
tion. Unfortunately, drug therapy that affects this that a subpopulation of preclinical patients with
pathologic process has not been identified. severe MR and cardiomegaly would benefit from
In the absence of evidence that medical ACE inhibition. Although this hypothesis has not
therapy can alter the progression of valvular been specifically tested, it is partly refuted by the
degeneration, interest has been directed toward results of SVEP; in that trial, a treatment effect
the possibility that drug therapy might improve was not observed in the subset of dogs that had
prognosis in subclinical MVD by decreasing radiographic cardiomegaly at study entry.
MR or by modifying the process of ventricular The reason that ACE inhibitors do not appear
remodeling. to improve prognosis in subclinical MVD is not


Figure 6-16. An electrocardiogram recorded from a 13-year-old Beagle with physical findings of mitral valve regurgitation.
There is P-mitrale, and the R amplitude exceeds 3 mV, suggesting left atrial enlargement and left ventricular hypertrophy, respec-
tively. (Lead II, 50 mm/s, 1 mV=1 cm.)
Chapter 6 Acquired Valvular Disease 125

known; however, it should be recognized that the Cough caused by Airway Compression
widely cited clinical trials of ACE inhibition in Some dogs with MVD develop a cough that ap-

people with heart disease generally have enrolled pears to result from compression of the mainstem
people with past myocardial infarction or idio- bronchi by an enlarged left atrium. This type of
pathic DCM. MVD in people is generally treated cough can develop prior to the development of
surgically, and, indeed, medical therapy is not pulmonary edema.
recommended for asymptomatic people with MR. Radiographically, there is an enlarged cardiac
Pathophysiologic differences between people with silhouette with distinct evidence of left atrial
ventricular myocardial dysfunction and dogs with enlargement. The mainstem bronchi may be
MVD might also be relevant. In contrast to the noticeably narrowed. The pulmonary veins are
effect of renin-angiotensin-aldosterone system sometimes distended, but the pulmonary intersti-
(RAS) suppression in dogs with experimentally tium and parenchyma have a normal appearance.
induced, primary myocardial disease, neither ACE It is important to recognize that primary respiratory
inhibitors nor angiotensin II antagonists favorably tract diseases such as tracheal collapse and chronic
affect ventricular remodeling in dogs with experi- bronchitis are common in the same patient group
mentally induced MR. However, the syndrome that develops MVD. With very few exceptions,
that results from acute disruption of the mitral clinical signs related to MVD do not occur in the
valve in the laboratory may differ markedly from absence of radiographic left atrial enlargement.
spontaneous valvular degeneration associated with When radiographic findings suggest that the
chronic, progressive MR. Therefore, the clinical cause of cough is airway compression but not
relevance of these research findings is uncertain. pulmonary edema, the use of an antitussive such
Theoretical considerations aside, definitive evi- as hydrocodone or butorphanol is rational.
dence that ACE inhibitors improve prognosis in Vasodilation causes a decrease in systemic vas-
subclinical MVD is lacking. Although it might be cular resistance and, in the setting of MR, can

argued that trials to date have had inadequate sta- increase stroke volume through a decrease in
tistical power, it is likely that a favorable effect of the regurgitant fraction. Potentially these effects
ACE inhibition, if one exists, is modest; the results can decrease left atrial and pulmonary venous
of VETPROOF suggest that 2 years of therapy with pressures and perhaps, reduce left atrial size.
enalapril may delay the onset of pulmonary edema Cough due to compression of the airways gener-
by approximately 4 months. Based on available ally is associated with considerable chamber en-
data, the author generally does not treat dogs with largement and this latter finding is a risk factor
subclinical MVD. On a pragmatic level, the prac- for the ultimate development of heart failure. Be-
titioner is sometimes presented with subclinical cause of the proven favorable effect of ACE inhi-
patients for which radiographic findings suggest bition in patients with heart failure due to MVD,
that the development of frank heart failure is im- it is reasonable to administer an ACE inhibitor
minent. In cases where there is marked left atrial in addition to an antitussive, when cough results
enlargement and pulmonary venous distension, the from bronchial compression.
author prescribes an ACE inhibitor. It is notewor- Some of the benefits of ACE inhibition likely
thy that long-term ACE inhibition has not been as- relate to their neuroendocrine effects. Because
sociated with detrimental effects. Furthermore, it is of this and because the ACE inhibitors are not
possible that these drugs have benefits that relate potent vasodilators, a case might be made for
to effects on other geriatric disorders such as hy- the use of hydralazine or perhaps amlodipine
pertension or renal disease. Based on this and the for dogs with MVD and cough due to bronchial
suggestion of a favorable effect in the VetProof compression. Caution must be exercised if these
trial, ACE inhibition may be a therapeutic consid- drugs are used and patients should be monitored
eration for some patients with cardiac enlargement for the development of systemic hypotension.
and subclinical MR; however, the evidence to Diuretic administration effectively reduces car-
support this approach is neither direct nor strong. diac volumes and may also be efficacious. The
argument can be advanced that this may result in
harmful activation of the renin-angiotensin axis.
Key Point Therefore, in this clinical situation, add furose-
Medical therapy that slows the progression of mide to the drug regimen only when ACE inhibi-
MVD has not been identified. tion in combination with an antitussive, fails to
result in clinical improvement.
126 Section II Cardiovascular Disease

Table 6-2 Suggested Strategies for Diagnostic and Therapeutic Management of Canine
Degenerative Valvular Disease
Cough caused by
Subclinical MR Airway Compression CHF Advanced CHF
Diagnostic X-rays as indicated X-rays X-rays X-rays
approach by clinical Echocardiography Echocardiography Echocardiography
circumstances (i.e., recommended not usually EKG when auscultation
prior to elective when radiographic necessary but provides suggests pathologic
anesthesia, loud evidence of left potentially useful arrhythmia
murmurs particularly atrial enlargement is ancillary information
if associated with equivocal in most cases
tachycardia) EKG when EKG when
EKG when auscultation auscultation suggests
auscultation suggests pathologic pathologic arrhythmia
suggests pathologic arrhythmia
Therapeutic Generally none Antitussive agent and Standard therapy for The following can be
approach indicated although in an ACE inhibitor CHF due to MR considered in addition
some circumstances, Short-term anti- consists of furosemide, to standard
the use of an ACE inflammatory dose an ACE inhibitor, and therapytreatment
inhibitor might be corticosteroids or moderate dietary salt should be tailored to
considered for patients therapeutic diuretic restriction the individual
with distinct cardiac trial considered for Triple diuretic therapy
enlargement (see text) refractory cases Amlodipine (or

When cough fails to respond to ACE inhibition marily of interventions that manipulate the deter-
and modest diuresis, it is important to consider minants of cardiac output and others intended to
the possibility that the cough results not from blunt the maladaptive neuroendocrine response
heart disease but rather from primary respiratory to cardiac dysfunction.
tract disease. In CHF due to MR, left ventricular filling pres-
sure (preload) is excessive, and the consequent
Treatment of Congestive Heart Failure caused increase in venous pressures causes tissue fluid to

by Mitral Valve Disease weep into the pulmonary interstitium and alveoli.
When MR causes clinical signs in people, the The administration of agents that reduce intravas-

disorder is treated surgically. Mitral valve re- cular volume, such as diuretics, or of agents that
pair with preservation of chordal attachments increase venous capacitance, such as nitroglyc-
is generally preferred to replacement of the erin, are therefore a mainstay of therapy.
valve with a prosthesis. Surgical treatment of Nitroglycerin is usually administered transder-
dogs with MVD has been reported. However, mally and is used most often as short-term therapy
expense and the need for expertise in open- in patients with fulminant edema, or occasionally
heart surgery performed during cardiopulmo- as adjunctive therapy in patients with advanced
nary bypass have limited the availability of this disease. The efficacy of transdermal nitroglycerin
approach. is uncertain, and in dogs with experimentally in-
Heart failure due to MVD generally is treated duced MR, the effect of nitroglycerin on filling
medically (Table 6-2). Unless the cause can be pressure did not differ from that of placebo.
definitively treated, heart failure is a terminal Furosemide, a potent agent that acts on the loop
syndrome. Therefore, medical management is in- of Henle, is the diuretic that is used most often
tended to alleviate clinical signs and to prolong in veterinary practice. It can be administered
life. Drug therapy of heart failure consists pri- orally or parenterally; the route of administration
Chapter 6 Acquired Valvular Disease 127

is chosen based upon the clinical status of the pimobendan increases the sensitivity of the con-
patient. The resultant decrease in intravascular tractile apparatus to available calcium, an effect
volume reduces left ventricular filling pressures, which also contributes to the inotropic effect.
allows lymphatic drainage of tissue fluid and, This latter property may be favorable because
resolution of edema. the increase in inotropic state is associated with a
It should be recognized that diuretics reduce pre- relatively low cost in terms of myocardial oxygen
load; this decrease in ventricular filling pressures consumption.
is generally well tolerated by patients with ven- Two recent clinical trials compared the ef-
tricular dilation and has obvious benefits when fects of pimobendan with an ACE inhibitor
edema is present. However, excessive diuresis in dogs with heart failure due to MVD. These
can result in hypotension related to low cardiac trials demonstrated that the clinical effects of
output, prerenal azotemia, and electrolyte distur- pimobendan and furosemide were not inferior
bances. It is generally believed that the optimal to established therapy consisting of furosemide
dose of furosemide is the lowest one that controls and an ACE inhibitor. For some clinical vari-
signs of congestion. ables, pimobendan was superior to the ACE
Importantly, many dogs with clinically evi- inhibitor. The effect of pimobendan when used
dent MVD cough in the absence of pulmonary together with an ACE inhibitor in dogs with
edema, and many of these patients have concur- valvular disease has not been addressed in
rent primary respiratory tract disease. Therefore, published trials to date. Therefore, the stage of
aggressive diuresis following radiographically disease at which pimobendan is most appro-
demonstrated resolution of pulmonary edema priately added to conventional therapy can be
is to be avoided. In most cases of CHF due to debated. It is reasonable to add pimobendan to
MVD, the administration of furosemide rap- the therapeutic regimen when there is clinical
idly and effectively resolves signs. Failure of deterioration despite administration of furose-
patients with MR and respiratory distress to mide and an ACE inhibitor. The concurrent use
respond promptly to diuretic administration of pimobendan, an ACE inhibitor, and furose-
should cause the practitioner to question the di- mide as initial therapy can probably be justi-
agnosis of CHF. fied when MVD results in severe heart failure.
Most patients that develop radiographic pulmo- When pet owners are constrained financially,
nary edema due to MR require lifelong diuretic and it is possible to prescribe only pimobendan
therapy. Early in the course of the syndrome, a or an ACE inhibitor, the available data suggest
dose of 1 mg/kg PO every 12 hours may be ade- that the use of either drug likely is appropriate.
quate, although the inevitable progression of MR In Beagles with mild MVD, chronic, oral adminis-
and CHF and renal tubular adaptations ultimately tration of pimobendan was associated with histo-
necessitate higher doses. logic valvular lesions that were more severe than
Moderate dietary salt restriction is suggested for those in a similar group of Beagles that received
patients with CHF due to MVD. benazepril. These data and a clinical case report
The benefits of ACE inhibition in CHF due to suggest that in some circumstances, pimobendan
MR have been demonstrated. Thus, the use might accelerate the development of degenerative
of an ACE inhibitor together with furosemide valvular lesions. Pimobendan is not indicated for
has become standard therapy for CHF due to the management of subclinical MVD.
MVD. When atrial tachyarrhythmias, particularly atrial
Pimobendan has recently been approved by the fibrillation, complicate MVD, the use of digoxin
United States Food and Drug Administration for (0.22 mg/m2 PO every 12 hours) is generally ac-
use in dogs; it is indicated for the management of the cepted. However, the role of digoxin in the man-
signs of mild, moderate, and severe CHF resulting agement of patients with CHF who are in normal
from DCM or atrioventricular valve insufficiency. sinus rhythm remains a point of controversy.
Previously, pimobendan had been licensed for Digoxin has two principal effects; it acts as a posi-
use in dogs with heart failure in Canada, Europe, tive inotrope and as a negative chronotrope. The
and Australasia. latter property is related to the autonomic effects
Pimobendan is an inodilator that has com- of the drug, which include a central vagomimetic
plex pharmacologic properties. It inhibits phos- effect and effects that may serve to normalize the
phodiesterase and therefore causes vasodilation baroreceptor dysfunction associated with CHF.
and an increase in inotropic state. Additionally, There is evidence to suggest that chronic activation
128 Section II Cardiovascular Disease

of the adrenergic nervous system is detrimental, adrenergic nervous system and RAS is ultimately
and that this abnormality may be partly reversed maladaptive and contributes to the progressive
by the administration of digoxin. nature of heart failure. The use of beta blockers
The need for digoxin in the patient with CHF due in this setting is consistent with this paradigm.
to MVD is difficult to assess. Because the com- Acutely, beta blockers have a negative effect on
monly used echocardiographic indices of contrac- cardiac performance and should be used in canines
tility depend on preload and afterload as well as with heart failure only with caution. Beta blocks-
myocardial function, they are difficult to interpret ers must be initiated at very low doses and titrated
when MR is severe. Furthermore, the results of to effect or target dose over the course of weeks.
clinical trials that enrolled people with heart fail- The use of beta blockers in patients with systolic
ure cast doubt on the intuitive notion that chronic failure is predicated on the belief that these agents
inotropic therapy is beneficial. preserve myocardial function. Although invasive
The effect of digoxin on dogs with heart failure measures may disclose myocardial function in dogs
and sinus rhythm has not been evaluated. How- with MR, the primary cause of clinical signs in pa-
ever, based on the results of a clinical trial that tients with MVD is likely the mechanical effect of
addressed the role of digoxin in people with heart the volume load. Nevertheless, studies of dogs with
failure, it seems likely that the magnitude of ef- experimentally induced MR suggest that beta block-
fect in dogswhether it is positive or negative ade may have a role in the management of MVD.
is probably small. Carvedilol is a third-generation beta blocker that
In patients with MVD and sinus rhythm, it is also an alpha adrenergic antagonist. Because of
seems most reasonable to reserve the use of this latter property, carvedilol is a weak vasodila-
digoxin for patients with advanced CHF and tor, which might make this beta blocker particu-
preserved renal function as digoxin is excreted larly well suited to the management of MVD.
almost entirely through the kidneys. When ad- The author considers the use of carvedilol, or a
ministering digoxin to dogs in sinus rhythm, less expensive alternative such as metoprolol or
aim for a blood concentration of 0.5 to 1 ng/mg atenolol, when echocardiographic findings sug-
on a sample obtained 8 to 10 hours postdose. gest incipient or patent myocardial dysfunction.
Higher concentrations likely are necessary and
appropriate when atrial fibrillation is present. Therapy of severe Congestive Heart Failure

caused by advanced Mitral Valve Regurgitation

Neuroendocrine Modulation The use of triple diuretic therapycombining
u0180 s0230

ACE inhibitors are part of the standard therapeu- furosemide with a thiazide and a potassium-

tic approach to heart failure caused by MR. It is sparing diuretic such as spironolactonecan be
likely that the favorable effect of ACE inhibition considered for patients that require high doses of
is not simply the result of vasodilation. In ad- furosemide to remain free of congestive signs.
dition to this mechanical effect, ACE inhibition The use of three different diuretic agents inter-
serves to protect the heart from the apparently feres with nephron function at anatomically and
detrimental effects of RAS activation. functionally distinct sites; together, the drugs may
Pharmacologic ACE inhibition generally is not have synergistic effects, allowing the use of lower
complete, and because aldosterone may con- doses of the individual agents. Additionally, the
tribute to the development of myocardial fibro- use of a potassium-sparing agent such as spirono-
sis, more complete suppression of the RAS may lactone serves to limit some of the adverse effects
yield positive results. Accordingly, the use of that are associated with the use of high doses of
spironolactonea weak diuretic that antagonizes loop diuretics such as furosemide.
the effect of aldosteroneis considered as adjunc- Despite proven efficacy in the management of
tive therapy for patients with severe CHF due to heart failure due to MVD, the ACE inhibitors
MVD. In humans with CHF, the use of subdiuretic are not potent vasodilators. In some patients with
doses of spironolactone prolongs survival. CHF due to severe MVD, the use of hydrala-
Beta blockers decrease mortality in people with zine or perhaps the vasoselective calcium chan-
heart failure. Because these drugs have a po- nel blocker, amlodipine, in addition to an ACE
tent negative inotropic effect, the mechanism by inhibitor may be helpful. When vasodilators are
which beta blockers improve survival is not in- used in addition to ACE inhibitors, the initial dose
tuitively obvious. However, it is now recognized should be low; ideally, the dose is titrated to effect
that seemingly compensatory activation of the based on serial blood pressure determinations.
Chapter 6 Acquired Valvular Disease 129


Figure 6-17. An early systolic, right parasternal long-axis echocardiographic image obtained from an 8-year-old, fe-
male spayed Papillion. The anterior mitral valve leaflet (arrow) was flailthe leaflet is perpendicular to plane of the mitral
annulusbecause of rupture of a chorda tendineae. LV, Left ventricle.

also develop azotemia when ACE inhibitors are


Key Point
The authors standard medical therapy for It should be recalled that there are essentially
heart failure due to MVD consists of furose-
no circumstances under which diuresis will in-
mide, an ACE inhibitor, and in some cases, di-
goxin. Pimobendan has been approved for the crease stroke volume and renal blood flow. In
treatment of mild, moderate, and severe CHF contrast, judicious vasodilation in the setting of
due to MVD. Spironolactone and beta block- MR can do exactly that. Thus, the development
ers may have roles as adjunctive therapy. of azotemia is usually managed first by a cau-
tious reduction in the diuretic dose. Should cre-
atinine values fail to decrease, the diuretic can be
discontinued; the patients respiratory rate and
Complications of Mitral Valve Disease and character should be carefully monitored. If azo-
its treatment temia persists after discontinuation of diuretic
therapy, the ACE inhibitor can be discontinued,

development of azotemia associated with


diuretic and Angiotensin-Converting Enzyme and cautious intravenous infusion of fluid can be
inhibitor administration initiated.
Monitoring of renal function is suggested for
Rupture of chordae tendineae

patients that are treated with diuretics and ACE

Rupture of chordae tendineae is a relatively com-

inhibitors. ACE inhibitors are not generally

thought to be directly nephrotoxic; however, ACE mon complication of MVD. When a primary
inhibition results in relatively selective dilation of chorda ruptures, the attached mitral leaflet be-
the efferent arteriole of the nephron, a hemody- comes suddenly flail (Figure 6-17), potentially
namic effect that can predispose to the develop- resulting in catastrophic MR, marked elevations
ment of prerenal azotemia. Those patients with in ventricular filling pressures, and fulminant pul-
preexisting renal disease and those receiving monary edema. Rupture of minor chordae may
overly aggressive doses of diuretics are most result in less impressive clinical signs or may be
likely to develop azotemia. In addition, patients subclinical.
with severe cardiac dysfunction that are criti- Rupture of a primary chorda tendinea may occur
cally dependent upon the effects of angiotensin in patients that have substantial, preexisting MR
II to maintain glomerular filtration fraction may and cardiac enlargement and result in clinical de-
compensation the severity of which varies. How-
ever, the development of acute pulmonary edema
130 Section II Cardiovascular Disease


Figure 6-18. Continuous wave Doppler study performed with the Doppler cursor through the right atrium of a dog with severe
endocardiosis. There is tricuspid valve regurgitation (TR); the peak velocity of the TR jet was nearly 5 m/s. This corresponds to a
systolic right atrialright ventricular pressure difference that is close to 100 mm Hg and provides evidence of severe pulmonary
hypertension. In this case, elevated left atrial pressure was partly responsible for pulmonary hypertension but the predicted
pulmonary artery pressure was out of proportion to any credible estimate of left atrial pressure. Reactive vasoconstriction of the
pulmonary arterioles may have contributed to the development of pulmonary hypertension.

in patients with normal cardiac dimensions is P is the pressure difference and v is the veloc-
uncommon. ity of the regurgitant jet). The right atrial pressure
Acute CHF due to chordal rupture is treated is approximated based on clinical findings; in
similarly to acute or decompensated heart failure the absence of right-sided CHF, the right atrial
caused by other disorders although there may be pressure is likely less than 10 mm Hg. Provided
a particular role for the intravenous administra- pulmonary stenosis (PS) is excluded by Doppler
tion of nitroprusside in addition to parenteral di- evaluation of the right ventricular outflow tract,
uretic administration. right ventricular and pulmonary artery pressures
The prognosis depends on numerous factors are equal during systole. Thus, measurement of
of which response to therapy is probably most the velocity of the TR jet can provide noninvasive
important. estimates of systolic pulmonary artery pressure
(Figure 6-18).
Pulmonary hypertension The cause of pulmonary hypertension associated

Pulmonary hypertension occasionally compli- with MVD is probably multifactorial. The pri-

cates the clinical presentation of MVD in the mary function of the right ventricle is to propel
dog. Doppler studies can provide noninvasive the stroke volume through the pulmonary vascu-
estimates of pulmonary artery pressure. Dop- lar tree to the left atrium. Elevations in left atrial
pler echocardiographic evidence of tricuspid pressure cause commensurate increases in right
valve regurgitation (TR) is commonly observed ventricular systolic pressure; if mean pulmonary
in patients with MVD. The velocity of the TR jet artery pressure does not exceed mean left atrial
is related to the systolic pressure difference be- pressure, there is no impetus for forward flow.
tween the right atrium and the right ventricle by The tendency for left atrial hypertension to cause
the modified Bernoulli equation (P = 4v2, where pulmonary hypertension is probably the primary
Chapter 6 Acquired Valvular Disease 131

explanation for high pulmonary artery pressures ten go on to develop CHF. When CHF develops, the
in most cases; however, in some patients, the disease is generally terminal. Even with palliative
increase in estimated pulmonary artery pressure medical therapy, survival is usually measured in
is disproportionate to any credible estimate of left months, with 8 to 14 months being typical.
atrial pressure. In these cases, pulmonary arte-
rial constrictionsometimes known as reactive
Infective Endocarditis

vasoconstriction probably contributes. Alterna-

tively, pulmonary hypertension may be also re- IE occurs occasionally in dogs and rarely in cats.

lated to the presence of concurrent pulmonary or The prognosis is generally grave, and most cases
airway disease. are terminal even with aggressive medical therapy.
There is no established therapy for patients with This latter point emphasizes the importance of de-
pulmonary hypertension associated with MVD. tecting IE, a disease that sometimes poses a consid-
Most vasodilators have a relatively predictable erable diagnostic challenge.
effect on the systemic vasculature; however, the
pulmonary arterioles respond inconsistently to
Prevalence and incidence

the commonly used vasodilator agents, and, in

consequence, it should be recognized that the IE is a relatively uncommon disease that is ob-

use of vasodilators in patients with pulmonary served occasionally in dogs but rarely in cats.
hypertension due to severe pulmonary vascular Mural endocarditis and infection of the tricuspid
disease is not without risk. If a vasodilator with valve are observed occasionally, as is infection
potent peripheral effects fails to decrease pulmo- of endocardial pacing leads; however, bacterial
nary vascular resistance, systemic hypotension or infection of the aortic or mitral valve leaflets is
detrimental increases in right ventricular pressure most common.
and myocardial oxygen demand may result. Middle-aged, large-breed male dogs, including
As initial therapy, interventions that reduce left German Shepherds and Boxers, are affected most
atrial pressure are reasonable. Diuretic therapy often.
should be tailored to rid the patient of radiographic In people, the presence of a congenital cardiac
evidence of pulmonary congestion or edema. Al- malformation is a risk factor for the development
veolar hypoxia is a stimulus for constriction of of IE. An association between congenital subval-
the pulmonary arterioles. If bronchoconstriction vular aortic stenosis and IE of the aortic valve has
associated with primary respiratory disease has been demonstrated, and it is likely that subvalvu-
contributed to the development of pulmonary lar aortic stenosis and, perhaps, other congenital
hypertension, the administration of bronchodila- malformations, are important factors in the epi-
tors may be helpful. demiology of IE in dogs.
When effective control of pulmonary conges-
tion or therapy of primary respiratory tract dis-

ease fails to lower pulmonary artery pressure,

and clinical signs such as weakness can plausi- Based on experimental studies, it is likely that the

bly be related to pulmonary hypertension, the following factors are important in the pathogen-
use of sildenafil in addition to an ACE inhibitor esis of infective valvular endocarditis:
can be considered. Sildenafil is an inhibitor of Endocardial damage (which may result from
phosphodiesterase-V that appears to have a rela- valvular insufficiency, stenosis, or a shunting
tively selective effect on pulmonary arterioles. lesion)
When possible, systemic blood pressure should Activation of clotting factors
be monitored when therapy with this drug is initi- Bacteremia and colonization of a noninfective
ated (see chapter 9). thrombus
The development of a noninfective thrombus
Prognosis precedes valvular infection. Episodes of bac-

The prognosis associated with the development of teremia can result in infection of the thrombus

MVD depends on numerous factors. The major- and the initiation of a variably aggressive in-
ity of patients with MR due to MVD succumb to flammatory process that results in distortion and
noncardiac disease. In the absence of noncardiac destruction of the valve leaflets and their associ-
disease, patients with cough or syncope and distinct ated structures.
radiographic evidence of left atrial enlargement of-
132 Section II Cardiovascular Disease

In clinical cases of canine IE, a congenital car- valve leaflets contributes to valvular incompe-
diac malformation may represent a predisposition tence. The hemodynamic consequences of MR
for the development of the disease. Prostatitis, have been discussed previously.
pyelonephritis, or even dental disease can pro- IE of the aortic valve typically results in aortic valve
vide a source for the development of bacteremia; incompetence, which is a potentially catastrophic
often, however, the site of bacterial entry into the hemodynamic lesion. When the aortic valve be-
bloodstream remains undiscovered. comes incompetent, the left ventricle is filled dur-
Degenerative valvular disease has no known as- ing diastole by the pulmonary venous return and
sociation with IE. Interestingly, despite the preva- by the blood that enters through the regurgitant
lence of dental disease in patients with MR due to orifice. When severe, the increase in ventricular
MVD, IE is extremely uncommon in this patient filling pressures (diastolic ventricular pressures) is
group. reflected back upon the pulmonary venous circula-
Gram-positive bacteria such as the streptococci tion, resulting in pulmonary congestion and edema.
and staphylococci are most often implicated in In contrast to MR, aortic valve insufficiency (AI)
the development of IE. Valvular infection with causes a substantial increase in left ventricular after-
gram-negative organisms such as Escherichia load and therefore, myocardial oxygen demand. As
coli is less common. a result, myocardial dysfunction (cardiomyopathy
With regards to the etiology of IE, there has been of overload) is observed commonly and early in the
recent interest in the fastidious, intracellular or- course of aortic valve IE.
ganisms of the genus Bartonella. Four species Embolization of fragments from the endocardi-
of Bartonella have been documented to cause tis lesion occurs commonly. Sites where infected
canine IE. Although geographical distribution of thrombi lodge include the spleen, the kidney, and
Bartonella IE may not be uniform, Bartonella is occasionally the brain. Most often, embolization
an important cause of IE in northern California of the spleen is clinically silent; infarction of the
and probably elsewhere. Patients with Bartonella kidneys or central nervous system can be cata-
infection are often concomitantly seropositive strophic, resulting in renal failure and nervous sys-
for tick-borne diseases and Bartonella itself tem signs such as head tilt. Embolization of joints,
may be arthropod borne. Bartonella spp. are resulting in bacterial arthritis, can also occur.
difficult to culture using standard microbiological
Clinical presentation

techniques. The diagnosis depends on docu-

mentation of serum antibodies to Bartonella or History

more specifically, demonstration of Bartonella IE in dogs is observed most commonly in a sub-

antigens through polymerase chain reaction acute form. In these cases, historical evidence of
testing performed on bacterial isolates or valve prior illness or of infectious disease may be lack-
tissue. ing. A congenital cardiac murmur may or may
not have been detected. IE is also observed in an
acute form.

Clinical signs in subacute IE are often vague;

The clinical signs of IE relate to sepsis, thrombo- lameness, inappetence, dyspnea, syncope, and ex-

embolism, and cardiac dysfunction. IE results in ercise intolerance are observed most commonly.
intermittent shedding of bacterial organisms into The lameness is often mild and may be difficult to
the bloodstream, resulting in episodes of bacte- localize. The embolization of infected thrombi to
remia. Signs of sepsis, including pyrexia and, joints contributes to lameness, although immune
rarely, circulatory collapse, may be observed. complex arthropathy may be of equal etiologic
Sequelae of sepsis related to chronic antigenic importance.
stimulation and the consequent development of Clinical signs of sepsis may be more prominent in
immune complex disease are observed fairly patients that develop acute IE. The sudden onset of
commonly in IE. Polyarthritis is observed often, fever and the development of a new cardiac mur-
and glomerulonephritis can also develop. mur in the critically ill suggest the presence of IE.
In canine IE, it is often the destruction of the
valve leaflets and associated structures that is of Physical findings

greatest clinical importance. The development Fever is a common but not necessarily a consis-

of infected thrombi results in failure of the valve tent finding in patients with IE. Published cases
leaflets to coapt. Occasionally, perforation of the series of canine IE reflect the experience of re-
Chapter 6 Acquired Valvular Disease 133

ferral centers and are therefore biased. At some tachyarrhythmias, including atrial fibrillation,
point in the natural history of the disease it is are also observed.
likely that most patients are pyrexic; however, The association of third-degree atrioven-
fever associated with IE can be intermittent and tricular block with IE deserves mention. Occa-
may resolve before clinical presentation. sionally an aggressive aortic lesion will invade
The pulse rate is often elevated, as some degree the interventricular septum or, alternatively,
of cardiac dysfunction is commonly present at embolize the nodal coronary artery, resulting
the time of presentation. in destruction of the atrioventricular node or AV
The respiratory rate is elevated, and respiratory bundle. This catastrophic complication is relatively
distress is usually apparent, in patients that have uncommon, but lesser degrees of atrioventricular
developed CHF. block or intraventricular conduction delays, such as
A cardiac murmur is present in the majority of left bundle branch block, are observed fairly often.
patients with established valvular infection. MR Electrocardiographic evidence of cardiac cham-
results in a systolic murmur that is most easily ber enlargement is observed in patients that
heard over the left cardiac apex. Aortic valve survive long enough for the volume overload as-
IE usually results in a diastolic decrescendo sociated with IE to result in chamber dilation and
murmur that is typically heard most easily over the hypertrophy.
left cardiac base. A concurrent systolic murmur
related to the increase in left ventricular stroke Echocardiographic Findings

volume associated with AI results in a murmur The term vegetative endocarditis is generally used

known as to-and-fro or bellows murmur. to refer to cases in which there is a macroscopic,

Diastolic murmurs are uncommon in veterinary infected thrombus associated with a valve leaflet.
patients and are usually soft; consequently, they The echocardiographic findings in vegetative IE
may escape detection. Despite this, they are of are distinctive. In most cases, nodular distortion
considerable diagnostic and prognostic impor- of the valve leaflets is readily apparent (Figure
tance; acquired diastolic murmurs in dogs most 6-20). Often the valvular abnormality is discrete
often result from aortic valve IE. and the lesion may oscillate independently of
When moderate or severe AI is present, the arte- valve motion.
rial pulses are hyperkinetic, or bounding, a physi- When these abnormalities are associated with
cal finding that should prompt consideration of the aortic valve leaflets, the diagnosis is usually
IE whenever signalment and other clinical find- assured.
ings are suggestive. Nodules affecting the mitral valve leaflets are of
lesser diagnostic specificity (Figure 6-21), as it
Diagnostic Findings

can be difficult to distinguish severe MVD from


Thoracic radiography infection of the mitral valve leaflets. To some

Radiographic findings in IE are variable. Car- extent, this distinction is made based upon the
diac enlargement is apparent when valvular le- patients signalment. As stated previously, IE
sions have imposed a chronic volume overload is very uncommon in elderly small-breed dogs
on the heart. Pulmonary congestion or edema is which are, of course, the patients most likely to
commonly observed (Figure 6-19). Occasion- develop severe MVD.
ally, IE results in severe and acute AI; this is The interpretation of subtle valvular abnormali-
one of the few clinical scenarios in which car- ties detected by echocardiography poses a diffi-
diogenic pulmonary edema is observed in as- cult clinical problem, and other, ancillary clinical
sociation with a normal or minimally enlarged data, including the results of blood cultures, must
cardiac silhouette. be considered.
The absence of a readily detectable valvular
Electrocardiography nodule on echocardiographic examination does

There are no electrocardiographic findings that not eliminate IE from the differential diagnosis.

are diagnostic of IE. However, all manner of When vegetative IE of the aortic or mitral valve is
cardiac arrhythmias can be observed in asso- present, there is often echocardiographic evidence
ciation with this disease. Ventricular tachyar- of left atrial and left ventricular enlargement. Pre-
rhythmias, including ventricular tachycardia, mature diastolic closure of the mitral valve and
are relatively common, and supraventricular diastolic flutter of the anterior mitral valve leaflet
indicate severe AI (Figure 6-22). Some degree of
134 Section II Cardiovascular Disease


Figure 6-19. Lateral (A) and ventrodorsal (B) thoracic radiographs obtained from a 1-year-old German Shepherd with aor-
tic valve endocarditis. The cardiac silhouette is enlarged and there is evidence of left atrial enlargement. Pulmonary opacities
indicate the presence of pulmonary edema.

systolic myocardial dysfunction is typically pres- is relatively mild, and evidence of acute inflam-
ent when cardiac enlargement results from AI. mation may or may not be present.
Doppler echocardiography is used to confirm the Abnormalities in the serum chemistries are not
presence of valvular incompetence. specific and, when present, are secondary to the
disease process. Azotemia is relatively common
Laboratory data and can be pre-renal, as a result of poor renal per-

In many cases of IE, the hemogram reveals leu- fusion, or it can result from renal infarction. Hypo-
kocytosis, but this finding is not consistently albuminemia, hyperglobulinemia, and elevations in
present. In subacute cases of IE, the leukocytosis serum alkaline phosphatase may also be observed.
Chapter 6 Acquired Valvular Disease 135


Figure 6-20. Two-dimensional echocardiographic image obtained from a Boxer with aortic valve endocarditis. This left apical
five-chamber view demonstrates the presence of a large, highly echogenic nodule attached to one of the aortic valve leaflets.


Figure 6-21. Two-dimensional echocardiographic short axis image obtained from a 5-year-old female spayed Doberman Pin-
scher with mitral valve endocarditis. There is a discrete nodule attached to anterior mitral valve leaflet (arrow).

Bacteria are cultivated from whole blood samples in Therapy


60% to 80% of IE cases. When possible, three whole-

Therapy of IE is directed toward the control of

blood samples are obtained over a 12- to 24-hour

sepsis, the prevention of thromboembolism, and
period from a central vein after aseptic preparation
the management of cardiac dysfunction that re-
of the overlying skin. When clinical circumstances
sults from valvular incompetence.
allow, blood samples are obtained prior to the
Antibacterial therapy is best guided by the re-
institution of antibacterial therapy, and the results
sults of bacterial culture and sensitivity testing
are used to guide treatment. Taking samples over a
of whole blood samples. When culture results are
shorter time period, say 1 to 3 hours, likely is reason-
unavailable, or when attempts to isolate bacteria
able when the clinical findings suggest that institu-
from blood are unsuccessful, antibiotics are cho-
tion of antibiotic therapy should not be delayed.
sen on an empirical basis.
136 Section II Cardiovascular Disease

Figure 6-22. M-mode echocardiograms obtained from dogs with severe aortic valve incompetence due to bacterial endocardi-

tis. A, An M-mode echocardiogram obtained at the mitral valve level. There is diastolic flutter of the anterior mitral valve leaflet and
premature closure of the mitral valveindirect echocardiographic evidence of severe aortic valve incompetence. B, An M-mode
echocardiogram obtained at the aortic level. The motion of the visible aortic valve leaflet is chaotic because it is flail, having been
all but destroyed by an aggressive endocarditis lesion.

Most often, IE in dogs results from gram-positive nous route because high serum levels of drugs are
organisms, and agents such as the clavulanate achieved quickly and with certainty.
potentiated penicillins or the cephalosporins are When clinical signs of sepsis are prominent and
appropriate. Azithromycin may have a role in blood culture results are negative, initial therapy
the management of IE due to Bartonella spp. using a combination of intravenous gentamicin
In general, bactericidal agents are preferred. A (or amikacin) and ampicillin (or a cephalosporin)
long course of therapy, 6 to 8 weeks, is generally is justified. When patients are free of gastroin-
recommended. There may be some advantage testinal signs such as vomiting or diarrhea, oral
to initiating antibiotic therapy using the intrave- antibiotic therapy is probably appropriate.
Chapter 6 Acquired Valvular Disease 137


Figure 6-23. Lateral radiographic projection of a clinically normal Cocker Spaniel. The dimensions used to calculate the vertebral
heart sum (VHS) are shown. The vertebral bodies, beginning at the fourth thoracic vertebra are used as a scale.

Cardioactive agents are chosen based on the results Prognosis

of radiographic and echocardiographic examina-
The long-term prognosis for patients with echo-
tions. When there is left atrial and left ventricular
cardiographic evidence of vegetative, subacute IE
enlargement due to AI, therapy with ACE inhib-
is grave. By the time the disease is detected, most
itors is generally employed. Furosemide (1 to 2
cases of IE have progressed to the extent that there
mg/kg PO every 12 hours) is used together with an
is irreversible damage to the valve. Failing surgi-
ACE inhibitor in cases where there is radiographic
cal valve replacement, which is rarely practical in
evidence of CHF. Digoxin may have a role in the
veterinary patients, the clinical picture of IE is one
management of patients with severe CHF. Careful
of progressive cardiac dysfunction. A few dogs die
attention to renal function must be paid when di-
of renal failure related to renal infarction or are eu-
goxin is used in patients with IE. In addition to the
thanized after septic thrombi have embolized to the
presence of CHF and the use of ACE inhibitors,
central nervous system. However, in most cases,
which are themselves risk factors for the develop-
ment of azotemia, patients with IE may develop b0110

renal dysfunction related to renal infarction. Frequently Asked Questions

Subjective evaluation of cardiac size from thoracic
Monitoring of therapy

radiographs is difficult. Are there objective criteria

As with other patients with CHF, it is prudent

that define radiographic cardiac enlargement?

to monitor serum electrolytes and renal func- Thoracic radiographs are indispensable in the diag-
tion. Further monitoring of patients with IE may nostic evaluation of dogs with MVD, but it is likely
include serial blood cultures and follow-up echo- that the accuracy of subjective evaluation of radio-
cardiographic studies. graphic cardiac size is dependent on observer experi-
It is tempting to believe that appropriate anti- ence. It is relevant that the patients that most often
develop clinically important MVD are small dogs that
biotic therapy will result in resolution of echo-
that have roughly cylindrical thoraces. In the lateral
cardiographically detected valvular lesions. The projection particularly, patients with this conforma-
valvular lesions of dogs with the more common tion tend to have a large cardiothoracic ratio even
form of IE, in which the presentation is subacute when the heart is, in fact, normal.
and there is echocardiographic evidence of severe One method that can be used to overcome some
valvular incompetence, do not generally resolve. of the limitations inherent in the subjective evaluation
Serial echocardiographic studies in these cases of radiographic cardiac size is the use of the vertebral
heart scale. Beginning at the fourth thoracic vertebra
usually demonstrate progressive valvular incom-
and using the vertebral bodies as a scale, the cranio-
petence and myocardial dysfunction. caudal and dorsoventral dimensions of the cardiac
silhouette are summed (Figure 6-23). This index of
cardiac size is less than 10.5 in most healthy dogs.
Higher values suggest cardiac enlargement.

death occurs as a result of medically refractory

138 Section II Cardiovascular Disease
Atkins CD, Keene BW, Brown WA, et al: Results of the
There is current interest in the use of spironolactone
veterinary enalapril trial to prove reduction in on-
as adjunctive therapy for heart failure in dogs. What
set of heart failure in dogs chronically treated with
are the indications for spironolactone in MVD?
enalapril alone for compensated, naturally occurring
Spironolactone is an antagonist of the mineralocor-
ticoid aldosterone. It is not a potent diuretic and in- mitral valve insufficiency, J Am Vet Med Assoc 231:
terest in the use of this drug primarily relates to its 1061-1069, 2007.
presumed extrarenal effects. Cardiac dysfunction is Buchanan JW: Chronic valvular disease (endocardiosis)
associated with neuroendocrine responses that result in dogs, Adv Vet Med 21:75, 1979.
in supraphysiologic aldosterone activity. Aldosterone Buchanan JW, Bucheler J: Vertebral scale system to mea-
is a ligand for specific renal receptors that mediate sure canine heart size in radiographs, J Am Ved Med
retention of sodium and excretion of potassium. Ad- Assoc 206:194, 1995.
ditionally, there are data that support a role for aldo- Bulmer BJ, Sisson DD: Therapy of heart failure. In
sterone in the development of myocardial fibrosis in Ettinger SJ, Feldman EC, eds: Textbook of veterinary
animals with experimentally induced cardiovascular internal medicine, ed 6, Philadelphia, 2005, WB
disease. Inhibition of aldosterone activity by spirono- Saunders.
lactone reduced mortality in people with severe heart Calvert CA: Valvular bacterial endocarditis in the dog,
failure and this effect was evident at a dose that did J Am Vet Med Assoc 180:1080, 1982.
not have a diuretic effect. Although invasive studies Chetboul V, Lefebvre HP, Sampedrano CC, et al: Com-
may disclose systolic myocardial dysfunction in dogs parative adverse cardiac effects of pimobendan and
with mild but experimentally induced MR, contrac- benazepril monotherapy in dogs with mild degenera-
tility is apparently preserved until late in the natural tive mitral valve disease: a prospective, controlled,
history of MVD. Based on this, it seems reasonable blinded, and randomized study, J Vet Intern Med
to reserve spironolactone for patients with heart fail-
21:742-753, 2007.
ure due to MVD. Additionally, the use of spirono-
DellItalia LJ: The renin-angiotensin system in mitral
lactone is apparently safe but not entirely benign.
regurgitation: a typical example of tissue activation.
Because this drug generally is used in conjunction
with ACE inhibitors, there is potentially a danger of Curr Cardiol Rep 4:97, 2002.
hyperkalemia resulting from excessively diminished Ettinger SJ, Benitz AM, Ericsson GF, et al: Effects of
aldosterone activity. Indeed, after publication of the enalapril maleate on survival of dogs with naturally
major study which documented the favorable effect acquired heart failure, J Am Ved Med Assoc 213:
of spironolactone in people, a number of reports of 1573-1577, 1998.
adverse effects appeared in the literature. Based on Griffiths LG, Orton EC, Boon JA: Evaluation of tech-
retrospective evaluation of clinicopathologic data, the niques and outcomes of mitral valve repair in dogs,
use of spironolactone together with ACE inhibitors J Am Ved Med Assoc 224:1941, 2004.
and furosemide is apparently safe in dogs; however, Haggstrom J, Hansson K, Kvart C, Swenson L: Chronic
it is prudent to monitor serum electrolytes and renal valvular disease in the cavalier King Charles spaniel
function. in Sweden, Vet Rec 131:549-553, 1992.
Haggstrom J, Kvart C, Pedersen HD: Acquired valvular
disease. In Ettinger SJ, Feldman EC, eds: Textbook
CHF, or suddenly from malignant arrhythmia even of Veterinary internal medicine, ed 6, Philadelphia,
when antibiotic therapy is successful in controlling 2005, WB Saunders.
signs related to sepsis. In general, when an echo- Haggstrom J, Pedersen HD, Kvart C: New insights into
degenerative valve disease in dogs, Vet Clin North
cardiographic diagnosis of IE is made in a dog,
Am Sm Anim Pract 34:1209-1226, 2004.
survival is usually measured in weeks or months.
Kvart C, Haggstrom J, Pedersen HD, et al: Efficacy of
With aggressive medical therapy, survival of 4 to enalapril for prevention of congestive heart failure
8 months is occasionally observed. The prognosis in dogs with myxomatous valve disease and asymp-
associated with more acute forms of IE that are tomatic mitral regurgitation, J Vet Intern Med 16(1):
treated early and aggressively is likely better. 80-88, 2002.
MacDonald KA, Chomel BB, Kittleson MD, et al: A
prospective study of canine infective endocarditis
Suggested Readings

in northern california (1999-2001): emergence of

Anderson CA, Dubielzig RR: Vegetative endocarditis in Bartonella as a prevalent etiologic agent, J Vet Intern
dogs, J Am Anim Hosp Assoc 20:149, 1984. Med 18:56, 2004.
Sisson D, Thomas WP: Endocarditis of the aortic valve in
the dog, J Am Ved Med Assoc 184:570, 1984.
Sisson D, Kvart C, Darke PG: Acquired valvular heart
disease in dogs and cats. In Fox PR, Sisson D, Moise
NS, eds: Textbook of canine and feline cardiology:
Chapter 7

Canine Cardiomyopathy
Mark A. Oyama

Dilated Cardiomyopathy
Prevalence and Signalment
Cardiomyopathy is defined as a primary disease of
the heart muscle of unknown etiology. Disease of Surveys indicate that between two and six dogs are
the heart muscle secondary to toxins, nutritional de diagnosed with DCM per 600 case referrals. In cer
ficiencies, endocrinopathies, and infectious agents tain breeds, the prevalence of DCM is remarkably
is often regarded as a secondary cardiomyopathy. high. Approximately 25% of Irish Wolfhounds,
The most common form of canine cardiomyopathy 50% of male Doberman Pinschers, and 33% of
is dilated cardiomyopathy (DCM), which is charac female Doberman Pinschers develop DCM. The
terized by progressive ventricular dilation and loss of typical age at diagnosis is between 6 and 8 years;
myocardial contractility. Other forms of cardiomyo however, it is not uncommon to diagnose DCM in
pathy, such as hypertrophic cardiomyopathy (HCM), dogs as young as 3 years and as old as 12 years.
are rare in dogs. DCM is most common in adult Male dogs appear to be more frequently affected,
large breed dogs, and in particular the Doberman especially in the Doberman Pinscher breed.
Pinscher, Irish Wolfhound, Scottish Deerhound, and
Great Dane. The important features of canine DCM
Natural History
include (1) the presence of an asymptomatic or occult
phase during which diagnosis of disease is difficult, The clinical progression of DCM is best described
(2) the high prevalence of congestive heart failure, as occurring in two distinct phases.
and sudden death in severely affected dogs, and (3)
the need for aggressive and comprehensive medical Asymptomatic Occult Phase
therapy to help alleviate clinical signs. Boxers with No clinical signs are evident; however, myocar
cardiomyopathy possess a unique pathophysiology, dial or electrical abnormalities are present and
clinical presentation, and natural history, such that may include:
disease is best described as arrhythmogenic right Increased left ventricular and atrial dimensions
ventricular cardiomyopathy (ARVC). Sudden death Decreased myocardial contractility
from ventricular arrhythmias is very common in Ventricular premature beats
Boxers with ARVC, much more so than chronic con The duration of the occult phase is highly vari
gestive heart failure. Secondary cardiomyopathies able and thought to last for months to years.
due to nutritional deficiencies appear in breeds of During this phase, progressive heart enlargement
small and medium size, most notably in the Ameri and worsening arrhythmias occur.
can Cocker Spaniel. A highly fatal juvenile form of Occult phase ends with the appearance of the first
DCM is seen in the Portuguese Water Dog. clinical signs of disease.
140 Section ii Cardiovascular Disease

Approximately 40% of Doberman Pinschers Weakness

experience sudden cardiac death as the first Occasional findings include:
clinical sign. Jugular vein distension or pulses
Overt Clinical Phase Ascites
Clinical signs develop Pale mucous membranes
Congestive heart failure Hypothermia
Syncope Pulmonary crackles
Exercise and activity intolerance Depressed mentation
Arrhythmias in the form of ventricular premature
beats, ventricular tachycardia, and atrial fibrilla
Diagnostic Tests
tion are common.
Death is due either to advanced congestive heart Ideally, all dogs should receive an electrocardio
failure that is refractory to medical therapy or gram (ECG), chest radiographs, echocardiogram,
sudden death. urinalysis, and serum chemistry. In many cases,
Between 30% and 50% of Doberman Pinschers additional diagnostics, such as 24-hour ambulatory
die suddenly ECG (Holter) monitoring, are performed.
Many dogs with advanced heart failure are eutha
nized due to chronic respiratory distress, severe Electrocardiography
activity intolerance, anorexia, and weight loss. Electrocardiography is the test of choice for de
tecting arrhythmias and may provide evidence of
History and Physical Examination Findings
heart enlargement; however a normal ECG does not
Asymptomatic Occult Phase rule out the presence of cardiomyopathy.
Common findings include: Asymptomatic occult phase
Soft systolic heart murmur Arrhythmias are often the first indication of
Irregular heart rhythm with pulse deficits disease and screening is recommended in
Occasional findings include: breeds at high risk for DCM.
Diastolic gallop rhythm Routine ECG detects frequent arrhythmias
Decreased intensity of heart sounds but may have limited sensitivity in dogs with
Weak femoral pulse quality infrequent or intermittent arrhythmias.
Jugular vein distension or pulses Detection of the following ECG signs is as
sociated with a high index of suspicion for
Overt Clinical Phase occult cardiomyopathy:
History may include exercise intolerance, syn One or more ventricular premature beats
cope, lethargy, anorexia, difficulty breathing, in a Doberman Pinscher or Boxer. In Box
coughing, abdominal distension ers, ventricular premature beats with a left
Common findings include: bundle branch block morphology (upright
Moderate intensity systolic heart murmur QRS complex in lead II) are highly sugges
Irregular heart rhythm with pulse deficits tive of ARVC (Figure 7-1).
Increased respiratory rate and effort Criteria for left ventricular or atrial enlarge
Increased bronchovesicular sounds ment (QRS duration > 0.06 sec, R wave am
Decreased intensity of heart sounds plitude > 3.0 mV, P wave duration > 0.04 sec)

Figure 7-1. Lead II ECG tracing from a 7-year-old male, castrated Boxer with arrhythmogenic right ventricular cardiomyopa-
thy. Ventricular premature beats with left bundle branch block morphology are a common finding in dogs with this condition.
25 mm/sec; 0.5 cm/mV.
Chapter 7 Canine Cardiomyopathy 141

In Irish Wolfhounds, atrial fibrillation is of The chest radiographs in Doberman Pinschers
ten an early sign of disease as opposed to are often misleading in that heart enlargement
other breeds where atrial fibrillation is as is less striking than in other breeds with simi
sociated with advanced stages of disease. lar clinical signs. In these instances, cardiac
Holter monitoring detects arrhythmias with ultrasound helps to determine the magnitude
greater sensitivity and is recommended in of left-sided heart enlargement and systolic
dogs at high risk (i.e., dogs with a familial dysfunction.
history of disease). The chest radiographs in Boxers with ARVC
Greater than 100 ventricular premature are usually normal.
beats in a 24-hour period is highly sugges
tive of occult DCM or ARVC. Echocardiography
A total of 50 to 100 ventricular premature Echocardiography is widely used to quantify
beats in a 24 hour period is suspicious for heart enlargement and systolic function. Routine
disease and should be followed by another echocardiography is not particularly sensitive in
Holter examination in 2 to 6 months. detecting early changes in occult disease, nor is it
Day-to-day variability in the frequency of particularly helpful after a diagnosis of end-stage
arrhythmia can produce false-negative re disease is made. As such, the utility of echocar
sults, and if the initial Holter examination diography increases as disease moves out of the
is inconclusive, multiple Holter examina occult phase to the overt clinical phase then de
tions may be indicated, especially in dogs clines again as the patient advances into end-stage
with a family history of disease or in those disease. Early in the course of disease, many dogs
that have experienced syncope. possess normal echocardiographic examinations,
During the overt clinical phase, the following despite having a significant numbers of ventricu
may be detected: lar arrhythmias.
Occasional to frequent ventricular or supra Echocardiographic criteria are used to help di
ventricular premature beats agnose occult DCM.
Ventricular tachycardia In Doberman Pinschers, a left ventricular
Criteria for left ventricular or atrial enlarge end-diastolic diameter (LVIDd) > 46 mm
ment (see previous section) or a left ventricular end-systolic diameter
Left bundle branch block (LVIDs) > 38 mm is highly suggestive of
Atrial fibrillation (Figure 7-2) early disease. These values may not be ap
plicable to Dobermans with very large body
weights, and LVIDd > 49 mm or LVIDs
Key Points
> 42 mm may be better guides in this
The author regards Holter monitoring as population.
the current gold standard for detection of In Doberman Pinschers, fractional shortening
occult DCM in Doberman Pinschers. Holter is an unreliable index for occult DCM, as this
monitoring is relatively easy to perform and
breed typically has fractional shortening val
equipment is readily available to the general
practitioner through human and veterinary ues in the mid or low 20% range. Similarly,
medical suppliers. Many veterinary telemedi- large-breed dogs with athletic lifestyles com
cine or remote consulting practices lease monly display fractional shortening values in
Holter units and assist in result analysis. the mid 20% range, and longitudinal echo
cardiographic studies or Holter monitoring is
required to determine whether disease is truly
Chest Radiography present.
Chest radiographs are relatively insensitive to mild In Irish Wolfhounds, occult disease is defined
increases in the heart size. A single set performed as LVIDd > 61.2 mm, LVIDs > 41 mm, frac
in the asymptomatic occult phase contributes tional shortening < 25%, end-systolic volume
relatively little to the immediate diagnosis; how index > 41 ml/m2, or E-point to septal separa
ever, serial radiographs are well suited to monitor tion > 10 mm.
progressive heart enlargement and progression of Newer ultrasound modalities such as Dop
disease. In the overt clinical phase, radiographs pler tissue imaging may be more sensitive in
are invaluable in helping to diagnose congestive detecting early abnormalities of myocardial
failure and to monitor response to treatment. contractility.
142 Section ii Cardiovascular Disease

Figure 7-2. Lead II ECG tracing from a dog indicating atrial fibrillation and left ventricular enlargement. Note the irregular
rhythm, lack of P waves, and widened QRS complex. 50 mm/sec; 10 mm/mV.

Figure 7-3. 2-dimensional echocardiogram of the left ventricle (LV) and atrium (LA) of a Great Dane with dilated cardiomyo
pathy. Note the dilated ventricular and atrial chambers. RV, Right ventricle; RA, right atrium.

As disease progresses from occult to overt, Decreased systolic thickening of the left ven
echocardiography helps monitor heart enlarge tricular wall and interventricular septum.
ment, assess contractility, and evaluate second The echocardiogram in Boxers with ARVC is
ary mitral regurgitation. Echocardiography is usually normal. Subtle right ventricular dilation
used in conjunction with chest radiographs to or wall motion abnormalities may be noted.
help decide when to initiate therapy.
Common echocardiographic findings in dogs
Concomitant Abnormalities in Moderate or
with advanced occult or overt clinical disease
Severe Dilated Cardiomyopathy
include the following:
Moderate to severe left ventricular and atrial Azotemia is commonly detected in dogs that
enlargement (Figure 7-3). are receiving diuretic therapy and is typically
Reduced systolic motion of the left ventricular prerenal in nature.
wall and interventricular septum (Figure 7-4). Mild azotemia (blood urea nitrogen < 60 mg/
Mild to moderate mitral regurgitation sec dl and creatinine < 2.5 mg/dl) usually does
ondary to mitral annulus dilation. not require specific treatment or cessation or
Incomplete systolic opening of the aortic reduction of diuretic therapy.
valves. More severe azotemia (blood urea nitrogen
Decreased aortic blood flow velocity. > 80 mg/dl and creatine > 3.0 mg/dl) can con
Increased mitral valve E-point to septal sepa tribute to patient morbidity and may require
ration (normal < 6 mm) (Figure 7-5). reduction of angiotensin-converting enzyme
Chapter 7 Canine Cardiomyopathy 143

Figure 7-4. M-mode echocardiogram of the left ventricle of a Cocker Spaniel with dilated cardiomyopathy. Note the decreased
systolic motion of the interventricular septum (arrow) and left ventricular free wall (arrowhead).

Figure 7-5. M-mode echocardiogram of the left ventricle and mitral valve of a Brittany Spaniel with dilated cardiomyopathy.
Electronic calipers are being used to measure the E-point to septal separation (EPSS), which is markedly increased over normal.

(ACE) inhibitor and diuretic dose or parenteral require specific treatment. Severe hypoka
fluid supplementation. lemia (K+ < 2.5 mEq/l) can cause cardiac
If fluids are administered, then administer arrhythmias and contribute to muscle weak
ing half-strength saline or Ringers solution ness. Reduction of potassium-wasting di
will reduce the sodium load to the patient. uretics (e.g., furosemide) or institution of
ACE inhibitor therapy can be temporarily potassium-sparing agents (e.g., ACE inhibi
discontinued or the dosage reduced. Initia tors, spironolactone) is performed. Clini
tion of the ACE inhibitor therapy should be cally important hyperkalemia is uncommon
delayed or done with caution. and usually associated with reduced car
Aggressive parenteral fluid therapy can ag diac output, poor renal perfusion, and renal
gravate congestive heart failure and should failure.
be used with caution. Mild hyponatremia is common and is di
Many instances can be treated by reduc lutional in nature. Serum concentration of
tion of diuretics and allowing the patient to sodium is decreased secondary to water re
drink enough water to reestablish hydration tention and expansion of the plasma volume
on their own. despite elevated total body sodium content.
Azotemia reduces renal clearance of digoxin Mild hyponatremia does not require spe
and predisposes to toxicity. Serum digoxin cific treatment. In the authors experience,
levels should be determined especially if the profound hyponatremia (Na+ < 130 mEq/l)
patient displays anorexia, vomiting, diarrhea, signals a poor prognosis. Treatment requires
or frequent arrhythmias. reduction of diuretic dose, water restriction,
Electrolyte abnormalities are common in dogs and dietary sodium supplementation.
with congestive heart failure due to DCM. Most Hypothyroidism is a common concurrent dis
changes are mild and do not require specific ease in middle-aged to older dogs, especially
treatment. in Doberman Pinschers. A causal relationship
Potassium levels may be either increased between hypothyroidism and DCM is doubtful.
or decreased. Mild hypokalemia (K+ = 2.5 Supplementation does not improve survival.
to 3.0 mEq/l) is commonly associated with Natriuretic peptides are produced by the atrial
high doses of diuretics and usually does not and ventricular tissues in response to increased
144 Section ii Cardiovascular Disease

wall stress. Their biologic actions counter

those of the renin-angiotensin-aldosterone sys
tem. Atrial and B-type natriuretic peptide are Standard treatment involves the use of diuretics,
elevated in dogs with symptomatic DCM and positive inotropes, and ACE inhibitors. Ventricu
reflect severity of disease. Atrial and B-type lar arrhythmias and atrial fibrillation requires use
natriuretic peptide are able to distinguish be of specific antiarrhythmics. More recently, beta
tween cardiogenic and noncardiogenic causes adrenergic blocking agents and combined posi
of dyspnea in dogs. In humans, natriuretic pep tive inotropic-vasodilator drugs have been used.
tides provide information regarding diagnosis, Treatment depends on the breed, stage of dis
prognosis, and efficacy of treatment. A similar ease, and presence of congestive heart failure or
utility is likely to exist for dogs. arrhythmias.
Cardiac troponin-I forms part of the actin-
myosin contractile apparatus and is released Drug Classes Used for Treatment
into circulation following myocyte injury or Diuretic therapy alleviates signs of congestion.
necrosis. Cardiac troponin-I is elevated in dogs As disease worsens, use of multiple diuret
with DCM and modestly correlates with degree ics helps achieve increased diuresis. Diuretic
of left ventricular hypertrophy. One study indi monotherapy increases activity of the renin-
cated that dogs with plasma cardiac troponin-I angiotensin-aldosterone system and concomitant
> 0.20 ng/ml have shorter survival times versus ACE inhibition should be used. Diuretic therapy
those with lower values. is commonly accompanied by mild azotemia
and hypokalemia. The potent loop diuretic, fu-
rosemide, is routinely used in symptomatic pa
Nutritional Deficiencies
tients. Thiazide diuretics, though less potent,
Taurine deficiency is a contributing cause of have a longer half-life, act at a site separate from
DCM in the American Cocker Spaniel, and a furosemide, and provide additional diuresis in pa
potential contributing factor in Dalmatians, tients already receiving high doses of furosemide.
Labrador Retrievers, and Golden Retrievers. Spironolactone is a weak potassium-sparing di
In contrast, the incidence of taurine-responsive uretic that is typically administered in conjunc
disease is virtually nonexistent in the traditional tion with a thiazide. Spironolactones beneficial
breeds of dogs with DCM. Recognition of tau effects are probably due to its anti-proliferative
rine deficiency is important in that heart func actions and subsequent reduction of ventricular
tion may be substantially improved following remodeling and fibrosis, rather than its very weak
supplementation. In any nontraditional breed of diuretic action.
dog, that is, in any dog that is not a Doberman Positive inotropic therapy is used to improve
Pinscher, Boxer, Great Dane, Irish Wolfhound, contractility. Drugs include digoxin, beta adren
or Scottish Deerhound, the author recommends ergic agonists (e.g., dopamine, dobutamine),
plasma taurine assay. Interestingly, most tau phosphodiesterase inhibitors (e.g., milrinone),
rine-deficient dogs are receiving an adequate and calcium sensitizers (e.g., pimobendan). As
meat-based diet, and abnormalities of taurine a positive inotrope, digoxin is a relatively weak
absorption, metabolism, or excretion are the and not useful in the emergency setting. Digoxin
likely cause of disease. is, however, useful as an antiarrhythmic used to
Most dogs with taurine deficient DCM have control the ventricular rate in patients with atrial
plasma taurine < 25 nmol/ml. fibrillation. The beta adrenergic agonists and
l-Carnitine deficiency is not a primary cause of phosphodiesterase inhibitors are administered
canine DCM; however, some dogs that are taurine using constant rate infusion and are useful in the
deficient require both l-carnitine and taurine in emergency setting. Pimobendan is a unique drug
order to improve. due to its combined inotropic and vasodilatory
Plasma l-carnitine concentration is not reflec properties. Survival and quality of life is likely
tive of myocardial tissue concentration and improved by this drug.
plasma assays are of little clinical utility. As Venous vasodilators reduce preload and arterial
such, diagnosis of myocardial l-carnitine defi vasodilators reduce afterload.
ciency requires myocardial biopsy. A presump ACE inhibitors blunt activity of the renin-
tive diagnosis of deficiency is often considered angiotensin-aldosterone system, reduce salt
when dogs are concurrently taurine deficient. and water retention, and elicit mild arterial
Chapter 7 Canine Cardiomyopathy 145

vasodilation. ACE inhibitors improve survival no known treatments that definitively slow pro
and quality of life in dogs with DCM. Dogs gression of disease in the occult state. Insofar as
with severe heart failure and poor renal per gradual derangement of neurohormonal activity is
fusion may become uremic while taking ACE associated with worsening cardiac function, use of
inhibitors, especially when high doses of di ACE inhibitors, beta blockers, and spironolactone
uretics are being concurrently used. has been suggested. Current recommendations are
Sodium nitroprusside elicits potent arterial based on small veterinary trials and extrapolation
and venous vasodilation and is very effective from human medicine. Three drug classes are typi
in cases of life-threatening heart failure. Due to cally considered during the occult phase.
the risk for hypotension, arterial blood pressure Use of beta blockade is scientifically supported in
monitoring is required during its use. Sodium virtually all human patients with left ventricular
nitroprusside is administered as a constant-rate systolic dysfunction with current or prior symp
infusion (CRI). toms, and consensus opinion extends this recom
Topical nitroglycerin produces minimal ve mendation to use in asymptomatic patients. In
nous vasodilation in dogs due to poor absorp dogs, sympathetic tone is increased during the oc
tion and low plasma concentrations. cult phase, thus providing rationale for administra
Antiarrhythmic agents suppress life-threatening tion of beta blockers in dogs with early disease.
ventricular arrhythmias and control the ventricu Use of ACE inhibition is scientifically supported
lar rate during atrial fibrillation. For ventricular in virtually all human patients with left ventricular
arrhythmias, drugs in classes I (e.g., lidocaine systolic dysfunction regardless of symptoms. In
and mexiletine), II (beta blockers), and III (e.g., dogs, the time course of ACE activation is uncer
sotalol) can be used alone or in certain combi tain. Although several studies indicate that height
nations. Drugs in class II and IV (calcium chan ened activity of the renin-angiotensin-aldosterone
nel blockers) and digoxin are used for atrial is not present in early disease, there is a need to
fibrillation. distinguish between circulating and local tissue
Beta-adrenergic blocking agents are extensively ACE activity. Though circulating ACE activity
used in humans with DCM. In dogs, little clini is not upregulated until later in disease, evidence
cal data exists. Beta-blocking agents blunt the suggests that a locally contained myocardial ACE
effects of chronic sympathetic nervous system system contributes much earlier in disease. Thus,
activity (i.e., tachycardia, arrhythmias, myocyte tissue-penetrating ACE inhibitors, such as benaz
death, ventricular remodeling, elevated activity epril or ramipril, may be beneficial.
of the renin-angiotensin-aldosterone system). Spironolactone is primarily used in humans with
Overly aggressive use may exacerbate conges symptomatic DCM; however, the benefit in pre
tive heart failure, and patients should be clini venting aldosterone-mediated remodeling may
cally stable before being titrated onto this class begin in earlier stages of disease.
of drug. Due to the high incidence of sudden death in
Inodilators are drugs that improve cardiac con Boxers and Doberman Pinschers, antiarrhythmic
tractility and elicit vasodilation. Pimobendan therapy is often initiated in asymptomatic dogs
is a calcium-sensitizing inodilator that increases based on Holter monitor findings. Dogs with runs
the myocardial response to calcium. Pimobendan
should be used in dogs with symptomatic disease
that are already receiving conventional therapy. Key Points
Pimobendan improves quality of life and is likely The natural history of cardiomyopathy is
to improve survival. substantially influenced by breed. Large- or
giant-breed dogs commonly develop atrial
fibrillation and congestive heart failure, while
Treatment of Asymptomatic Occult Disease Doberman Pinschers and Boxers with ARVC
Treatment in the occult phase represents both an commonly exhibit syncope, ventricular ar-
opportunity and a challenge. Clearly, treatments rhythmias, and sudden death. Thus, in Great
Danes, Irish Wolfhounds, and similar affected
that slow progression in this phase would help
breeds, treatment efforts should focus on the
delay or prevent symptomatic disease, yet the dis resolution of heart failure, whereas in Dober-
covery of effective drugs is hindered by the diffi man Pinschers and Boxers, antiarrhythmic
culty in performing large-scale prospective clinical therapy is commonly prescribed.
trials with sufficient statistical power. There are
146 Section ii Cardiovascular Disease

of ventricular tachycardia or R-on-T phenome Oral pimobendan (0.25 mg/kg every 12 hours)
non are started on sotalol (1.5 to 2.0 mg/kg every may be useful if intravenous positive inotrope
12 hours) or the combination of mexiletine (5 to therapy is not available.
8 mg/kg every 8 hours) and atenolol (0.3 to 0.4 When given orally, digoxin requires several days
mg/kg every 12 hours). The efficacy of this treat to reach effective concentration, and as such, has
ment in preventing sudden death is unproven. little role as an emergency positive inotrope. In
travenous digoxin commonly produces toxicity
Treatment of Overt Clinical Disease
and is not recommended.
Treatment of Severe Life-Threatening Supplemental oxygen therapy is administered either
Congestive Heart Failure in an oxygen cage (fraction of inspired oxygen =
Congestive heart failure is relieved through aggres 40%) or given nasally (50 to 100 ml/kg/min).
sive diuretic, vasodilator, and positive inotropic One of the most difficult clinical decisions is
therapy. whether or not to specifically treat ventricular
Manual removal of heart failure fluid should be arrhythmias. Overly aggressive treatment may
performed in all patients with clinically significant cause hypotension or predispose to even more
pleural or abdominal effusion, as this will rapidly malignant arrhythmias.
improve respiratory effort and alleviate distress. Ventricular premature beats and short runs of
Intravenous or intramuscular furosemide (3 to 8 mg/ ventricular tachycardia that occur at relatively
kg) is administered. When given parenterally, dura slow heart rates (< 160 bpm) typically do not
tion of effect is approximately 2 hours; therefore, require treatment. Often, resolution occurs
additional doses should be administered if the pa spontaneously once congestive heart failure
tients respiratory rate and effort have not improved and hypoxia are successfully treated.
within this time period. Patient recovery can be sig Rapid ventricular arrhythmias that are life-
nificantly hindered due to insufficient dosing of fu threatening are accompanied by clinical signs
rosemide during the first 12 hours of treatment. (i.e., weakness, syncope, hypotension, blanch
Efficacy of diuretic therapy is assessed by mon ing of mucous membranes). Intravenous lido-
itoring patient respiratory rate and effort, urine caine (2 mg/kg IV bolus followed by CRI of
output, and body weight. To confirm the reso 40 to 80 mcg/kg/min) or procainamide (6 to
lution of pulmonary edema or to reassess pa 8 mg/kg IV bolus followed by CRI of 20 to 40
tients that are not responding to therapy, chest mcg/kg/min) is often effective.
radiographs are performed 12 to 24 hours after Due to the high incidence of sudden death in
initiation of therapy. Boxers and Doberman Pinschers, aggressive anti
The presence of severe underlying renal dys arrhythmic therapy in these species is more com
function may necessitate lower doses and less monly warranted, and especially in dogs that have
frequent dosing. previously experienced syncope. Once stabilized,
Sodium nitroprusside (2 to 5 mcg/kg/min CRI) either oral sotalol or combination of mexiletine
is a very effective vasodilator. Nitroprusside can and atenolol are prescribed (see next section).
produce profound hypotension, and arterial blood
pressure monitoring is required when using it. Transitioning the Improved Emergency Patient
The infusion rate is adjusted to elicit a 15 mm Hg to Chronic Oral Treatment
decrease in mean blood pressure as long as the Aggressive emergency therapy successfully resolves
mean value does not fall below 70 mm Hg. acute heart failure in approximately 75% of dogs. In
Intravenous positive inotropes such as dopamine most dogs, significant improvement in clinical signs
(2 to 10 mcg/kg/min CRI) or dobutamine (5 to will be apparent within 48 hours. Patients refractory to
15 mcg/kg/min CRI) help improve cardiac out therapy beyond this point have a grave prognosis. As
put. High doses may aggravate ventricular ar the patient becomes increasingly stable, intravenous
rhythmias or cause sinus tachycardia. medications are gradually reduced and replaced with
Milrinone is a potent positive inotrope that acts oral medications. During this time, patient hydration
downstream of the myocardial beta adrenergic status, body weight, appetite, respiratory effort, elec
receptor. It increases contractility in patients re trolytes, and renal function continue to be monitored.
ceiving beta blockers or in patients that are not Once the patients respiratory rate and effort has im
responding to dopamine or dobutamine therapy. proved, parenteral furosemide is discontinued in fa
Milrinone is administered as a 30 to 50 mcg/kg vor of oral furosemide (typical oral dose: 1 to 2 mg/kg
loading bolus given intravenously over 10 min every 8 to 12 hours). Nitroprusside and dopamine
utes then CRI of 1 to 8 mcg/kg/min. or dobutamine are gradually reduced over 12 to 24
Chapter 7 Canine Cardiomyopathy 147

hours and replaced by an ACE inhibitor (enala- Treatment of Dilated Cardiomyopathy

pril 0.5 mg/kg every 12 hours or benazepril 0.5 accompanied by Atrial Fibrillation
mg/kg every 24 hours) and digoxin (0.003 mg/kg Atrial fibrillation commonly occurs in dogs with
every 12 hours) or pimobendan (0.25 mg/kg every advanced DCM. The incidence of atrial fibrillation
12 hours). Due to the potential for side effects (i.e., is higher in giant-breed dogs (e.g., Great Danes,
anorexia, vomiting) some clinicians stagger the ini Irish Wolfhounds) than in Doberman Pinschers
tiation of digoxin and ACE inhibitor. In these cases, and Boxers. Atrial fibrillation with rapid ventricu
digoxin is withheld for 3 to 5 days until the patient is lar rates (> 180 bpm) exacerbates congestive heart
known to be tolerating the ACE inhibitor. In patients failure and low cardiac output. Conversion of atrial
with atrial fibrillation, the urgency for digoxin treat fibrillation back to normal sinus rhythm is usually
ment is more acute, and digoxin can be started first, futile, and management is targeted at slowing the
followed by an ACE inhibitor in 5 to 7 days. ventricular rate. One of three drugs can be adminis
Lidocaine or procainamide is gradually reduced tered for this purpose.
over 12 to 24 hours and replaced by sotalol (1.5 to Digoxin(0.003 mg/kg every 12 hours)
2.5 mg/kg every 12 hours) or a combination of mex- Diltiazem (0.5 to 2.0 mg/kg every 8 hours) or Dil-
iletine (5 mg/kg every 8 hours) and atenolol (0.3 to tiazem XR (1.5 to 4.0 mg/kg every 12 to 24 hours)
0.4 mg/kg every 12 hours). Atenolol(0.25 to 1.0 mg/kg every 12 hours)
Aggressive use of beta adrenergic blocking anti In most instances, digoxin is preferred due to
arrhythmics, such as sotalol or atenolol, may ex its concomitant positive inotropic effects. If rate
acerbate heart failure (see next section). Gradual control is not achieved by digoxin alone, then the
titration of these agents may be required. addition of diltiazem or atenolol is warranted.
Dietary sodium restriction (40 to 70 mg Na/100 kcal). Overly aggressive dosing of atenolol or ateno
lol co-administered with diltiazem can produce
Treatment of Refractory Heart Failure bradycardia, heart block, and hypotension. Intra
Patients that are already receiving high doses of venous administration of digoxin is not recom
loop diuretics may benefit from additional diuret mended due to the high likelihood of toxicity. In
ics that target areas of the nephron other than the patients that require immediate rate control due
loop of Henle. to extremely rapid ventricular rates, oral loading
Hydrochlorothiazide (1 to 4 mg/kg every 12 to 48 of digoxin (0.006 mg/kg for the first one or two
hours) is a moderately potent diuretic that acts in doses) or intravenous diltiazem (0.1 to 0.2 mg/kg
the distal convoluted tubule and has a longer half- IV bolus then 2 to 6 mcg/kg/min CRI) can be
life than furosemide. Initially, it is given in con attempted.
junction with furosemide and gradually increased The ideal heart rate for dogs with DCM and atrial
as needed to control congestion. Hydrochlorothi fibrillation is not known; however, most clinicians
azide is also supplied as a tablet combined with use a value of 150 bpm as their threshold between
equal amounts of spironolactone (hydrochloro- an acceptable rate and need for more aggressive
thiazide-spironolactone; 2 to 4 mg/kg every12 to treatment.
24 hours). 24-hour ambulatory ECG (Holter) monitoring
In patients with right heart failure or severely de is the preferred method to determine mean heart
creased cardiac output, absorption and renal deliv rate and efficacy of long-term oral treatment.
ery of oral furosemide may be decreased. In these
cases, substituting subcutaneous injections of fu Additional Oral Medications
rosemide often restores effectiveness. Usually, the In addition to the combination of diuretics, ACE
total daily dose of furosemide can be modestly inhibitor, and pimobendan, other medications are
decreased when administered in this fashion. likely beneficial in DCM. The use of these medica
End-stage DCM is often accompanied by inappe tions is based on beneficial effects demonstrated in
tence and weight loss. The author has occasion human or animal model studies. As clinical data be
ally prescribed anabolic steroids (stanozolol 1 to come increasingly available in dogs, the use of these
2 mg per dog every 12 hours) to counteract this medications will continue to grow. The following
catabolic state. The long-term safety of this treat recommendations are based on a limited number of
ment is questionable. reports in dogs and the authors own experience.
Pimobendan(0.25 mg/kg every 12 hours), when In addition to their antiarrhythmic use, beta adren
added to conventional therapy often helps control ergic blockers such as metoprolol and carvedilol
heart failure and improves appetite and demeanor are used to slow progression of heart enlargement
of patients with refractory disease and systolic dysfunction. Initiation of these drugs
148 Section ii Cardiovascular Disease

is done in patients with clinically stable heart c alcium overload, myocardial oxygen demand,
disease, and as such, beta blocking agents should and arrhythmia formation. Agents with combined
not be used in patient with active signs of con vasodilatory properties may offer additional adv
gestion (the exception would be emergency beta vantages in patients with severe DCM.
blocker use to control rapid atrial fibrillation). Ini Pimobendan (0.25 mg/kg PO every 12 hours)
tiation of beta blockade can acutely worsen con results in substantial improvement in quality of
tractility; thus patients are gradually titrated onto life. Pimobendan is typically used in patients
the medications over 4 to 8 weeks. Adverse side with severe disease, and as such, is used in con
effects include bradycardia, hypotension, and ex junction with diuretics, ACE inhibitors, and oc
acerbation of congestive heart failure. Clinicians casionally, digoxin. Benefit from pimobendan
who prescribe beta blockers must be prepared to during occult disease is possible, but requires
manage acute heart failure secondary to drug ini additional study.
tiation. In humans, beta blockers slow progression Aldosterone antagonists, such as spironolactone,
of disease and improve survival but do not dramat act as mild diuretics but even more importantly,
ically improve quality of life. Beneficial effects re reduce the proliferative effects of aldosterone
quire several months of continuous treatment, and within the myocardium and vasculature. Other
in dogs with end-stage disease, treatment may not beneficial properties include blunting of sym
be practical. Accordingly, both the maximum ben pathetic nervous activity and normalization of
efit and the minimum risk of beta blocker use are baroreceptor function. In the presence of severe
probably early in the course of disease. heart disease, ACE inhibition alone may not be
Metoprolol (initial dose of 0.1 to 0.2 mg/kg PO sufficient in suppressing aldosterone production,
every 12 hours followed by gradual titration to and in humans with heart failure, spironolactone
0.4 to 0.8 mg/kg PO every 12 hours over 4 to 8 improves survival.
weeks). Spironolactone (1 to 2 mg/kg PO every 12 hours)
Carvedilol(initial dose of 0.1 mg/kg PO every is commonly prescribed with hydrochlorothia
12 hours followed by gradual titration to 0.5 zide in dogs with severe heart disease. Due to
mg/kg PO every 12 hours over 4 to 8 weeks). its anti-proliferative effects, spironolactone
Calcium-sensitizing agents purportedly increase may also be beneficial in the occult and early
cardiac contractility while reducing cellular symptomatic stages of disease.
Amino acid deficiency is present in some breeds
with DCM (e.g., American Cocker Spaniels).
Key Points
Taurine supplementation (500 mg PO every
Beta blockade represents one of the cornerstones 12 hours for Cocker Spaniels) is recommended
of treatment in human patients with DCM. In in dogs with low plasma taurine concentration.
these patients, beta blockers slow progression of Concurrent l-carnitine supplementation (1
disease, improve systolic function, and prolong
g every 12 hours for Cocker Spaniels) is rec
survival. These benefits are dose dependent and
aggressive therapy yields the greatest results. In ommended in dogs with taurine deficiency.
canine patients, little is known about the ideal Alternatively, due to the relative expense of
timing, dose, and drug that should be used. In l-carnitine compared to taurine, l-carnitine is
healthy dogs, oral carvedilol doses ranging from withheld during the initial three months of tau
0.5 to 1.5 mg/kg PO every 12 hours blunt re- rine treatment and administered only to those
sponse to sympathetic stimulation with isopro- dogs that have not responded to taurine alone.
terenol. The appropriate dose for dogs with heart l-Carnitine deficiency was detected in a fam
disease is unknown, but it is likely to be lower ily of Boxers with left ventricular dilation and
than that used in healthy dogs. In dogs with systolic dysfunction. Supplementation (50
experimental mitral valve disease, oral carve- mg/kg PO every 8 to 12 hours) should be
dilol at 0.4 mg/kg PO every 24 hours reduced
considered in dogs with this presentation. The
heart rate, whereas in a small study of dogs with
advanced naturally occurring DCM, oral carve- value of supplementation in Boxers with ar
dilol at 0.3mg/kg PO every 12 hours did not re- rhythmias and no left ventricular dilation (which
sult in any measurable improvement in echocar- is the most common presentation) is doubtful.
diographic heart size or systolic function. Thus, Dogs that respond to amino acid supplementa
the effective dose of carvedilol in affected dogs tion can often reduce or discontinue conventional
is likely to be > 0.3mg/kg PO every 12 hours. heart failure medications (i.e., furosemide, ACE
inhibitors, digoxin); however, taurine and/or
Chapter 7 Canine Cardiomyopathy 149

c arnitine supplementation should continue in majority of dogs reported to have HCM are male
definitely. and of young age (typically < 3 yrs), suggesting a
Heart disease is accompanied by elevations of heritable etiology. The left ventricular hypertrophy
circulating cytokines and alterations of energy associated with HCM can be symmetrical (i.e., af
production, both of which may contribute to the fecting both the interventricular septum and left
heart failure syndrome of weight loss, muscle ventricular posterior wall equally) or asymmetric
wasting, and poor appetite. (in humans, the septum is typically more affected
Fish oil supplements can reduce interleu than the posterior wall). In the authors experience,
kin concentrations and help improve cardiac most cases of canine HCM involve symmetric
cachexia. LV hypertrophy. Significant left ventricular hy
Coenzyme Q10 is part of the mitochondrial re pertrophy causes diastolic dysfunction, left atrial
spiratory transport chain and supplementation enlargement, heart failure, and arrhythmias. Most
may improve quality of life. dogs with HCM are asymptomatic and the diag
The benefit of supplementary antioxidant vita nosis is made during evaluation of a heart murmur
mins E, A, or C is unknown. or arrhythmia. Echocardiography is the diagnostic
method of choice. Treatment is aimed at abolish
ing the obstructive component of disease with beta-
blocking agents (atenolol 0.5 to 1.0 mg/kg every
The time course from occult to symptomatic DCM 12 to 24 hours), alleviating heart failure with di
is highly variable and can be years. During this uretics, and suppressing arrhythmias. Sudden death
phase, serial echocardiographic and electrocardio appears to be more common than congestive heart
graphic exams are recommended. Sudden death can failure. Many dogs with HCM remain asymptom
occur during the occult phase, especially in Boxers atic for years.
and Doberman Pinschers. Once clinical signs such
as congestive heart failure develop, the long-term
prognosis is poor. Survival times derived from clin Frequently Asked Questions
ical studies are difficult to assess due to nonstan What Causes DCM?
dardized treatment, lack of ACE inhibitor use, and The etiology of primary DCM is unknown. DCM is a
statistical issues surrounding euthanasia. Median description of the hearts response to injury (i.e., dila
survival time is likely 3 to 4 months in Doberman tion and systolic dysfunction), and as such, may be the
Pinschers and 5 to 6 months in other breeds. Dogs end result of multiple causes. In fact, given the forms of
that survive greater than 7 months may do well DCM that are unique to different breeds, it is likely that
more than one etiology exists. Possible causes include
for an extended period of time. One-year survival genetic/familial, immune-mediated, infectious, toxic,
is approximately 10% to 15%. The presence of or nutritional. DCM in Doberman Pinschers may in
atrial fibrillation, biventricular congestive failure, volve specific components of the cytoskeleton or extra
and young age at time of presentation (< 5 years) cellular matrix. Cellular energy production is markedly
are associated with worse prognosis. Although the reduced in affected Doberman Pinschers, but whether
overall survival rate is disheartening, it is difficult these changes are primary abnormalities or secondary
to assess how any individual dog may fare. The au changes has yet to be determined. Boxers with ARVC
are thought to possess abnormal calcium cycling, which
thor suggests aggressive intravenous management is detected in certain forms of ARVC in humans.
of dogs with fulminant heart failure and reevalua
tion after 24 to 72 hours of therapy. Combination Therapy with Beta Blockers and
There is a wealth of data supporting use of beta block
Hypertrophic ers in humans with DCM. Although these agents are
Cardiomyopathy effective at slowing pathologic ventricular remodel
ing and improving survival, they do relatively little
Hypertrophic cardiomyopathy (HCM) is an un to improve quality of life or exercise tolerance. In
common myocardial disease of dogs. HCM is char contrast, pimobendan, though not proven to improve
acterized by idiopathic concentric left ventricular survival in humans, has a marked benefit on quality
of life in dogs. A practice adopted by some cardiolo
hypertrophy, and can lead to heart failure or sud gists is to combine pimobendan and beta blocker use
den death. HCM, if accompanied by systolic ante in dogs with symptomatic DCM. The positive ino
rior motion of the mitral valve and left ventricular tropic effect of pimobendan may increase the like
outflow tract obstruction, is specifically referred to lihood of successful titration and tolerance of beta
as hypertrophic obstructive cardiomyopathy. The
150 Section ii Cardiovascular Disease
Kittleson MD, Keene B, Pion PD, Loyer CG: Results
blockers, and thereby achieve both increased quality
of the multicenter spaniel trial (MUST): taurine- and
and quantity of life.
carnitine-responsive dilated cardiomyopathy in Ameri
can cocker spaniels with decreased plasma taurine con
centration, J Vet Int Med 11(4):204-211, 1997.
Monnet E, Orton EC, Salman M, Boon J: Idiopathic di
Suggested Readings lated cardiomyopathy in dogs: survival and prognos
tic indicators, J Vet Int Med 9(1):12-17, 1995.
Borgarelli M, Tarducci A, Tidholm A, Haggstrom J: Ca
OGrady MR, OSullivan ML: Dilated cardiomyopa
nine idiopathic dilated cardiomyopathy. Part II: Patho
thy: an update, Vet Clin North Am Small Anim Pract
physiology and therapy, Vet J 162(3):182-195, 2001.
34(5):1187-1207, 2004.
Calvert CA, Pickus CW, Jacobs GJ, Brown J: Signal
Tidholm A, Svensson H, Sylven C: Survival and prog
ment, survival, and prognostic factors in Doberman
nostic factors in 189 dogs with dilated cardiomyopa
pinschers with end-stage cardiomyopathy, J Vet Int
thy, J Am Anim Hosp Assoc 33(4):364-368, 1997.
Med 11(6):323-326, 1997.
Tidholm A, Haggstrom J, Borgarelli M, Tarducci A:
Fuentes VL, Corcoran B, French A, et al: A double-blind,
Canine idiopathic dilated cardiomyopathy. I.
randomized, placebo-controlled study of pimobendan
Aetiology,clinical characteristics, epidemiology and
in dogs with dilated cardiomyopathy, J Vet Int Med
pathology, Vet J 162(2):92-107, 2001.
16(3):255-261, 2002.
Chapter 8

Feline Cardiomyopathy
Richard D. Kienle

Introduction sumed primary myocardial disease that do not

The term cardiomyopathy literally means heart meet the criteria for making a diagnosis of hyper-
muscle disease and designates a disorder of the trophic or dilated cardiomyopathy.
heart in which the primary abnormality lies within The widespread use of echocardiography in vet-
the muscle tissue (myocardium). Primary indicates erinary practice allows for more frequent and ac-
the myocardial disease is not secondary to valvu- curate recognition of myocardial disease in cats.
lar disease, pericardial disease, coronary vascular
disease, systemic or pulmonary hypertension, con- Key Point
genital abnormalities, or systemic disease. Most
In domestic cats, cardiomyopathies are the
primary cardiomyopathies are of unknown etiol-
dominant form of cardiac disease.
ogy (idiopathic). A secondary cardiomyopathy is a
disease that affects the myocardium secondary to
infectious, toxic, metabolic, or other disease pro-
cesses. The World Health Organization has cat-
egorized the types of cardiomyopathies and based Cardiomyopathies are classified according to
the categorization scheme primarily on the domi- their morphologic appearance. Within each
nant pathophysiology produced by the myocardial classification, a wide range of morphologic and
disease. clinical presentations may be seen. In some cats
it may be difficult to comfortably place a cats
myocardial disease into one of these categories.
Feline Cardiomyopathies Also, since cardiomyopathies are so common in
cats it is common for other forms of cardiac dis-
General Comments
ease to be misidentified as one of the forms of
The majority of cardiomyopathies diagnosed in cardiomyopathy.
cats are idiopathic (primary). Only one etiology,
taurine deficiency in dilated cardiomyopathy, Primary Cardiomyopathies
has been identified for a feline cardiomyopathy. Hypertrophic cardiomyopathy (HCM)
Intermediate (or intergrade) cardiomyopathy and Idiopathic dilated cardiomyopathy (DCM)
restrictive cardiomyopathy are poorly defined Restrictive cardiomyopathy (RCM)
clinical entities in cats. These diagnoses have Unclassified cardiomyopathies (UCM)
been assigned to many feline patients with pre- Arrhythmogenic right ventricular cardiomyopathy
152 Section II Cardiovascular Disease

Key Point Biventricular CHF is present when elevated

systemic and pulmonary venous, and therefore
In this chapter, I chose not to perpetuate the capillary, pressures manifest as any combination
pretense that what have been called RCM
of the previously mentioned signs, or as pleural
and intermediate cardiomyopathy represent
distinct and well-known disease processes effusion.
for which substantiated recommendations Low-output heart failure, or cardiogenic shock, is
regarding treatment and prognosis can be inadequate cardiac output, often a result of myo-
made. The term unclassified cardiomyopathy cardial failure.
has been used as a reminder that the only High-output heart failure is CHF, left or right
conclusions that can be drawn about these sided, resulting from excessive flow through a
cats hearts is that they have myocardial dis- capillary bed.
ease. Myocardial failure is a reduction in myocardial
contractility characterized by a reduced shorten-
ing fraction and an increased end-systolic dimen-
Specific/Secondary Cardiomyopathies sion on the echocardiogram.
Nutritional (taurine deficiency)
Metabolic (hyperthyroidism, acromegaly) Key Point
Infiltrative (neoplasia, amyloidosis) It is important to realize that heart failure
Inflammatory (toxins, immune reactions, infec- and myocardial failure represent heart dis-
tious agents) ease, and that heart failure, either conges-
Genetic (HCM, DCM) tive or low-output, may, in some cases,
Toxic (doxorubicin, heavy metals) be a result of myocardial failure; however,
heart failure can be, and often is, present
in the absence of myocardial failure. Simi-
Clinical Classification and Pathophysiology larly, myocardial failure may be present in
Abnormalities in myocardial function during sys- association with or in the absence of heart
failure (Figure 8-1).
tole or diastole can underlie or influence the clini-
cal signs observed. Systolic dysfunction is present
when the ability of the ventricle to eject blood is
Signalment and Presenting Complaints
impaired and may result in signs of low output
and possibly congestive heart failure (CHF). Dia- Key Point
stolic dysfunction is present when the ability of The clinical presentation, physical exam find-
the ventricle to relax is impaired and may result ings, radiographic findings, and electrocar-
in signs of CHF. diographic (ECG) findings are similar for all
forms of myocardial disease and generally
Key Point cannot be used to differentiate among them.
Ideally an understanding of the underlying Echocardiography is necessary to determine
etiology of a disease dictates specific therapy the specific disorder that is present.
to reverse the condition; however, in most
cases, treatment of cardiac disease is pallia- The typical clinical presentation, physical exam
tive. Therefore, when tailoring rational ther- findings, radiographic findings, and ECG find-
apy for a patient with cardiac disease, the ings will be discussed in this section. The echo-
clinical status of the patient is the primary cardiographic findings will be discussed with the
consideration. specific disease later.
The most common historical clues in cats with
Right-sided CHF is present when elevated sys- myocardial disease include:
temic venous, and therefore capillary, pressures Dyspnea/tachypnea
resulting from cardiac disease manifest as ascites Poor general condition, weakness, lethargy, or,
or peripheral edema. rarely, exercise intolerance
Left-sided CHF is present when elevated pulmo- Anorexia
nary venous, and therefore capillary, pressures Acute posterior paresis or paralysis
resulting from cardiac disease manifest as pulmo- Coughing and abdominal distention, common
nary edema (and likely also as pleural effusion findings in dogs with cardiac disease, are rare
incats). findings in cats with cardiac disease.
Chapter 8 Feline Cardiomyopathy 153

Key PointS
Heart Disease
A normal thoracic radiograph does not pre-
clude the diagnosis of a cardiomyopathy.
Many asymptomatic cats with mild chang-
es and normal LA size will have a normal
thoracic radiograph.
Echocardiography, including Doppler
echocardiography, is essential for nonin-
vasive determination of a functional and
anatomic diagnosis. Before assigning a
diagnosis of cardiomyopathy based solely
Low Congestive upon morphologic/functional appearance,
Heart a concerted effort should be made to rule
Failure out cardiac and extracardiac diseases that
might mimic the echocardiography of pri-
mary myocardial diseases.
Other diagnostic tests do not usually con-
tribute to the diagnosis of myocardial dis-
Figure 8-1. Venn diagram illustrates the various potential ease but are important for determining the
combinations of congestive heart (backward) failure, low-out- overall status of the patient, identifying con-
put (forward) heart failure, and myocardial failure (each repre-
comitant disorders, and assessing the effi-
sented by a circle) that may be detected in patients with heart
disease (the box). As all the circles reside in the box, each rep-
cacy or untoward effects of therapy. When
resents a form of heart disease, and the overlapping portions possible, routine biochemistries, urinalysis,
of the circles illustrate how the conditions may coexist. and hemogram should be performed prior
to pharmacologic intervention to establish
Physical Examination baseline values for the patient and to rule
out concurrent or secondary metabolic or
Early detection of disease should be a primary
hematologic disturbances.
goal. A thorough physical examination, with Chemical and cytologic evaluation of pleural
careful attention to auscultation, should be per- fluid with respect to protein concentration
formed. Many patients present with acute onset and cellularity can help determine whether
of dyspnea, paresis, lethargy, or anorexia; how- CHF underlies the production of pleural fluid.
ever, the majority of patients is asymptomatic and Cats with CHF can develop true chylous
will be identified after a murmur, gallop sound, effusion.
or other abnormality is identified during a routine Plasma and whole blood taurine concen
physical examination. The most common physi- trations should be measured in all cats
cal clues suggesting myocardial disease include: with echocardiographically documented
Systolic murmur (commonly heard along the ster- myocardial failure (see Taurine Deficiency
Induced Myocardial Failure).
nal border). This murmur may relate to either mitral
regurgitation or outflow tract obstruction or both.
Gallop sound, At normally rapid heart rates these
gallop sounds often represent a summation of the der and alert the clinician to secondary ramifications
third and fourth sounds. that may require attention; however, neither elec-
Dysrhythmia trocardiography nor thoracic radiography provides
Tachypnea/dyspnea adequate evidence for ruling out, confirming, or clas-
Muffled or harsh lung sounds sifying feline cardiac disease. Contrast radiography
Hypothermia or, preferably, echocardiography, is required to con-
Jugular pulses/distention firm or rule out and categorize myocardial disease.
Acute paresis associated with pain in regions Electrocardiography often shows:
with evidence of reduced peripheral perfusion Intraventricular conduction abnormalities (left
bundle branch block, left anterior fascicular
block pattern, pre-excitation syndrome)
Ancillary Tests
Increased amplitude of R waves
Thoracic radiography and electrocardiography may Ventricular arrhythmias are common but are
direct or reinforce suspicion that a cardiac disorder is generally mild with relatively infrequent single
present. They may also further characterize the disor- premature ventricular contractions.
154 Section II Cardiovascular Disease

Figure 8-2. A, Lateral thoracic radiograph from a cat with dilated cardiomyopathy demonstrates severe generalized cardio-
megaly. B, Dorsoventral thoracic radiograph from the same cat as in A.

Occasionally cats will have more complex ar- radiography. The author often delays radiography
rhythmias. Some cats with severe LA enlarge- until after stabilizing the patient (Figure 8-4).
ment will develop atrial fibrillation. Diagnostic and potentially therapeutic thoraco-
Thoracic radiography is most useful for detect- centesis should precede radiography in dyspneic
ing gross cardiac enlargement and clinical se- cats.
quelae to cardiac dysfunction (e.g., pulmonary
venous congestion, pulmonary edema, enlarged
great veins, pleural effusion) (Figures 8-2 and
8-3). Restraint for radiographic procedures can Therapy should be based upon the clinical
be life threatening to dyspneic cats. Extreme andfunctional classification of the disease
caution should be taken before proceeding with process in the individual patient and not by
Chapter 8 Feline Cardiomyopathy 155

Figure 8-3. Lateral thoracic radiograph from a cat with hypertrophic cardiomyopathy demonstrates marked left atrial enlarge-
ment, pulmonary venous engorgement, and pulmonary edema.

Dyspneic Cat All patients with evidence of significant and

Take life-threatening CHF (pulmonary edema, pleural
Airway Yes
or very pale
? appropriate
effusion) require immediate therapy (i.e., appro-
priate combinations of pleurocentesis, diuretics,
Pleurocentesis Furosemide is the diuretic of choice in cats. Fu-
Pleural Diagnostic &
rosemide should be administered intravenously
air or
? therapeutic
(1 to 2 mg/kg every 1 to 2 hours as needed) or
intramuscularly (1 to 2 mg/kg every 2 hours as
No needed) depending upon the stress level of the
Stabilize prior to
further diagnostics or
? Much
cat. Dosing must be dramatically reduced once
the respiratory rate begins to reduce. Generally,
stressful therapeutics Yes
aggressive diuretic therapy is continued until the
O2, If tolerated, respiratory rate is below 40 breaths per minute.
furosemide, sq or im
consider steroid if Not all cats respond well to being placed in an
history suggests oxygen cage. Carefully observe patients after
feline asthma placing in a closed oxygen cage and opt for a
Further diagnostics, quiet, unoxygenated environment if the patient
including radiography, appears more distressed in the oxygen cage.
and therapeutics
Tranquilization with an agent such as acepro
Figure 8-4. Algorithm outlining choices and decisions en-
mazine may be indicated to calm distressed
countered in the management of life-threatening dyspnea in
the cat. The most important point illustrated is not to proceed patients.
with stressful diagnostic or therapeutic procedures until the The use of topical nitroglycerin as a preload
patient is stable. Stressed cats die. reducing agent in acute and chronic situations
is recommended by some, but evidence of ef-
f ollowing a standard approach based solely ficacy is lacking.
upon the diagnosis. Cats with significant pleural effusion will benefit
With only two exceptions, the indications for most from immediate pleurocentesis. Patients
and benefits of therapeutic intervention in with significant pericardial effusion and cardiac
asymptomatic cats with myocardial disease are tamponade require pericardiocentesis and should
controversial. These exceptions are: not receive diuretics prior to pericardiocentesis.
Myocardial failure secondary to taurine deficiency Maintenance therapy is generally aimed at mini
Thyrotoxic heart disease mizing signs and prevent acute crisis. Lower doses
Dyspneic cats are easily stressed and may acutely of furosemide (6.25 mg twice a day to 12.5 mg
deteriorate and die if stressful diagnostic or thera- three times a day PO) are indicated for chronic
peutic interventions are initiated too early. An al- maintenance control of CHF. Angiotensin-convert-
gorithm for management of the dyspneic cat is ing enzyme (ACE) inhibitors (enalapril 0.25 to 0.50
presented in Figure 8-4. mg/kg PO every 24 to 48 hours or benazepril 0.25
156 Section II Cardiovascular Disease

to 0.50 mg/kg PO every 24 hours) are also quite Medical therapiesmost are untested and
effective in cats with CHF. Antiarrhythmic drugs unproven
may be indicated to control significant arrhythmias. Anticoagulation with heparin (220 units/kg IV fol-
Inotropic agents may be indicated in patients with lowed 3 hours later by maintenance dose of 66 to
myocardial failure or low-output heart failure. 200 U/kg SQ four times a day) is used to prevent
The judicious use of intravenous fluids may in- further thrombosis. Adjust dose to maintain the acti-
frequently be indicated in patients with signs of vated partial thromboplastin time at or slightly above
low-output heart failure, primarily in situations the upper limit of the normal reference range.
where the patient has stopped taking in oral Vasodilation with acepromazine (0.2 to 0.4 mg/
fluids, has received excessive treatment with kg SQ three times a day) or hydralazine (0.5 to
diuretics, or has concurrent renal dysfunction 0.8 mg/kg PO three times a day) is used to pro-
and there is concern about maintaining adequate mote collateral blood flow.
renal perfusion. Streptokinase and urokinase are significantly
Specific therapies designed to alter the natural less expensive than newer fibrinolytic agents
history of disease should be instituted concur- (e.g., tissue plasminogen activator), but little
rently and may, in some cases, in time, eliminate clinical experience has been reported. Tis-
the need for drugs to control heart failure (see sue plasminogen activator: Though clinically
specific conditions discussed later). effective thrombolysis has been documented in
All cats with myocardial failure should be sup- the cat, expense, morbidity associated with rapid
plemented with taurine (see section on Taurine reperfusion, and inability to prevent recurrence
DeficiencyInduced Myocardial Failure) until make this option impractical in most cases.
proven to be not taurine deficient and not taurine
Several strategies to prevent an initial thromboem-
bolic event or to avoid recurrence of aortic throm- Inadequate information is available to make broad
boembolism in cats with cardiomyopathy have generalizations regarding prognosis for cats with
been devised and recommended. None of these myocardial diseases. Although echocardiography
strategies has been evaluated by controlled studies. provides the basis for diagnosis, clinical and ra-
Low-dose aspirin (25 mg/kg PO every 2 to 3 diographic data should be strongly considered for
days) is the most widely employed prophylactic prognostication.
measure. Although aspirin is known to exert anti- Cats with severe myocardial disease and
thrombotic effects, there is no objective evidence noevidence of heart failure may survive for
of its efficacy for the prophylaxis of systemic long periods of time. Conversely, cats with
aortic thromboembolism in cats. Recurrence of much less severe echocardiographic evidence
thromboembolic events in aspirin-treated cats of disease presenting with significant and
were as high as 75% in one study. difficult to control signs of heart failure may
Lovenox (enoxaparin),a low molecular weight survive for very short periods under the best of
heparin, has shown promise in anecdotal clini- situations.
cal settings. No large clinical trials have been The long-term prognosis for cats with thrombo
completed. The most commonly used dose is embolic disease is grave because mortality asso
1 mg/kg SQ every 12 to 24 hours. ciated with individual episodes is high, and recur-
Left untreated, the outcome of arterial occlusion rence is common despite prophylaxis.
will depend upon the extent of occlusion and time
to spontaneous reperfusion, either via the primary
vessel or the collateral circulation. Cats may lose
the affected leg(s) because of ischemic necrosis, Gross examination of the heart provides use-
die of toxemia, remain paralyzed from peripheral ful anatomic information and should be per-
nerve damage, or regain full or partial function of formed when possible to confirm antemortem
the leg. Overall, response to presently available findings.
conservative or aggressive clinical intervention In most cases histopathologic evaluation adds
has been poor. little useful information and, unless readily avail-
Therapeutic options include: able at low cost, is not recommended unless
Surgical removal of emboli specific indications are present (see the section
Catheter embolectomy Specific Diseases).
Chapter 8 Feline Cardiomyopathy 157

due to a de novo mutation in these cats, or is asso-

ciated with a completely different disease process
is unknown although suspicion of inheritance has
HCM is a disease of the ventricular (primarily left been reported in mixed breed cats.
ventricular [LV]) myocardium characterized by
mild to severe thickening (concentric hypertrophy)
Clinical Classification and Pathophysiology
of the papillary muscles and ventricular walls. The
word primary in this context means that the hyper- HCM is characterized by enlarged papillary
trophy is due to an inherent problem in the myocar- muscles and a thick LV myocardium with a
dium and is not secondary to a pressure overload or normal to small LV chamber. These changes
to hormonal stimulation. may be mild, moderate, or severe and may
be symmetrical or asymmetric. When it is se-
vere, the concentric hypertrophy by itself
General Comments
increases chamber stiffness. In addition, blood
When any other disease process that may lead flow and especially blood flow reserve to severely
to concentric hypertrophy is present, the diag- thickened myocardium is compromised, which
nosis of HCM is excluded. Secondary disor- may cause myocardial ischemia, cell death, and
ders typically produce symmetric concentric replacement fibrosis. Increased concentrations of
hypertrophy and typically produce a maximum circulating neurohormones may also stimulate
increase in wall thickness of 50% or less, even interstitial fibrosis. These also increase chamber
with severe disease. If severe or asymmetric stiffness and are probably the primary reasons
concentric hypertrophy is present in a patient for the marked diastolic dysfunction seen in this
with one of these disorders, then concomitant disease. The stiff chamber causes an increase in
HCM should be considered. diastolic intraventricular and LA pressures, LA
HCM is the most commonly diagnosed cardiac enlargement, and may lead to CHF. The concen-
disease in cats and its prevalence appears to be in- tric hypertrophy may also result in a decrease in
creasing; however, echocardiographic screening afterload because of the increase in wall thickness
for the disease has also become more prevalent which may result in a decrease in end-systolic
over the past ten years so increased awareness volume, often to zero (cavity obliteration).
and ease of diagnosis may be a major contribut- Abnormal papillary muscle orientation and other
ing factor to this increase. unexplained factors commonly produce SAM of
In most cases the etiology is unknown (idio- the mitral valve. In one survey of 46 cats, SAM
pathic). The disease is known to be inherited in was present in 67% of cases. Cats with HCM and
some breeds of cats. The first family of cats SAM are commonly said to have the obstructive
with an inherited form of HCM was identified in type of HCM or to have hypertrophic obstructive
Maine coon cats in 1992 and reported in 1999. cardiomyopathy. SAM of the mitral valve pro-
The disease is inherited as a simple autosomal duces a dynamic subaortic stenosis that increases
dominant trait in this breed and 100% expressed systolic intraventricular pressure in mid to late
in experimental cats housed in a colony. A fam- systole. The dynamic subaortic stenosis increases
ily of American shorthair cats, primarily with the velocity of blood flow through the subaortic
systolic anterior motion (SAM) of the mitral region and often produces turbulence. Simultane-
valve,but with other evidence of HCM as well ously, when the septal leaflet is pulled toward the
has also been identified. The disease in this interventricular septum, this leaves a gap in the
breed also appears to be inherited as an auto mitral valve creating mitral regurgitation which is
somaldominant trait. In addition to these breeds, typically only mild to moderate in degree. These
there is anecdotal evidence of HCM being in- abnormalities are by far the most common cause
herited in numerous other breeds, including of the heart murmur heard in cats with HCM. The
Persian, British shorthair, Norwegian forest, Rag- degree to which SAM and mitral insufficiency
doll, Turkish van, and Scottish fold cats, along contribute to the development of left-heart failure
withothers. in cats with HCM is unknown and deserves fur-
HCM is most likely inherited when it is identified ther study.
in a specific breed; however, HCM is most com- Sudden death may occur in any individual and may
monly identified in domestic (mixed-breed) cats. be unrelated to disease severity. The incidence of
Whether the disease is inherited in these cats, is sudden death in cats with HCM is unknown.
158 Section II Cardiovascular Disease

Pleural effusion is common in cats with heart failure. Cats with severe HCM and moderate to severe
It can be a modified transudate, pseudochylous, or heart failure are usually presented to a veterinar-
true chylous in nature.Theexactpathophysiology ian because of respiratory abnormalities (tachy-
of pleural effusion secondary to heart failure is un- pnea and/or dyspnea) due to pulmonary edema,
known. The most likely possibility is that feline vis- pleural effusion, or both.
ceral pleural veins drain into the pulmonary veins Cats with HCM may develop systemic
such that elevated pulmonary vein pressure causes thromboembolism.
the formation of pleural effusion. Cats with HCM may die suddenly, often with no
Thrombi in cats with HCM may form in the prior clinical signs referable to heart disease or
left atrium or left auricle. LA thrombi commonly failure. The cause of the sudden death in these
break loose (become emboli) and are carried by blood cats is unknown.
flow most commonly to the terminal aorta where they In humans, sudden death appears to be either due
lodge. These thromboemboli occlude aortic blood to an arrhythmia, acute worsening of the outflow
flow and elaborate vasoactive substances that con- tract obstruction associated with stress or exer-
strict collateral vessels. The net result is cessation of cise, or a large thrombus occluding flow in the
blood flow to the caudal legs resulting in acute paresis/ left.
paralysis and pain. The incidence of sudden death in feline HCM
is probably under represented in the veterinary
literature because cats that die suddenly are not
Signalment and Presenting Complaints
presented or reported to veterinarians.
In cats the disease has been observed as young
as 6 months of age and as old as 16 years of age.
In Maine coon cats that are going to develop
severe disease, HCM most commonly develops Cats with severe HCM have papillary muscle hy-
to its most severe stage in males by around 2 pertrophy, markedly thickened LV walls (7 to 10
years of age. Females are more variable but most mm), and usually an enlarged left atrium (Figure
frequently develop to an end-stage of wall thick- 8-5). The hypertrophy can be global, affecting all
ening by three years of age. The average age of areas of the LV wall or can be more regional or
onset and rate of progression in mixed breed cats segmental. Segmental forms can have the entire or
is unknown. a region of the interventricular septum or free wall
Males are affected more commonly than females. primarily affected, the apex primarily affected,
Cats with HCM may be completely asymptom- or the papillary muscles (and often the adjacent
atic, may be presented to a veterinarian with sub- free wall) primarily affected. Papillary muscle
tle signs of heart failure, may have moderate to hypertrophy may be the only manifestation of the
severe heart failure, or may be presented because disease.
of thromboembolic disease. Sudden death is also Because of these forms, HCM is a diagnosis that
a common presentation. should be made by examining several different
Asymptomatic cats can have mild to severe LV two-dimensional echocardiographic views and
thickening; however, those with severe thicken- measuring wall thicknesses in diastole from the
ing usually go on to develop heart failure. Cats thickest region or regions on the two-dimen-
with severe disease that appear to have no clini- sional images. M-mode echocardiography may
cal signs may show subtle signs of heart fail- miss regional thickening unless it is guided by
ure (e.g., tachypnea) that may be detected by the two-dimensional view. The LV end-diastolic
an observant owner. The respiratory rate is of- or end-systolic dimension may be normal or
ten increased in these cats at rest and they may decreased and end-systolic cavity obliteration
become more tachypneic or even dyspneic if may occur. An enlarged left atrium indicates
stressed. Stressed cats with severe HCM may increased LV end-diastolic pressure. Occa-
recover quickly following stress or may go on to sionally, a thrombus is imaged in the LA or its
develop fulminant heart failure. Cats with mild appendage.
to moderate thickening may never develop clini- SAM of the mitral valve may be identified by
cal signs referable to their disease and may live two-dimensional or, more commonly, by M-mode
normal lives. In others, the LV wall may pro- examination (Figure 8-6). Color flow Doppler
gressively thicken and complications may de- echocardiography can be used to demonstrate
velop when they are older. the hemodynamic abnormalities associated with
Chapter 8 Feline Cardiomyopathy 159

Figure 8-5. Echocardiograms from a cat with hypertrophic cardiomyopathy. A, Right parasternal long-axis view shows concen-
tric hypertrophy of the left ventricle (LV) and left atrial (LA) dilation. B, Right parasternal short-axis view shows the thick interven-
tricular septum and left ventricular wall and a comparatively small left ventricular chamber. C, M-mode echocardiogram at the
level of the left ventricle, showing the thickened myocardium and small LV cavity.
160 Section II Cardiovascular Disease

Figure 8-6. M-mode echocardiogram of the mitral valve from a cat with hypertrophic cardiomyopathy demonstrates systolic
anterior motion of the mitral valve. The mitral valve moves toward the interventricular septum in early systole (unlabeled arrows) and
returns to normal position shortly before the beginning of diastole. LV, Left ventricle; RV, right ventricle; MV, mitral valve. (Courtesy
Mark D. Kittleson, D.V.M., Ph.D.)

SAM. Two turbulent jets originating from the LV are likely many cats with mild to moderate HCM
outflow tract are seenone regurgitating back in the cat population that never progress to a more
into the left atrium and the other projecting into severe form of the disease, condemning owners to
the aorta. Spectral Doppler can be used to deter- pill their cat twice or even once a day for the rest
mine the pressure gradient across the region of of the cats life is questionable, given the lack of
dynamic subaortic stenosis produced by the SAM. data. Many veterinarians feel compelled to treat a
The pressure gradient roughly correlates with the patient with a disease, and some owners demand
severity of the SAM although it can be quite la- treatment for their pet, even if there is only a theo-
bile, changing with the cats level of excitement. retical case for using a drug. Consequently, when-
SAM is not present in all cats with HCM. The ever HCM is diagnosed in a cat the veterinarian
majority of cats with severe HCM have SAM. must explain the situation to each owner and try to
However, on the other end of the spectrum, some let the owner make an informed decision based on
cats develop SAM before they have any evidence their wishes and life style. Because no intervention
of wall thickening, when their papillary muscles is known to change the course of the disease, there
are thickened or long. Although the basilar region is no mandate to treat at this stage.
of the interventricular septum is often thickened Two classes of agents, oral beta blockers and oral
in diastole in cats with HCM, the basilar LV out- calcium channel blockers, have been advocated
flow tract does not need to be narrowed for SAM to improve LV filling and cardiac performance
to occur. in cats with HCM. Although there is no clear
Diastolic dysfunction in cats with severe HCM evidence as to which therapy is more beneficial
has been documented using Doppler tissue imag- in symptomatic individuals, many cardiologists
ing and measures of transmitral flow and relax- believe patients with documented HCM should
ation time. Cats with severe HCM routinely have receive one or the other as part of their chronic
a decrease in early diastolic wall motion of the LV management. Whatever the initial choice, re-
free wall and mitral valve annulus using Doppler sponse to therapy should dictate whether dose
tissue imaging. In addition, peak E wave veloc- adjustment, changing drug class, or discontinua-
ity is reduced, peak A wave velocity is increased, tion of therapy is warranted.
isovolumic relaxation time is prolonged, and rate
of deceleration of early inflow is reduced. Adrenergic Beta Blockers
Atenolol: 6.25 to 12.5 mg/cat every 12 hours.
Atenolol is supplied as 25 mg tablets.
There currently is no evidence that any drug alters Calcium Channel Blockers
the natural history of HCM in domestic cats until Diltiazem is currently the preferred calcium
they are in heart failure. Diltiazem, atenolol, bena- channel blocker. Beneficial effects include less-
zepril, and enalapril are commonly administered ened edema formation and decreased wall thick-
to cats with mild to severe HCM that are not in ness in some cats. Exactly how these beneficial
heart failure on an empirical basis. Because there effects occur is open to debate. Only a few cats
Chapter 8 Feline Cardiomyopathy 161

experience a clinically significant decrease in In general, cats that present with heart failure
wall thickness in my experience. have a poor prognosis. A median survival time
Cardizem7.5 mg PO every 8 hours. This product after diagnosis of about 3 months is reported. Cats
is supplied as 30 mg tablets. One-quarter tablet is that present in heart failure and respond favorably to
given every 8 hours. therapy may do well for prolonged periods of time.
Dilacor XR: 30 mg PO every 12 hours. This In general, cats presenting with aortic throm-
product is supplied as 120, 180, and 240 mg cap- boembolism have a poor prognosis. A median
sules. Each large capsule can be opened to yield survival, after diagnosis, of about 2 months is re-
two, three, or four 60 mg tablets, which are then ported. Cats that survive the thromboembolic epi-
halved to achieve a 30 mg dose. sode may do well for extended periods; however,
CardizemCD: 45 mg PO every 24 hours. Cardi- these cats are generally at high risk for recurrence
zem CD is supplied as 180 mg capsules that con- of thromboembolism.
tain many smaller capsules. The larger capsule Owners should always be warned of the potential
can be opened and the smaller capsules divided for sudden death. The exact incidence of sudden
into a number that produces an appropriate dose. death in cats with HCM is unknown. It is in some
The smaller capsules can be divided into groups cats, it is the first and only clinical sign.
of four (45 mg each) and placed in smaller gelatin
capsules for administration. One capsule is then
administered once per day.
In severe cases the entire LV wall may be im-
pressively thick. Papillary muscle hypertrophy is
Key Point usually prominent, and the LV cavity is usually
decreased in size owing to encroachment. Both
The authors generally use diltiazem first in cats symmetric and asymmetric (asymmetric septal
without outflow tract obstruction, tachycardia
hypertrophy) forms of hypertrophy are recog-
or arrhythmias. The authors generally use aten-
olol first in cats with outflow tract obstruction,
nized in cats. The left atrium is often enlarged,
tachycardia or arrhythmias. The authors may and, occasionally, a thrombus is present within
switch to the alternate therapy if the response the left atrium.
is suboptimal or becomes suboptimal. Cats with milder forms have less dramatic wall
thickening and normal or near-normal LV cham-
ber size. The LA may be normal or only mildly
enlarged. Occasionally, the disease is manifested
only by papillary muscle hypertrophy with nor-
Prognosis is generally based upon clinical pre- mal LV free wall and septal thickness. There is
sentation, echocardiographic evidence of elevated considerable variability in the degree and loca-
intracardiac pressures, and response to therapy. tion of the hypertrophy.
Inadequate data has been published to reach de- Myocyte hypertrophy is the hallmark of histo-
finitive conclusions; therefore, statements on prog- pathologic examination with approximately 30%
nosis are largely based upon clinical experience of the cases also having myocardial fiber disarray
and conjecture. involving at least 5% of the septal myocardium.
Asymptomatic cats with mild to moderate
hypertrophy and no LA enlargement are believed
Feline (Idiopathic) Dilated
to have a good long-term prognosis. Reported
average survival times are generally in the
range of 4 to 6 years. Asymptomatic cats with DCM is a disease of the ventricular myocardium
obvious wall thickening and LA enlargement (predominantly left) characterized by primary
are likely at higher risk for developing heart fail- myocardial failure.
ure. These cats are also believed to be at risk for
developing thromboembolic disease. Asymptom-
General Comments
atic cats with severe wall thickening and normal
LA size are occasionally observed. Although Prior to 1987, DCM was one of the most com-
it is tempting to predict that these cats are at monly diagnosed heart diseases in cats. Most
greater risk for progressive disease, inadequate cases at that time were likely a secondary car-
data are available. diomyopathy associated with nutritional taurine
162 Section II Cardiovascular Disease

deficiency. Primary idiopathic DCM is currently The degree to which alterations in diastolic func-
not a common cardiac condition in cats. Because tion contribute to decompensation of patients with
there are no published reports defining differences DCM is likely larger than previously appreciated.
between cats with myocardial failure associated
with taurine deficiency and with idiopathic DCM,
Signalment and Presenting Complaints
there is very little, if anything, known about idio-
pathic DCM in cats. The reported age at diagnosis ranges from 5
There is no reason to expect that clinical findings months to 14 years (mean age 7 to 8 years).
and results of ancillary tests (other than blood No sex predilection is evident.
taurine concentration and funduscopic examina- Cats with DCM may have a variable period of
tion) should be dramatically different between lethargy, anorexia, and malaise prior to overt
these disorders. signs of CHF.
Myocardial failure secondary to other causes Cats may present with no prior signs and an acute
(e.g., long-standing congenital or acquired LV onset of CHF or systemic thromboembolism.
volume overload or toxic, ischemic, nutritional,
or metabolic problems that may underlie myo-
Physical Examination
cardial failure) must be ruled out to definitively
assign a diagnosis of idiopathic DCM. Physical examination is similar to that of other
The underlying etiology remains unknown and may forms of myocardial disease.
represent a common endpoint to many processes.
Ancillary Tests
Key Point
Ancillary tests are similar to taurine deficiency
Although myocardial failure secondary to myocardial failure (see next section); however,
taurine deficiency is now quite rare in cats, one must rule out taurine deficiency using whole
all cats with myocardial failure should be as-
blood and plasma taurine assays.
sumed to be taurine deficient until shown not
to be taurine responsive.
For acute CHF, see the earlier section on treatment of
CHF in the Therapy section of General Information.
The underlying abnormality leading to clini- Cats with DCM and signs of low-output heart
cal manifestations in cats with idiopathic DCM failure (cardiogenic shock) represent a therapeu-
is primary systolic myocardial failure. End- tic challenge. Suggestions based upon clinical
systolic LV volume increases owing to a reduc- experience with cats with myocardial failure as-
tion in myocardial pump function. As a result, sociated with taurine deficiency are presented in
stroke volume and cardiac output decrease. Neu- the section on this disorder.
rohumoral compensatory mechanisms promote
an increase in intravascular volume and end-dia-
stolic pressures, stimulating eccentric hypertrophy
(dilation). At these larger LV end-diastolic vol- There are no reports documenting the clinical char-
umes, the geometry of the ventricle is such that acteristics of cats with idiopathic DCM thatdo not
small changes in chamber dimension during sys- respond to taurine supplementation. There is no
tole provide adequate stroke volume and cardiac evidence that clinical intervention alters the pro-
output; however, working at these larger volumes gression of myocardial failure in patients that do
is energetically inefficient for the ventricle. At any not respond to taurine supplementation. The ex-
point in this degenerative process that end-diastolic pected survival time for patients is more a function
pressures rise too high or cardiac output drops too of their clinical condition at the time of diagnosis
low, the patient may present with signs of CHF or than of the treatment they receive.
low-output heart failure, respectively (Figure 8-7). Asymptomatic cats diagnosed because a murmur
The factors that contribute to patients going from or gallop is identified during a routine physical
asymptomatic, well-compensated myocardial examination may survive for years with myocar-
failure, to a symptomatic, uncompensated state dial failure before developing signs of CHF or
are poorly understood. low-output heart failure.
Chapter 8 Feline Cardiomyopathy 163




Figure 8-7. Dilated cardiomyopathy in a cat. A, Right parasternal long-axis view showing dilation of the left atrium (LA)
and left ventricle (LV). B, Systolic color Doppler image of the same view as in A showing modest secondary mitral and tricus-
pid valve regurgitation. C, Left apical four-chamber view showing the dilated left atrium and ventricle. D, Right parasternal
short-axis view showing left ventricular dilation. E, Right parasternal short-axis view at the heart base showing moderately
severe left atrial dilation. F, M-mode recordings at the level of the ventricles [1], mitral valve [2], and aortic valve [3]. There
is marked dilation of the left atrium and left ventricle and decreased left ventricular systolic motion. In addition, the opening
motion of the mitral valve is decreased, and the distance between the open mitral valve and ventricular septum (EPSS) is
markedly increased (10 mm). RA, Right atrium; RV, right ventricle. (From Nyland TG, Mattoon JS: Small animal diagnostic
ultrasound, ed 2, Philadelphia, 2002, WB Saunders.)

Cats presenting with signs of CHF or low-out-

put heart failure have a very guarded prognosis.
These cats usually either die soon after admission There is currently no information available, but thereis
from cardiogenic shock or succumb to refractory no reason to suspect that findings should be different
CHF or thromboembolism. Based upon a small from taurine-deficient cats with myocardial failure or
number of documented cases, expected survival patients with DCM in other species in which there
is 1 to 2 months after diagnosis. are no specific or pathognomonic changes found.
164 Section II Cardiovascular Disease

Although not reported, in my experience cats with

Feline Restrictive RCM are more likely to have intraventricular con-
Cardiomyopathy duction abnormalities (left bundle branch block,
RCM is a diverse group of conditions characterized left anterior fascicular block pattern, pre-excitation
by restriction of diastolic filling. Specific clinical and syndrome) on electrocardiograms and seem to have
morphologic criteria for this diagnosis in the cat have a higher frequency of ventricular arrhythmias.
not been as clearly defined as they have in humans. There is often very dramatic LA enlargement on
thoracic radiographs and pulmonary veins are often
enlarged and tortuous. When CHF is present, pulmo-
General Comments
nary edema is more common than pleural effusion.
Without the use of invasive diagnostic procedures The echocardiographic findings in RCM (Figure
or necropsy examination, it is not possible to dis- 8-8) are quite variable. Severe LA dilation is a com-
tinguish this disorder from infiltrative diseases of mon feature. The LV internal dimensions are normal
the myocardium and UCM. or mildly reduced and LV systolic function is generally
This disorder is uncommon in the authors experi- normal. Two-dimensional echocardiography may dem-
ence. Much of what follows is summarized from the onstrate loss of normal LV symmetry and distorted
literature and not from direct clinical experience. or fused papillary muscles. Some authors report
increased endocardial echogenicity. Mitral regur-
gitation is detectable with spectral and color-flow
Doppler in most affected cats. Intracardiac throm-
In the most widely recognized form in cats, endo- bus (most commonly left atrium) may be present.
cardial, subendocardial, or myocardial fibrosis or
infiltration results in diastolic dysfunction.
LV pathology predominates. In most cases systolic
function is preserved. Papillary muscle fibrosis, dis- For acute CHF, see the earlier section on treat-
tortion of the mitral valve apparatus, and changes ment of CHF in the Therapy section of General
in LV geometry may contribute to the development Information.
of mitral regurgitation and left-sided CHF. No specific therapy for controlling the fibrous tis-
Similar pathophysiology may result from pericar- sue reaction is available.
dial fibrosis (restrictive pericarditis) or infiltrative Beta blockers or calcium channel blockers are not
neoplastic and inflammatory diseases of the epi- effective for improving diastolic function due to
cardium or myocardium. Signs referable to bi- fibrosis. Negative chronotropic, dromotropic, and
ventricular restriction predominate in pericardial antiarrhythmic effects of these drugs may be ben-
disease. eficial in cats with ventricular or supraventricular
Signalment and Presenting Complaints
Signalment is difficult to report accurately because
there is little agreement among cardiologists as As with other forms of cardiomyopathy, progno-
to which cases fall within this classification. Pre- sis is difficult to predict for individual cases prior
senting complaints are similar to those of other to observing the initial response to therapy; how-
forms of myocardial disease. ever, in general the prognosis is relatively poor
even when initial response to therapy is good.
Average survival time in the authors experience
Physical Examination
is usually only 4 to 6 months.
Physical examination findings are similar to that A high incidence of serious arrhythmias, sys-
of other forms of cardiomyopathy. temic thromboembolism, and refractory CHF has
been reported by some authors.
Ancillary Tests
As with other forms of myocardial disease, ancil-
lary tests rarely help discriminate the diagnosis. The postmortem changes are unique to this form
In general the findings are similar to what is dis- of cardiomyopathy and may be used to differenti-
cussed earlier in the chapter. ate it from other disorders.
Chapter 8 Feline Cardiomyopathy 165



Figure 8-8. Atypical (restrictive?) cardiomyopathy in the cat. A, Right parasternal long-axis view showing marked dilation of
the left atrium (LA), right atrium (RA), and right ventricle (RV). Note that the left ventricle (LV) is neither dilated nor thickened.
B, Right parasternal short-axis view from the same cat as in A showing marked right and left atrial dilation. In addition, a ball-like
thrombus is visible within the dilated left auricle (arrow). C, Right parasternal long-axis view of another cat with biatrial dilation,
a nonhypertrophied and nondilated left ventricle, and mild secondary tricuspid valve regurgitation. D, M-mode recording at the
mitral valve level from the same cat as in A and B. The right ventricular wall, septal, and left ventricular wall thicknesses are normal,
but all show mildly hyperdynamic systolic motion. The mitral-septal distance (EPSS) is normal. (From Nyland TG, Mattoon JS:
Small animal diagnostic ultrasound, ed 2, Philadelphia, 2002, WB Saunders.)

Patchy or diffuse endocardial, subendocardial, or

General Comments
myocardial deposition of fibrous tissue is charac-
teristic. Fibrosis without eosinophilia is the most In recent years, increasing numbers of cats have
common form reported in the cat. Fibrous adhe- been recognized with obviously abnormal hearts,
sions between papillary muscles and the myocar- many presenting in heart failure, but not fitting
dium, with distortion and fusion of the chordae into any recognized disease classification. It is not
tendineae and mitral valve leaflets, may be noted. known whether these cases represent a single dis-
As with most cardiomyopathies, the LV appears ease category. It is not known whether these cases
to be most severely affected. represent a congenital or acquired disease. It is not
Extreme LA and left auricular enlargements are known whether these cats are afflicted by a primary
common. myocardial disease or by a secondary condition.
Although no controlled studies have been per-
formed, taurine deficiency or metabolic abnor-
Unclassified Feline malities (e.g., hyperthyroidism) have not been
Cardiomyopathies consistent findings in affected cats.
The author (and other colleagues) has chosen to apply
the term unclassified cardiomyopathies to a diverse
set of cardiac presentations in cats. They are unclas-
sified because the lesions do not conform to expecta- The pathophysiology is unknown; however, clini-
tions for HCM or DCM, or to other known cardiac cal observations suggest diastolic dysfunction,
disorders. What follows is intended to describe the similar to that described for RCM, is the predom-
spectrum of lesions that are labeled UCM. inant functional abnormality in these cats.
166 Section II Cardiovascular Disease

For cats with chronic CHF, diuretics and ACE in-

Signalment and Presenting Complaints
hibitors are recommended (see previous section)
No sex, breed, or age predispositions are known.
Cats in this category are generally older adults.
Presenting complaints are believed to be similar
to other forms of myocardial disease. The prognosis is generally based upon clinical pre-
sentation, echocardiographic and radiographic evi-
dence of elevated diastolic pressures, and response
Physical Examination
to therapy.
Physical examination is similar to that of other Asymptomatic cats with mild LA enlargement are
forms of myocardial disease. believed to have a good long-term prognosis. Asymp-
tomatic cats with marked LA enlargement are likely
to be at higher risk for developing heart failure.
Ancillary Tests
In general, cats that present in heart failure have
Common thoracic radiographic findings include a poor prognosis. Although cats that present in
often severe left or bi-atrial enlargement. When heart failure and respond favorably to therapy
CHF is present, pulmonary edema is more com- may do well for prolonged periods of time.
mon than pleural effusion although both may be In general, cats with aortic thromboembolism
observed. have a poor prognosis. Cats that survive the throm-
By nature of the definition the echocardiographic boembolic episode may do well for extended
findings are extremely variable. In my opinion, the periods; however, these cats are generally at high
most consistent echocardiographic finding is severe risk for recurrence of thromboembolism.
dilation of the left atrium (see Figure 8-7). The left
ventricle is usually normal sized or only mildly di-
lated; however, severe LV dilation may be observed
Taurine DeficiencyInduced
along with normal wall thickness (eccentric hyper-
Myocardial Failure
trophy). Various patterns of mild regional myocar- Taurine deficiencyinduced myocardial failure is
dial hypertrophy are observed in the septum or LV associated with low plasma, whole blood, and tis-
free wall of some cats. Enlargement of the right sue taurine concentrations that and may be revers-
heart is variable but may be marked in some cases. ible after taurine supplementation. In 1987 it was
Systolic contractile indices may be normal or mildly determined that many cats presenting with DCM
depressed. Mitral, and on occasion tricuspid, regur- were taurine deficient and that supplementation
gitation can be detected with spectral and color-flow with taurine reversed the myocardial failure.
Doppler in most affected cats. It is generally mild Therefore, much of the literature published be-
but may be moderate in some cases. A thrombus fore 1987 referring to idiopathic DCM in cats
may be observed within the LA (Figure 8-9). should be considered to be referring to this condi-
tion, not to idiopathic DCM.
General Comments
For acute CHF, see the earlier section on treat-
ment of CHF in the Therapy section under Supplementation of commercial cat foods with
General Information. additional taurine has greatly reduced the preva-
As the underlying etiology and pathophysiology lence of this near-uniformly fatal condition.
have not been defined, no specific therapy can be Not all taurine-deficient cats develop myocardial
recommended for these disorders. failure. The other factor(s) required for taurine
With the presumed pathophysiology of this deficiency to lead to the development of myocar-
group of disorders, the use of calcium chan- dial failure are unknown. A genetic predisposi-
nel blockers to support or improve diastolic dys tion has been proposed.
functionmakessense; however, no studies have It is reasonable to assume that nutritional taurine
confirmed that this therapy has any benefit for deficiency combined with other causes of myo-
supporting CHF or improving survival in cats with cardial failure (e.g., long-standing congenital or
UCM. I generally use diltiazem in these cats (see acquired LV volume overload or toxic, ischemic,
earlier HCM section) unless there is a direct contra- nutritional, endocrine, or metabolic problems)
indication or untoward effects of the medication. may lead to synergistic complicating effects.

Chapter 8 Feline Cardiomyopathy

Figure 8-9. Echocardiograms from a cat with an unclassified form of cardiomyopathy. A, Right parasternal long-axis view. There is marked dilation of both left and right atria and mild dilation of
the right ventricle. LV, Left ventricle; LA, left atrium; RV, right ventricle; RA, right atrium. B, Right parasternal short-axis view shows the marked right and left atrial dilation. In addition, a thrombus is
visible within the dilated left auricle. AO, Aorta. C and D, M-mode recordings at the ventricular level and aortic level, respectively. The right ventricular wall, septal, and left ventricular wall thickness
are normal. The left ventricular chamber is only mildly dilated, and the left ventricular shortening fraction is in the low normal range (30%). The left atrium is markedly dilated.
168 Section II Cardiovascular Disease

A precise requirement for taurine cannot be de- Diet history should be accurately ascertained
termined for all foods because the requirement during the initial workup of any cat with myocar-
is dependent upon many factors. No commercial dial failure. Many owners have managed to for-
diet should be assumed to be taurine sufficient mulate diets with inadequate amounts of taurine
until the manufacturer has provided feeding and need to be educated to prevent recurrence.
trial data documenting that the food maintains In addition, it is likely that a small number of
normal taurine concentrations in blood and tis- cases will continue to be the result of commer-
sue during a trial of at least 6 months. cial cat foods containing inadequate amounts of
taurine, and the veterinary profession, to whom
these cats will present for diagnosis and treat-
ment, remains the most effective sentinel for de-
The hemodynamics and pathophysiology are be- tecting patterns with regard to diet and disease
lieved to be similar to idiopathic DCM as previ- occurrence.
ously outlined. Cats diagnosed with any form of myocardial fail-
In most cases, taurine deficiency is believed to ure should have plasma and whole blood taurine
be nutritionally derived, as a result of inadequate concentrations determined from blood samples
amounts of taurine in the diet. The role that tau- obtained prior to supplementation. Even a single
rine, an essential amino acid in the cat, plays in dose of taurine may make interpretation difficult
the maintenance of myocardial function remains and proper sample handling is critical for accu-
unknown. rate results.
The following guidelines should be used in han-
dling samples for taurine analysis:
Signalment and Presenting Complaints
Submit both heparinized plasma and heparin-
Signalment and presenting complaints are similar ized whole blood.
to those of other forms of cardiomyopathy. Place the sample on wet ice or centrifuge the
sample and separate plasma immediately.
Make sure the sample contains no clots or he-
Physical Examination
The physical examination is similar to that of Store and ship samples frozen (dry ice or ice
other forms of cardiomyopathy. packs).
Funduscopic evaluation may reveal the presence Normal values:
of taurine deficiencyinduced central retinal Plasma: taurine greater than 60 nmol/ml (at
degeneration. risk when less than 30 nmol/ml). Note: Plasma
taurine concentration is very labile; 24 hours of
fasting can cause plasma concentrations to fall
Ancillary Tests
below 30 nmol/ml.
Ancillary tests do not provide a definitive diag- Whole blood: taurine greater than 200 nmol/
nosis. The results of electrocardiography and ml (at risk when less than 100 nmol/ml).
thoracic radiographs are similar to other forms of Whole blood taurine concentration is not as
myocardial disease. The echocardiographic find- labile. Fasting does not significantly affect
ings are similar to those for idiopathic DCM. values.
The primary echocardiographic abnormality is an
increase in end-systolic diameter (more than 12
mm) with a reduced shortening fraction (less than
35%). The end-diastolic dimension is also often During the initial phase of therapy, proper
enlarged (more than 17 mm) (Figures 8-10 and supportive and symptomatic care for CHF (as
8-11). Significant LA enlargement is common. described previously under general comments
The E-point to septal separation (EPSS) is often on therapy) is essential if CHF is present. Cats
increased (> 2 mm). The right ventricle and right with documented taurine deficiency should be
atrium are variably affected. Mitral regurgitation supplemented with 250 mg every 12 hours un-
may be detected with spectral and color-flow til echocardiographically determined LV dimen-
Doppler. In some cases, a thrombus is observed sions normalize. This usually occurs within 4 to
within the body of the left atrium or in the left 6 months. Clinical improvement is usually evident
auricular appendage. within about 2 weeks.
Chapter 8 Feline Cardiomyopathy 169

Figure 8-10. Two-dimensional echocardiograms from a cat with myocardial failure associated with taurine deficiency. Right
parasternal long-axis (A) and short-axis (B) views, respectively, demonstrate marked dilation of all four cardiac chambers. LV, Left
ventricle; LA, left atrium; RV, right ventricle; RA, right atrium.

Diuretics and ACE inhibitors can be discontin- nmol/ml). Taurine supplementation can be dis-
ued when signs of CHF resolve, and radiographic continued once echocardiographic values return
improvement in cardiac size is noted. The ACE to within normal limits, and the cat is eating a diet
inhibitor should be removed first and then the with adequate amounts of taurine.
diuretic tapered over a period of 2 weeks. The Taurine concentration in plasma and whole blood
owner should be taught to monitor respiratory should be monitored periodically to be certain
rate while withdrawing heart failure medications, that the diet fed is maintaining concentrations
and clinical and radiographic evaluation should within acceptable limits. If taurine concentrations
be repeated 1 week after withdrawing medica- are depleted again, then many cats will again de-
tions to detect any decline in the cats condition. velop myocardial failure.
Digoxin is not routinely administered as a part of ther-
apy, but there is no contraindication to doing so. When
used initial dose should be one fourth of a 0.125 mg
tablet PO every 48 hours. Digoxin levels are taken 6 Because results of taurine analysis are not imme-
to 8 hours after the seventh dose and are used to adjust diately known and a recent dietary change may
therapy. I rarely increase the dose to more than one normalize taurine values, all cats with myocar-
fourth of a 0.125 mg tablet PO every 24 hours. dial failure should be supplemented with taurine
The diet should be altered to maintain normal and given an initially guarded-to-grave prognosis.
plasma taurine concentrations (greater than 60 In one large study, 30% of cats with myocardial
170 Section II Cardiovascular Disease

failure died within the first week after diagnosis. enlarged. There are no specific histologic or elec-
Hypothermia and thromboembolic disease were tron microscopic lesions.
associated with a poor prognosis. Taurine supple- In the past, many of these cases were classified as
mentation did not provide benefit with regard to RCM or intermediate cardiomyopathy. The echo-
survival until 2 weeks after treatment is begun. cardiographic appearance in many cases suggests
Cats that survive 1 week and respond to treat- that the hemodynamics resemble those of RCM;
ment for CHF can be upgraded to a fair progno- however, few cases have documented characteristic
sis. Catsthat survive 2 weeks and are shown to histopathologic lesions. The term intermediate sug-
be taurine deficient can be upgraded to a good gests a combination of or transition between states.
prognosis. There is no evidence that this represents a combina-
Most taurine-responsive cats have complete re- tion of or a transitional state between two forms of
versal of echocardiographic and clinical evidence cardiomyopathy. In fact, as stated previously, there
of myocardial failure after supplementation with is no evidence that these cases represent a single dis-
taurine (see Figure 8-11). Occasionally cats may ease entity or are proven to be a cardiomyopathy.
have residual mild myocardial failure (LV short- The whole blood analysis is most important.
ening fraction 25% to 30%); however, these cats
are generally asymptomatic and rarely require
any form of therapy other than maintaining nor-
Thyrotoxic Heart Disease
mal plasma taurine concentrations. Thyrotoxic heart disease is cardiac changes result-
ing from direct and indirect effects of elevations in
circulating thyroid hormone (hyperthyroidism).
The most predominant pathologic features are
General Comments
severe LV and LA enlargement. The LV walls
may appear thin and the papillary muscles and A frequently recognized secondary cardiomyop-
trabeculations are less prominent than normal. athy that may be confused with primary myocar-
The right ventricle and right atrium may also be dial diseases in older cats


Figure 8-11. M-mode echocardiograms from a cat with myocardial failure associated with taurine deficiency before (A) and
after (B) taurine supplementation and diet modification. Before therapy the left ventricle was markedly dilated, and the left ven-
tricular shortening fraction was severely reduced. Those parameters both normalized after taurine supplementation. EDD, Left
ventricular dimension at end-diastole; ESD, left ventricular dimension at end-systole.
Chapter 8 Feline Cardiomyopathy 171

Thyrotoxic heart disease or hyperthyroidism does energy economy of the heart and increases the
not cause HCM. overall work of the heart. Additionally, the thyro-
The prevalence and severity of thyrotoxic heart toxic heart, although hyperkinetic when the patient
disease has been decreasing in recent years, is at rest, has less reserve capacity available for
likely as a result of increased awareness and when increased cardiac work is necessary (e.g.,
therefore early diagnosis and treatment of exercise). This situation, placed on top of preex-
hyperthyroidism. isting cardiac disease (e.g., HCM, RCM, or DCM,
valvular disease) can lead to decompensation of a
previously well-compensated cardiac disease.
Reduced systemic vascular resistance in the pres-
The effects of thyroid hormone on the heart are ence of an increased intravascular volume (not
believed to be both direct and indirect. documented in cats) associated with significant
Direct actions increases in cardiac output are what define the
Increased protein synthesis (mitochondrial, high-output state of the cardiovascular system
ion pump, and contractile proteins) in hyperthyroid cats. This high-output state can
Alteration of myosin subtype (slow to fast (especially in the presence of underlying primary
type myosin; V3 to > V1) cardiac pathology, such as valvular insufficiency)
Less economical energy conversion from progress to result in clinically apparent signs of
chemical (adenosine triphosphate) to me- CHF in hyperthyroid cats.
chanical (force) by the myocardium Despite the reduced systemic vascular resistance
Increased rate of calcium cycling by the sar- that is part of the high-output, hyperthyroid state,
coplasmic reticulum hypertension, rather than hypotension, is ob-
Up-regulation of cardiac beta receptors served in many (87% of 39 cats in one study)
Enhanced rate of spontaneous depolarization hyperthyroid cats. Hypertension resolves in most
by sinoatrial node cells treated cases once a euthyroid state is reached.
Shortened action potential duration
Indirect actions
Signalment and Present Complaints
Enhanced metabolic demand by other tissues
results in a high-output state; the heart must Cats are generally older, with no gender or breed
increase its throughput to meet the increased predispositions.
demands of the peripheral tissues that are sim- Most cats present for routine examination or be-
ilarly stimulated to a higher metabolic state cause of signs or symptoms of hyperthyroidism
by the excess circulating thyroid hormone. (e.g., polyphagia, polyuria/polydipsia, weight loss).
Reduced systemic vascular resistance (not the Occasionally cats present with CHF or low-out-
same as hypotension) plays an important role put heart failure.
in the overall cardiac status of patients with
hyperthyroidism. Afterload is reduced while
Physical Examination
preload is increased in the presence of an in-
creased intravascular volume. Classic signs of hyperthyroidism, including evi-
In some, hypertension is a predominant find- dence of weight loss, unkempt hair coat
ing and leads to: Systolic heart murmur or gallop rhythm may be
Significant concentric hypertrophy of the present
left ventricle Sinus tachycardia is usually present
Risk of retinal detachment or hemorrhage A thyroid nodule may be palpable
The sum of these effects when there is excess
thyroid hormone (hyperthyroidism) is a heart
Ancillary Tests
that operates at a faster rate (tachycardia), is
hypertrophied, can contract faster and more Electrocardiography
powerfully (enhanced contractility), and has a Sinus tachycardia is commonly present
propensity to abnormal electrical depolarizations Tall R waves suggestive of LV hypertrophy or
(arrhythmias). dilation
Although these might at first glance sound like Variable arrhythmias, including atrial prema-
beneficial changes (bigger, faster, stronger, more ture complexes and ventricular premature com-
excitable), the thyrotoxic state greatly strains the plexes
172 Section II Cardiovascular Disease

Uncommonly, intraventricular conduction dis- Key Point

turbances are seen
Thoracic radiography: Common findings include We have found beta blockade therapy ben-
eficial in cats with hyperthyroidism that are
Generalized cardiomegaly with or without LA
unable to complete specific antithyroid ther-
enlargement apy because of concurrent renal insufficiency.
When CHF is present, pulmonary edema and Beta blockers are also helpful in controlling
pleural effusion are equally likely to be present. cardiovascular signs of thyrotoxicosis pend-
Echocardiography ing a euthyroid state in cats started on me-
Reported echocardiographic changes in cats thimazole (Tapazole).
with hyperthyroidism include increased aortic
root dimension, LA enlargement, increased
end-diastolic or end-systolic LV dimensions, in most cases. The authors recommend beta-
mild to moderate concentric hypertrophy of the adrenergic blockade in the following situations:
LV free wall or septum, and an increased (or, To manage significant supraventricular or ven-
rarely, decreased) LV shortening fraction. tricular tachyarrhythmias
In the authors experience the typical echo- In hyperthyroid cats undergoing anesthetic pro-
cardiographic changes in cats with hyperthy- cedures
roidism without CHF include hyperkinetic LV
wall and septal motion with mild LV dilation
(eccentric hypertrophy) and varying degrees
of LA enlargement. In general the LV wall Asymptomatic cats can be managed very well
andseptal thicknesses are not excessive in re- without the use of specific cardiovascular therapy
lation to the chamber dimensions and do not prior to appropriate therapy for the hyperthyroid
resemble the typical changes associated with state, and most evidence indicates that the cardio-
HCM. vascular changes are reversible.
There are reports of cats with myocardial failure Most cats with CHF can be managed successfully
demonstrating marked increases in LV end-dia- if the hyperthyroid state is controlled.
stolic and end-systolic dimensions, moderate to Most cats with severe systolic myocardial fail-
severe LA enlargement, and a reduction in short- ure have a poor prognosis, as the changes appear
ening fraction. The relationship of this presenta- to be irreversible unless influenced by taurine
tion to a deficiency of the amino acid taurine is deficiency.
unknown, but may also represent late irrevers-
ible changes associated with hyperthyroidism.
Acromegalic Heart Disease
Acromegalic heart disease is cardiac changes result-
ing from direct and indirect effects of elevations in
For acute CHF, see the section on treatment circulating growth hormone (hypersomatotropism).
of CHF in the Therapy section under General
General Comments and Historical
Signs of CHF may be difficult to control prior to
beginning to control the hyperthyroid state. Be-
gin with pharmacologic manipulations; thyroid- A syndrome resembling acromegaly in humans
ectomy or the physical isolation required after has been reported in a group of middle-aged and
radioactive iodine therapy present a high risk to older cats with growth hormonesecreting tumors
uncompensated animals. Once signs of CHF are of the pituitary gland.
well controlled and the hyperthyroid state is at- In 14 cases all affected cats had insulin-resistant di-
tenuated, more specific therapy may be pursued. abetes mellitus and enlargement of the liver, heart,
In cats with asymptomatic thyrotoxicosis, therapy kidneys, or tongue. Various cardiovascular abnor-
is generally aimed at controlling the hyperthyroid malities were seen in most of the affected cats.
state (i.e., Tapazole, thyroidectomy, or radioac- An increase in serum growth hormone concen-
tive iodine therapy). tration in about 60% of the cats with HCM but
Beta-adrenergic blockade is a common recommen- without signs of acromegaly. Growth hormone
dation in the literature. There is no contraindication is a known inducer of myocardial hypertrophy,
to its use, but benefits have not been documented and cats with acromegaly can have quite severe
Chapter 8 Feline Cardiomyopathy 173

concentric hypertrophy of the LV myocardium. Documentation of a pituitary mass on com-

Whether the increase in serum growth hormone puted tomographic scan or magnetic resonance
concentration is the cause, is the result, or is un- imaging provides further support.
related to feline HCM is unknown. A definitive diagnosis requires demonstration
of increased baseline serum growth hormone
The pathogenesis of heart disease in cats with
acromegaly is unclear. The importance of a di-
recttrophic effect of excessive growth hormone on Generally, therapy is aimed at controlling the
the myocardium as opposed to secondary effects diabetic state and renal failure. If CHF is present,
resulting from volume expansion, hypertension, supportive care (diuretics and vasodilators) may
or other secondary effects requires further study. also be beneficial.
The increased plasma growth hormone concen- Successful therapy for feline acromegaly has not
tration in some cats with HCM suggests a poten- been reported. Potential therapeutic modalities
tially important role for growth hormone in cats include radiation therapy, medical therapy, and
with hypertrophic heart disease. hypophysectomy.
Supportive therapy for CHF should be employed
in those cats with consistent clinical findings.
Signalment and Presenting Complaints
(See the section on treatment of CHF in the
Cats with acromegaly generally do not present Therapy section under General Information.)
for signs referable to cardiovascular disease. Of the six reported cases of CHF, four of these
Presenting complaints commonly include poly- cats died, three of which had concurrent renal
uria/polydipsia and weight loss referable to un- failure.
controlled diabetes.
Although no breed predilections have been iden-
tified, almost all of the reported cases have oc-
curred in older neutered male cats. The short-term prognosis is good. Pituitary tu-
mors grow slowly, and neurologic signs are
uncommon; the diabetes can be relatively well
Physical Examination
controlled with high doses of insulin.
Systolic murmurs were noted in 9 of the 14 cats Mild to moderate CHF responds fairly well to
described. symptomatic therapy.
Physical features of acromegaly include progna- Most cats eventually died or were euthanized
thia inferior, cranial and abdominal enlargement, owing to refractory CHF or renal failure. Re-
organomegaly (especially kidneys and liver), in- ported survival ranged from 4 to 24 months after
creased body size, and weight gain. diagnosis.
Signs of CHF may develop late in the course of
the disease.
LV hypertrophy is the hallmark pathologic feature.
Ancillary Tests
Myocardial histologic lesions include myofiber
Electrocardiography: abnormalities were not de- hypertrophy, multifocal myocytolysis, interstitial
tected in any of the 14 cats reported. fibrosis, and intramural arteriosclerosis.
Thoracic radiography: radiographic cardiomeg-
aly was identified in 12 of 14 cats.
Echocardiography: septal and LV wall concentric Neoplastic Infiltration
hypertrophy, resembling HCM, was identified in ofthe Heart
seven of eight cats examined.
General Comments and Historical
The diagnosis of acromegaly is tentatively
based on the presence of insulin-resistant dia- Rare in cats
betes mellitus or renal failure in a cat with clin- Echocardiography is generally required for non-
ical features of acromegaly. surgical detection.
174 Section II Cardiovascular Disease

Cardiac tumors reported in cats include: neutrophils. A viral etiology was suspected but
Lymphoma never identified.
Chemodectoma One report describes a transmissible myocarditis/
Hemangiosarcoma diaphragmitis in cats. No organism has been iso-
Metastatic pulmonary carcinoma lated, but transmission between cats by injecting
Metastatic mammary gland carcinoma. blood from infected cats into other cats does re-
Lymphoma is the most common tumor of the feline liably reproduce the disease. All cats developed
myocardium. Reported cardiac abnormalities in high fever (103.8 to 105.7 F), were lethargic,
cats with lymphoma include complete heart block, and were partially anorexic. Complete blood
pericardial effusion, and CHF. counts and chemistries were normal in all cats
Echocardiographic findings in cats with diffuse for 6 weeks except for an elevation of creatine
neoplastic infiltration of the myocardium can phosphokinase in three of seven cats. The dis-
mimic those of HCM. ease resolved on its own in these cats. Necropsy
Regression of neoplastic infiltration was reported revealed pale 1 to 3 mm discrete foci surrounded
in one cat with lymphoma following treatment by hemorrhage on ventricular myocardium and
with combination chemotherapy. on the diaphragm. No clinical signs referable to
the cardiovascular system were noticed.
The relationship of endomyocarditis to the other
Drugs, Toxins, and Physical Injury
cardiomyopathies of cats is unknown. Other re-
A large number of drugs and toxins are reported ported causes of myocarditis in cats include toxo-
to cause myocardial injury in domestic animals, plasmosis and metastatic infection from sepsis or
but very few are likely to be encountered in clinical bacterial endocarditis.
small animal practice. Of these, doxorubicin has
received the most attention in cats.
Decreased fractional shortening and increased
LV end-systolic dimensions were reported in four HCM is very common and probably represents
of six experimental cats given cumulative doses the largest percentage of cardiac diseases cur-
of doxorubicin of 170 to 240 mg/m2. However, rently diagnosed in the cat.
clinical signs of heart failure were not observed Presumed myocardial diseases that cannot be
even after a cumulative dose of 300 mg/m2, and classified into one of the known primary disor-
no cat showed electrocardiographic abnormali- ders, but that also lack common features allow-
ties during the study. As in other species, patho- ing classification as a single clinical entity, are
logic studies revealed extensive areas of myocyte increasing in frequency. Little is known about the
vacuolization and myocytolysis. Similar clinical etiology, pathophysiology, therapy, and progno-
observations have been reported in cats with ma- sis associated with these UCMs.
lignancies treated with doxorubicin. None devel- Of the secondary cardiomyopathies discussed,
oped overt heart failure, and arrhythmias were only nutritional (taurine-responsive) DCM and
only rarely observed. thyrotoxic heart disease are encountered with
With the possible exception of heat stroke and anyfrequency. Both of these disorders have
hypothermia, physical causes of myocardial beenwell classified, and both respond dramati-
damage are infrequently recognized in cats. Trau- cally to appropriate specific therapy. The other
matic myocarditis appears to be either uncom- secondary cardiomyopathies occur infrequently
mon or unrecognized in most cats that experience and are generally poorly understood. The gen-
thoracic trauma. eral approach, diagnosis, and therapy for these
disorders are similar to those for other feline
Infectious Myocarditis
One must recognize that the associated clinical
Infectious myocarditis is infrequently recog- and diagnostic findings frequently overlap, often
nized in cats. Liu and associates described a syn- making a definitive diagnosis difficult. Echocar-
drome of acute nonsuppurative myocarditis in diography is the one diagnostic aid that reliably
25 young cats (mean age 2.6 years). Most cats allows differentiation among the different cardio-
died unexpectedly, and necropsy revealed focal myopathies encountered in cats; however, even
or diffuse infiltration of the endocardium and with a thorough ultrasound examination, distinc-
myocardium with mononuclear cells and a few tions are still often unclear.
Chapter 8 Feline Cardiomyopathy 175

Frequently Asked Questions per nutritionist instructions) so perhaps heat is

damaging the taurine in the home-made food.
There was a young male cat that was admitted for rou-
Commercial manufacturers put in higher levels of
tine orchiectomy. His pre-operative complete blood
taurine into canned food recipes to allow for this
count, chemistry screen and urinalysis were normal.
intraprocessing destruction of taurine.
His pre-operative thoracic radiographs also appeared
3. Though most DCM cases are taurine deficiency
normal. Physical examination was within normal lim-
associated, some DCMs are not clearly associated
its, except the cat appeared small for his age.
with low blood levels.
The lightly sedated cat was subjected to mask induc-
4. It is important to test taurine levels before any
tion with isoflurane because the attending veterinari-
taurine supplementation is started.
an sometimes used this approach in quiet healthy cats.
They were able to intubate, but not resuscitate this pa- In cats, what do the UCMs represent? Key points to
tient. Why did this cat die during this induction? consider:
In this case, post-mortem confirmed cardiomyopathy 1. Cats do not always fall into clear categories of
it was not a laryngospasm. Key points to consider: heart disease.
1. HCM can be present, and the thoracic radiographs 2. Even with echocardiography the parameters may
still be normal. not clearly fit into one specific type, but rather
2. Many cats with cardiomyopathy are asymptomatic. share features of more than one type.
3. Sudden death may occur in otherwise healthy 3. Most cases of cardiomyopathy in cats are
appearing cats. idiopathic.
4. As per the anesthesia chapter, caution is needed as 4. These UCMs only allow one to assume cardiac
follows, quoted, Mask induction with isoflurane disease is presentno more.
or sevoflurane is not recommended in cardiac
patients. Most animals become very excited during
mask induction, even with adequate preanesthetic
medication, which could predispose to arrhythmias
and increased myocardial work secondary to the
Suggested Readings
stress response. Atkins CE: The role of noncardiac disease in the develop-
Cats are not good candidates for mask induction. Safe ment and precipitation of heart failure, Vet Clin North
combination anesthetic regimens are available that Am Small Anim Pract 21:1035, 1991.
make the technique of inhalant induction by mask un- Fox PR: Feline myocardial disease. In Fox PR, ed: Canine
necessary today. In the past, many of these anesthetic and feline cardiology, New York, 1988, Churchill Liv-
accidents were attributed to rare adverse primary ingstone.
anesthetic reactions if cause of death was not deter- Fox PR: Myocardial diseases. In Ettinger SJ, ed: Text-
mined by testing. book of veterinary internal medicine, ed 2, Philadel-
What is the significance of SAM in a cat with cardio- phia, 1989, WB Saunders.
myopathy? Key points to consider: Harpster NK: Feline myocardial diseases. In Kirk RW,
1. Key point is the pressure gradient across the region ed: Current veterinary therapy IX, Philadelphia,
of dynamic subaortic stenosis produced by the 1986, WB Saunders.
SAM. The pressure gradient roughly correlates with Jacobs G, Panciera DL: Cardiovascular complications of
the severity of the SAM although it can be quite feline hyperthyroidism. In Kirk RW, Bonagura JD,
labile, changing with the cats level of excitement. eds: Kirks current veterinary therapy XI, Philadel-
2. SAM is not present in all cats with HCM. The phia, 1992, WB Saunders.
majority of cats with severe HCM have SAM. Kittleson MD: Management of heart failure: concepts,
3. SAM can develop in advance of chamber wall therapeutic strategies, and drug pharmacology. In
changes, so it may be an early finding in some cats. Fox PR, ed: Canine and feline cardiology, New York,
A cat is diagnosed with DCMand you have not seen 1988, Churchill Livingstone.
a case since changes in food formulations 20 years Kittleson MD, Kienle RD: Small animal cardiovascular
ago? Key points to consider: medicine, St Louis, 1998, Mosby.
1. Taurine is not processed as efficiently in some dog Liu SK, Tilley LP: Animal models of primary myocardial
breeds when compared with othersthis may disease, Yale J Biol Med 53:191-211, 1980.
happen in certain lines/breeds of cats perhaps too? Liu SK, Maron FJ, Tilley LP: Feline hypertrophic cardio-
(conjecturenot yet confirmed in published studies) myopathy, Am J Path 102:388-395, 1981.
2. It is known that the commercial processing of Pion PD, Kittleson MD, Rogers QR: Cardiomyopathy in
tinned cat foods results in the destruction of some the cat and its relation to taurine deficiency. In Kirk
of the taurine due to presumed damage from high RW, ed: Current veterinary therapy X, Philadelphia,
temperature processing. The owner is using a high 1989, WB Saunders.
temperature pressure cooker to make her home- Pion PD, Kittleson MD: Therapy for feline aortic throm-
made diet (she is not simmering constituents as boembolism. In Kirk RW, ed: Current veterinary ther-
apy X, Philadelphia, 1989, WB Saunders.
Chapter 9

Cor Pulmonale and Pulmonary

Lynelle R. Johnson

Introduction The pulmonary circulation maintains low right

Cor pulmonale is defined as right-heart failure ventricular pressure in the face of increases in
caused by pulmonary or thoracic disease. It may be cardiac output through recruitment of closed cap-
characterized by clinical signs of fluid accumulation illaries and distension of existing capillaries.
or by radiographic or echocardiographic evidence Distribution of pulmonary blood flow is altered by
of right ventricular overload. By definition, pul- hypoxic pulmonary vasoconstriction and is also
monary hypertension (PH) must be present in cor modulated by endothelial release of vasoconstric-
pulmonale in order for the right heart to fail. Heart- tors and vasodilators. Hypoxic pulmonary vaso-
worm disease with pulmonary vascular obstruction constriction is a protective mechanism that prevents
is the most common cause of cor pulmonale in the de-oxygenated blood from entering the circulation
canine population, although any pulmonary vas- by preferentially constricting vascular supply to
cular obstruction has the potential to result in PH poorly ventilated lung regions. Thus, local alveolar
and cor pulmonale. Pulmonary arterial obstruction hypoxia results in local vascular constriction that
can result from lodging of clot material (pulmonary preserves gas exchange. However, global hypoxia
thromboembolism [PTE]) or from embolization of or diseases that disrupt the normal response to hy-
fat, septic material, neoplastic cells, or heartworms poxia can result in a deleterious rise in pulmonary
in the pulmonary arteries or capillary bed. artery pressure. Alterations in endothelium-derived
mediators can also impact pulmonary artery pres-
sures. The most potent vasoconstrictor is endo-
Cor Pulmonale thelin-1; thromboxane A2 and superoxide also
and Pulmonary mediate vasoconstriction. Vasodilators produced
Thromboembolism by the endothelium include nitric oxide and pros-
tacyclin. Release and activity of these vasoreactive
mediators can be altered in disease states, and im-
Pulmonary circulatory pressures are maintained balance among the various mediators can result in
at a level much lower than systemic pressures in a rise in pulmonary artery pressure.
order to reduce the workload on the thin-walled PTE results in abnormal gas exchange, altered vas-
right ventricle. Normal pressures in the dog and cular control, changes in pulmonary mechanics,
cat are reported as a systolic pulmonary artery and loss of ventilatory control. Physical obstruc-
pressure of 15 to 25 mm Hg, end-diastolic pulmo- tion of large pulmonary arteries leads to increased
nary artery pressure of 5 to 10 mm Hg, and a mean vascular pressure and reactive pulmonary vaso-
pulmonary artery pressure of 10 to 15 mm Hg. constriction from release of clot associated factors
Chapter 9 Cor Pulmonale and Pulmonary Thromboembolism 177

such as thromboxane that increase vascular resis- Box 9-2 Predisposing conditions for
tance. Secondary alterations in pulmonary physi- pulmonary thromboembolism
ology worsen and perpetuate derangements in gas
exchange. Release of humoral mediators such as Immune mediated hemolytic anemia
serotonin from platelets results in bronchoconstric- Neoplasia
tion and increased airway resistance. Surfactant Sepsis
function is altered leading to loss of elastic recoil Protein-losing nephropathy/enteropathy
and atelectasis, decreased pulmonary compli- Cardiac disease
ance, and increased right-to-left shunting. Work of
Central catheter use
breathing increases because of augmented alveolar Hemodialysis
dead space from nonperfused lung regions. Total parenteral nutrition
Hip replacement surgery
Cor pulmonale can result from disorders that im-
pact the pulmonary vasculature, such as obstruc- rapidly lysed and removed by the local fibrinolytic
tive or obliterative diseases of the pulmonary system; however, occlusion of larger pulmonary
circulation, or sustained hypoxic vasoconstric- arteries or massive showering of emboli to a large
tion associated with chronic parenchymal or circulatory volume can lead to acute right ventric-
tracheobronchial disease. Rarely, an increase in ular overload.
pulmonary blood flow will result in PH. Not all
animals with associated disorders will develop
Clinical Presentation
PH and cor pulmonale, and it is likely that ge-
netic or other influences will determine the vas- History and Clinical Signs
cular response. PH and cor pulmonale appear to Dogs or cats with PH and cor pulmonale can
be encountered more commonly in dogs than in be of any age, depending on the underlying eti-
cats. Primary PH is relatively uncommon; how- ology of elevated pulmonary artery pressures.
ever, various pulmonary conditions can lead to Generally there is a history of signs referable to
secondary PH in the dog or cat, including chronic the pulmonary system or to congestive failure.
tracheobronchial disorders, pneumonia, or inter- Animals can display any combination of signs
stitial lung disease (Box 9-1). A minority of these including lethargy, weakness, cough, respiratory
animals will develop overt clinical signs of right- distress, tachypnea, abdominal distention, and
heart failure. syncope. Historical features and clinical signs are
PTE is a secondary condition that occurs in as- not specific for PH or cor pulmonale but instead
sociation with diseases that cause blood stasis, reflect the underlying cardiopulmonary disease.
alter endothelial integrity, or increase coagulabil- PTE is generally a disorder of older animals, and
ity. PTE has been linked most commonly with history and clinical signs reflect the underlying
immune-mediated hemolytic anemia, neoplasia, disease process. Difficulty in clinical recognition
sepsis, protein losing nephropathy, cardiac disease, of this disorder is high, and animals with PTE are
and hyperadrenocorticism (Box 9-2). Clinically often presented for signs of weight loss, lethargy,
silent pulmonary embolism occurs in a majority and anorexia rather than for respiratory signs, al-
of dogs (82%) undergoing total hip replacement though tachypnea is often present on admission.
surgery. Small pulmonary thromboemboli are Secondary PTE should be suspected in an animal
with a predisposing condition that develops an
Box 9-1 Causes of cor pulmonale acute onset of tachypnea, cyanosis, and/or hypox-
emia that is refractory to oxygen therapy.
Pulmonary vascular disease
Heartworm disease
Chronic pulmonary thromboembolism
Chronic pulmonary disease Key Point
Tracheobronchial disease or collapse PTE occurs secondary to a variety of underly-
Pulmonary fibrosis/interstitial pneumonia ing conditions. Affected animals may present
Pneumonia for signs reflecting the primary condition or
Primary pulmonary hypertension for refractory respiratory distress.
178 Section ii Cardiovascular Disease

arterial oxygenation does not exclude the diagno-

Physical Examination
sis of PTE. Some but not all animals with PTE will
Animals with cor pulmonale will generally dis- respond to supplemental oxygen administration
play tachypnea or respiratory distress due to with normalization of arterial oxygen. Animals
fluid accumulation (ascites or pleural effusion) with additional cardiac or pulmonary pathology
or because of underlying pulmonary disease. A that increases shunt fraction will not necessarily
systolic heart murmur due to mitral or tricuspid have a complete response to exogenous oxygen
regurgitation is found in the majority of dogs supplementation.
with PH. Animals that develop clinical signs
of overt right-heart failure will display jugu- Radiographs
lar venous distention, ascites, or subcutaneous Radiographic evidence of right-heart enlarge-
edema. ment in an animal with lung or pulmonary vas-
Dogs and cats with PTE have tachypnea and hy- cular disease is supportive of cor pulmonale.
perpnea that is not alleviated by oxygen admin- (Figure 9-1) Retrospective review of radiographs
istration. Cough is relatively uncommon. Harsh in animals with PTE may allow the detection of
lung sounds or loud bronchovesicular sounds can regional oligemia, lack of normal vascular ta-
be detected; however, crackles or wheezes are pering, or enlarged central pulmonary arteries;
less common. Physical examination abnormali- however, in the clinical setting, radiographic
ties will reflect the underlying disease, such as changes appear less obvious, because PTE is of-
pale mucous membranes in the case of immune ten not suspected in the large proportion of dogs
mediated hemolytic anemia or a pot-bellied ap- that die with PTE.
pearance due to Cushings disease. Thoracic radiographic abnormalities are com-
mon in PTE but are rarely specific. Pulmonary
infiltrates may be interstitial, alveolar, or lobar in
Diagnostic Testing
dogs and cats. Alveolar infiltrates may represent
Laboratory Testing hemorrhage, edema, or infarction. Cardiomegaly
Basic laboratory tests generally reflect the under- and mild to moderate pleural effusion are com-
lying disease and do not add to the diagnosis of mon in dogs and cats. Importantly, normal chest
PH, cor pulmonale, or PTE. The diagnosis of PTE radiographs are reported in 7% to 27% of dogs
is particularly problematic. Testing for plasma and cats with necropsy confirmed PTE, and PTE
d-dimer, a breakdown product resulting from the should be a top differential diagnosis in an animal
action of plasmin on cross-linked fibrin, has been with marked respiratory distress and normal tho-
shown in human medicine to have high sensitiv- racic radiographs.
ity but low specificity in the diagnosis of PTE. In
veterinary medicine, several diseases can result
in a positive d-dimer test, although the magnitude Key Point
of the elevation may enhance the suspicion of Normal chest radiographs in a tachypneic
pulmonary embolization. It is unclear whether a animal that fails to respond to oxygen admin-
negative test excludes the possibility of PTE. istration should be considered suggestive of
Pulse oximetry and arterial blood gas analysis are pulmonary embolism.
useful for detecting abnormal gas exchange. He-
moglobin saturation (SpO2) is related to arterial
oxygen partial pressure by a sigmoidal relation-
ship, with values above 95% indicating normox- Electrocardiography
emia. Below 95%, values for SpO2 lie on the Reported abnormalities with right ventricular en-
exponential part of the curve, and small changes in largement due to PH or PTE include deep S waves
SpO2 reflect very large changes in arterial oxygen. in leads II and aVF and a right axis deviation. Right
Thus, pulse oximetry provides only a crude esti- atrial enlargement is supported by tall or peaked P
mate of lung function. Arterial blood gas analysis waves; however, electrocardiographic evaluation
provides more precise assessment of oxygenation of right heart enlargement is insensitive, and ab-
and can be used to follow response to therapy. normalities have been reported in<15% of dogs
Arterial blood gas analysis often reveals hypox- with PH. The electrocardiogram should be closely
emia, hypocapnia, and increased alveolar-to-arte- examined for rhythm disturbances, which may be
rial gradient in dogs with PTE; however, normal found in up to 25% of dogs with PH.
Chapter 9 Cor Pulmonale and Pulmonary Thromboembolism 179

Figure 9-1. There is generalized enlargement of cardiac silhouette on the right lateral (A) and dorsoventral (B) views. Pulmo-
nary arteries are enlarged and appear to taper slowly. Numerous pleural fissure lines are identified, and there is a diffuse heavy
interstitial and peribronchial pattern identified within the lung.

Echocardiography Doppler echocardiography can be used to esti-

Two-dimensional echocardiography can provide mate pulmonary artery pressure when tricuspid
subjective evidence of PH leading to cor pul- regurgitation or pulmonic insufficiency is pres-
monale (when pulmonic stenosis has been ruled ent. (Figure 9-2) Using the modified Bernoulli
out). Supportive evidence of right ventricular equation (Pressure gradient=4velocity2),
overload includes right ventricular concentric spectral Doppler allows reasonably accurate es-
hypertrophy and dilation, dilation of the main timation of right ventricular systolic pressure via
pulmonary artery, systolic flattening of the inter- measurement of tricuspid regurgitation velocity,
ventricular septum, and paradoxical septal motion. and estimation of pulmonary artery diastolic
180 Section ii Cardiovascular Disease

Figure 9-2. Tricuspid regurgitant jet in a dog with pulmonary hypertension. Based on the modified Bernoulli equation, the right
ventricular-to-right atrial pressure gradient is 85 mm Hg. (Courtesy Dr. Fiona Campbell, University of California, Davis)

pressure via measurement of pulmonic insuffi- identify reversible vasoconstriction. Lowering

ciency velocity. PH is documented by a tricuspid of the pressure gradient in response to inter-
regurgitant jet>2.8 m/sec or a pulmonic insuf- vention would suggest a potential response to
ficiency jet>2.2 m/sec. medical therapy. Unfortunately, sedation or gen-
Echocardiographic features consistent with pul- eral anesthesia is required for catheterization,
monary embolization overlap with those found and animals with PH are at increased risk
in PH. In addition, a thrombus can occasionally for anesthetic complications. Therefore, this
be visualized within the heart or great vessels. procedure is rarely performed in the clinical
Therefore, animals with predisposing conditions situation.
that develop an acute onset of respiratory distress Pulmonary angiography has been considered the
could benefit from echocardiographic assessment gold standard for diagnosis of PTE in humans;
for right ventricular dilatation, pulmonary artery although contrast helical computed tomography
enlargement, or septal flattening that might sug- is being used increasingly more often. Neither
gest pulmonary embolization. imaging modality is used commonly in veteri-
nary medicine because anesthesia is required,
Key Point and patients with severe PH or PTE are high-risk
Echocardiography should be considered in anesthetic candidates. Definitive angiographic
dogs suspected of PTE. diagnosis of PTE depends on visualization of an
intraluminal filling defect in a pulmonary artery
or loss of visualization of an artery.
Catheterization and advanced imaging Ventilation:perfusion scanning uses technetium-
Direct measurement of pulmonary artery pres- 99mlabeled macroaggregated albumin as a
sure through right heart catheterization is the vascular marker and technetium-99mlabeled di-
gold standard for diagnosing PH. Cardiac ethylenetriaminepentacetic acid as a ventilatory
catheterization also allows performance of marker to define segmental or lobar perfusion
acute pharmacologic testing of vasodilators to defects in areas of normal ventilation. Ventilation
Chapter 9 Cor Pulmonale and Pulmonary Thromboembolism 181

scans are rarely performed on nonanesthetized drugs require sophisticated or complicated de-
animals; however, perfusion scanning alone can livery and result in only minimal reductions
be completed without anesthesia and can assist in pulmonary artery pressures. Although these
in documentation of perfusion deficits. This is reductions are statistically significant and pro-
a safe, noninvasive technique for evaluation of vide some clinical benefit in human patients, it
PTE, although it is somewhat nonspecific be- is unclear whether these small changes in pul-
cause perfusion deficits can reflect true regions of monary arterial pressures would be beneficial in
thrombosis or simply a lung region experiencing veterinary patients.
hypoxic pulmonary vasoconstriction. An orally available nitric oxide donor silde-
nafil (Viagra), which causes accumulation of
cyclic guanosine monophosphate in vascular
smooth muscle and resultant vasodilation, has
Currently, little is known about the optimal some efficacy in reducing pulmonary artery
therapy for either PH or PTE. In animals with pressures in both humans and experimental
cor pulmonale, cautious diuretic therapy is animals. Occasional reports in dogs suggest
warranted to reduce fluid accumulation, and that it might also be beneficial in some veteri-
judicious use of thoracocentesis or abdomino- nary patients. Supplementation with arginine
centesis can be used to improve respiration. has been investigated for use in human medi-
Excessive removal of fluid is to be avoided since cine since arginine is converted into nitric oxide
animals may develop volume contraction or through combination with molecular oxygen. A
systemic hypotension. nonselective endothelin antagonist (Bosentan)

Therapy of PH has not been well defined in vet- has been shown to be efficacious in lowering
erinary medicine. Systemic vasodilators are not pulmonary artery pressures in patients with PH,
generally effective in lowering pulmonary artery although again, the reduction in pressure was
pressures and can cause deleterious side effects quite modest. Endothelin antagonists have not
because of excessive hypotension. Standard treat- been evaluated in veterinary patients. Anti-
ment of the underlying cardiopulmonary condi- coagulants may be beneficial by reducing in situ
tion should be employed and may lessen PH. thrombosis, progressive vascular occlusion, and
Anticoagulant therapy is recommended in hu- continued proliferative vascular disease.
man patients with PH associated with PTE or to
limit in situ thrombosis that can result in progres-
sive vascular obstruction. Low molecular weight
heparin therapy is often used because of reduced
risk of bleeding due to its favorable factor X:
factor II activity. However specific information
on pharmacokinetics and pharmacodynamics
of the available products is currently lacking in
Frequently Asked
veterinary medicine. Ultra-low-dose aspirin
(< 1 mg/kg every 24 [dog] to 72 [cat] hours) can What clinical findings would support the diagnosis
be used also in an attempt to inhibit platelet ag- of cor pulmonale and how could this be confirmed?
gregation. Newer antiplatelet drugs are currently Animals with clinical signs relative to cor pulmonale
generally display respiratory abnormalities (tachy-
under investigation.
pnea, hyperpnea, and/or cough) and may also exhibit
Insight into various therapies for PH has been signs of right-heart failure (ascites, jugular venous
gained by reviewing treatment of primary PH distention, and/or subcutaneous edema). Radiographi-
in humans, which is partially mediated by al- cally, cor pulmonale is evident as right-sided heart en-
terations in endothelium-derived vasodilators largement. Right atrial enlargement and dilation of the
and constrictors and by vascular proliferation. caudal vena cava support the diagnosis. Two-dimen-
Drugs that have been employed include intra- sional echocardiography reveals eccentric dilation of
the right ventricle. With chronic PH or PH in a young
venous or inhaled prostacyclin (a breakdown
animal, right ventricular hypertrophy can be found.
product of arachidonic acid metabolism) and In the presence of tricuspid regurgitation or pulmonic
inhaled nitric oxide. These vasodilators are se- insufficiency, Doppler echocardiography can confirm
lective for the pulmonary circulation and have PH by detection of a velocity jet greater than 2.8 or
more pronounced impact on pulmonary pres- 2.2 m/sec, respectively.
sures than systemic pressures. However, these
182 Section ii Cardiovascular Disease
Glaus TM, et al: Clinical and pathological characterisa-
What tests confirm the diagnosis of PTE and provide
tion of primary pulmonary hypertension in a dog, Vet
support for institution of anticoagulant therapy?
Rec 154:786, 2004.
Unfortunately, ante-mortem diagnosis of PTE re-
Johnson L, Boon J, Orton EC: Clinical characteristics of
mains challenging, and definitive diagnosis is often
not achieved in the clinical setting. Suspicion for PTE 53 dogs with Doppler derived evidence of pulmonary
should be present in an animal with a recognized hypertension: 1992-1996, J Vet Intern Med 13:440,
predisposing condition (see Box 9-2) that develops 1999.
an acute onset of respiratory distress. Normal chest Johnson LR, Lappin MR, Baker DC: Pulmonary throm-
radiographs do not preclude the diagnosis. Support- boembolism in 29 dogs: 1985-1995, Vet Intern Med
ive evidence of PTE would include a positive d-dimer 13:338, 1999.
test, echocardiographic evidence of right ventricular Koblik PD, Hornoff W, Harnagel SH, et al: A compari-
overload, and perfusion deficits on pulmonary scin- son of pulmonary angiography, digital subtraction
tigraphy in an animal with refractory respiratory angiography, and 99mTc-DTPA/MAA ventilation-
distress. Anticoagulant therapy with low molecular perfusion scintigraphy for detection of experimental
weight heparin would often be instituted in a patient pulmonary emboli in the dog, Vet Radiol Ultrasound
with these findings. Thrombolytic therapy is rarely 30:159, 1989.
employed because of the risk of generating a sys- La Rue MG, Murtaugh RJ: Pulmonary thromboembo-
temic fibrinolytic state or creating ischemia-reperfu- lism in dogs: 47 cases (1986-1987), J Am Vet Med
sion injury. Because of the difficulty in establishing Assoc 197:1369, 1990.
a diagnosis of PTE and the morbidity and mortality Liska WD, Poteet BA: Pulmonary embolism associated
associated with this secondary complication, prophy- with canine total hip replacement, Vet Surg 32:178,
lactic anticoagulant therapy should be considered in 2003.
animals with recognized predisposing conditions.
Michelakis ED, et al: Long-term treatment with oral
What type of treatment can be considered for PH? sildenafil is safe and improves functional capac-
Aggressive management of underlying cardio- ity and hemodynamics in patients with pulmonary
pulmonary conditions should be instituted. Ani- arterial hypertension, Circulation 108(17):2066,
mals with chronic bronchitis or small airway col- 2003.
lapse often require steroids (oral or inhaled) and Nelson OL, Andreason C: The utility of plasma d-dimer
extended-release theophylline (10 mg/kg PO ev- to identify thromboembolic disease in the dog, J Vet
ery 12 hours [dog] or 15 to 19 mg/kg PO in the Int Med 17:830, 2003.
evening [cat]). Interstitial lung diseases are less likely Norris CR, Griffey SM, Samii VF: Pulmonary throm-
to respond to medical therapy. In either group of ani- boembolism in cats: 29 cases (1987-1997), J Am Vet
mals with respiratory dysfunction, supplemental oxy- Med Assoc 215:1650, 1999.
gen therapy either at home or in the hospital setting
Pyle RL, Abbott J, MacLean H: Pulmonary hypertension
can improve clinical presentation. Use of sildenafil
and cardiovascular sequelae in 54 dogs, Intern J Appl
(0.5 to 2.0 mg/kg every 8 to 12 hours) can be consid-
Res Vet Med 2:99, 2004.
ered for animals with severe PH. Blood pressure and
echocardiographic monitoring for side effects and ef- Schermerhorn T, Pembleton-Corbett JR, Kornreich B:
ficacy are recommended. Pulmonary thromboembolism in cats, J Vet Int Med
18:533, 2004.
Schober K, Baade H, Ludewig E, et al: Cor pulmonale in
terrier breed dogs with chronic-progressive, idiopathic
Suggested readings pulmonary fibrosis: 19 cases (1996-2001), Tierarztliche
Praxis Ausgabe K, Kleintiere/Heimtiere 30:180, 2002.
Bach JF, Rozanski EA, MacGregor J, et al: Retrospec- Thomas D, Steiz M, Rtanabe G, et al: Mechanism of
tive evaluation of sildenafil citrate as a therapy for bronchoconstriction produced by thromboemboil in
pulmonary hypertension in dogs, J Vet Intern Med dogs, Am J Phys 206:1207, 1964.
20(5):1132-1135, 2006. Uehara Y: An attempt to estimate the pulmonary artery
Berger M, Haimowitz A, Van Tosh A, et al: Quantitative pressure in dogs by means of pulsed Doppler echocar-
assessment of pulmonary hypertension in patients diography, J Vet Med Sci 55:307, 1993.
with tricuspid regurgitation using continuous wave
Doppler ultrasound, J Am Coll Cardiol 6:359, 1985.
Fluckiger MA, Gomez JA: Radiographic findings in dogs
with spontaneous pulmonary thrombosis or embo-
lism, Vet Rad 23:124, 1984.
Chapter 10

Heartworm Disease
Clay A. Calvert and Justin David Thomason

Introduction Larvae development to the third stage usually

Heartworm disease is a common problem in tropi- requires 1 to 2.5 weeks, depending on the ambi-
cal and subtropical regions. Heartworm infection ent temperatures. Mosquitoes can survive the de-
has spread throughout most areas of the United velopment of only low numbers (<10) of larvae.
States, but the prevalence is still low at high el- Larvae development within the mosquito requires
evations and in most northern states. Endemic foci an average daily temperature of at least 57 Fahr-
frequently occur in regions with otherwise low enheit. The cooler the temperature, the longer
prevalence and it is difficult to eliminate heart- the time required for L3 to develop and vice
worms from a region once they have been estab- versa. Transmission is unlikely to occur during
lished. Wild animal reservoirs include wolves, the cold months of the year, even in most south-
coyotes, foxes, California gray seals, sea lions, ern regions of the United States. This is because
raccoons, and ferrets. when the temperatures are moderately low, the
time required for development from L1 to L3 may
exceed the life-span (30 days) of the mosquito.
Heartworm Disease Third-stage larvae (L3) infect the dog via the bite
wound created during feeding.
Etiology and Life Cycle
Larvae migrate through the subcutaneous tissues
Heartworm infection is produced by the parasite and vascular adventitial tissues for about 100
Dirofilaria immitis and is transmitted to dogs mostly days. During this time, two molts occur. Young
by 10 to 15 species of mosquitoes. Mosquitoes can adults (L5 larvae) enter the vascular system at 3
transmit infective larvae (L3) 2 to 3 weeks after in- to 3.5 months post-infection and are in the small
gesting a blood meal. Infection rates vary among pulmonary arteries after 5 to 6 months.
cats in endemic regions but are usually 10% to 20% In the dog, adult worms and microfilaria are
of that of dogs within the same enzootic region. Be- thought to have a natural life-span of 3 to 5 years
ing male, a large breed, and outdoors increases the and 1 to 2 years, respectively.
risk of infection in dogs.

Canine Infection Life Cycle Key Point

Female mosquitoes are the intermediate hosts Adult worms are present in the pulmonary ar-
and acquire the first-stage larvae (microfilaria) by teries approximately 6 months after transmis-
feeding on infected dogs. Two molts then occur sion from the mosquito.
to produce the infective L3 stage.
184 Section II Cardiovascular Disease

Heartworm Disease
Life Cycle
Heartworms invade the Mature heartworms (6-7
heart and pulmonary months) may also
arteries, reach maturity in reproduce and release
6-7 months, and shed microfilariae (heartworm
antigen into the offspring) into the
bloodstream. bloodstream.

Larvae remain in tissue

Microfilariae are ingested
for approximately two
by a mosquito.
months, then develop into
immature adults and
travel to the pulmonary
arteries in 3-4 months.

Infective larvae are

transferred to the dog Microfilariae develop into
through the wound infective larvae within the
produced by the mosquito.
IDEXX Corp., 1990
Figure 10-1. Life cycle of Dirofilaria immitis. (Courtesy Idexx Corp., Westbrook, Maine.)

See Figure 10-1. Feline Infection Life Cycle

Microfilaria can appear after 6 months, in- Some mosquito species do not like to feed on
crease in concentration for 6 months, plateau cats and cats are relatively resistant to infection,
for several months, and then decrease in con- requiring a greater L3 inoculation. Therefore, the
centration as long as super-infection does not infection rate in unprotected cats is at least 80%
occur. lower than that of unprotected dogs. The numbers
Microfilaria-specific antibody-mediated, occult of infective larvae that mature are fewer than in
infections occur in the presence of persistent host dogs, and the pre-patent period is usually 1 to 2
antibody excess. Antibody-dependent leukocyte months longer. The natural survival time of adult
adhesions entrap microfilaria in the pulmonary worms in the cat is thought to be no more than
microcirculation. Between 10% and 67% of all 2 years.
heartworm infections are occult, and some of
these are due to immune-mediated host reaction.
In most endemic regions, the incidence of occult
infections is approximately 20% to 25% of all Heartworm infection is most common in tropi-
infections. Dogs administered macrolide prophy- cal and subtropical climates. Infection is in-
laxis that are, or become, infected will not have evitable in chronically unprotected dogs along
microfilaremia. the southern Atlantic and Gulf coasts and other
Microfilaria-leukocyte (neutrophils and eosino- highly endemic regions. The prevalence in cats
phils) complexes are engulfed by phagocytic varies by geographic region. It is much lower
cells of the mononuclear phagocyte system, re- than dogs in some areas, similar to dogs in some
sulting in granulomatous inflammation. areas, and the incidence is probably underesti-
Predominately eosinophilic inflammation, with mated. Dogs housed outdoors have a four- to
minimal granulomatous inflammation, produces five-fold increased risk compared to those
allergic pneumonitis. housed indoors. Infection is most common
Progressive granulomatous inflammation oc- in dogs 4 to 7 years of age, but in highly en-
casionally occurs and leads to lethal pulmonary demic regions infection is common in younger
eosinophilic granulomatosis. dogs.
Chapter 10 Heartworm Disease 185

blood flow become impaired to varying degrees

and severe arterial disease results in pulmonary
Disease onset and severity largely reflect the hypertension, increased right ventricular after-
number of adult heartworms. In infected cats, the load, and eventually right-sided congestive heart
average number of adult worms is 3 to 6, depending failure (CHF). Parenchymal lung disease (in-
on the concentration of infected mosquitoes and the farction and consolidation) develops secondary
ambient temperature in any given region. to pulmonary arterial thromboembolism and in-
creased vascular permeability.
Worm Location
Until the adult worm burden exceeds 50 in a 25
kg dog, nearly all worms are located in the pul- Dogs
monary arteries. Worm burdens of approximately The history in dogs with heartworm infection
75 are associated with worms located in the right varies considerably. Many infections are dis-
atrium. Caval syndrome typically is associated covered in asymptomatic dogs by immunodiag-
with worm burdens of 100 or greater. nostic screening. Some dogs are totally without
signs; others have unexplained tachypnea, exer-
Response to Live Worms in Dogs cise intolerance, or cough. Signs consistent with
Pulmonary pathology is produced beginning with pulmonary hypertension, with or without overt
the young adults. Even if infection is identified 7 right-sided CHF, are associated with severe heart-
months post-infection, the L5 have already been worm disease.
in the pulmonary arteries for a few months and
some pathology has occurred. Pulmonary arterial Cats
endothelial damage and subsequent myointimal The history in cats also varies considerably. Leth-
proliferation most severely affects the caudal and argy and decreased appetite may be reported by
intermediate lung lobes, which are those receiv- the owners. Coughing, emesis, and sudden or epi-
ing the highest blood flow. sodic dyspnea are typical signs in cats. However,
Pulmonary lobar arterial enlargement, tortuosity, and sudden death may be the first sign of infection.
obstruction of smaller branches begin within a few CHF is uncommon.
weeks of worm arrival. Intrapulmonary blood flow
is obstructed as the disease progresses, and blood is
Clinical Signs
diverted to less severely affected lobes. Small down-
stream arterioles become damaged and leak plasma The clinical signs associated with heartworm in-
and inflammatory cells into the surrounding lung fection reflect the adult worm burden, duration of
parenchyma. This causes interstitial and alveolar infection, and host-parasite interaction. Respiratory
lung infiltrates and granulomatous inflammation. signs are most prominent.
Pulmonary arterial obstruction and lung inflam-
mation cause fever, coughing, dyspnea, he- Dogs
moptysis, leukocytosis, and thrombocytopenia. Exercise intolerance, coughing, dyspnea, and re-
Pathology is more severe and accelerated in ac- spiratory crackles occur in dogs with moderate and
tive dogs, relative to inactive dogs, for any given advanced heartworm disease. Hemoptysis occurs
worm burden. Small dogs do not tolerate heart- with severe disease and is caused by pulmonary
worm infection as well as large dogs. thromboembolism. It can be seen before, but oc-
curs more often after adulticide treatment. Acute
Response to Live Worms in Cats dyspnea and increased pulmonary radiographic
The response in cats and ferrets is similar to that infiltrates may develop secondary to spontaneous
of dogs but there is more pulmonary arterial mus- worm death. Syncope is associated with severe
cular hypertrophy and the barrier to oxygen dif- pulmonary arterial disease and pulmonary hyper-
fusion is more severe than in the dog. Mortality in tension. Signs of elevated central venous pressure
cats and ferrets is higher than in dogs. indicate severe pulmonary hypertension with in-
cipient or overt right-sided CHF. Physical find-
Response to Dead Worms ings include prominent jugular pulse, distended
The most severe disease is seen in response to jugular veins, hepatomegaly, and ascites.
dead worm fragments that are swept into small Hemoglobinuria commonly occurs in associa-
arterioles. Pulmonary vascular compliance and tion with caval syndrome (i.e., acute hemolytic
186 Section II Cardiovascular Disease

crisis caused by obstruction of the vena cava with Box 10-1 Clinical Signs Associated with
adult worms) and occasionally when severe pul- Feline Heartworm Disease
monary arterial disease results in hemolysis due
to fibrin-thrombus related RBC trauma. Throm- Acute Signs Chronic Signs
bocytopenia is usually a consequence of these Sudden death* PIE syndrome
complications. Respiratory Coughing
Nephrotic syndrome occasionally occurs as the Pulmonary embolism Dyspnea
result of severe glomerular disease (amyloidosis Collapse; shock Cardiopulmonary
or immune complex glomerulonephritis). Mani- Hemoptysis Lethargy
festations include proteinuria, hypoalbuminemia, Dyspnea; cough Weakness
hypercholesterolemia, ascites and occasionally Pneumonitis Right-sided CHF
Dyspnea; cough Anorexia
peripheral edema and azotemia.
Neurologic Gastrointestinal
Blindness Vomiting
Cats Seizures
Clinical signs in cats are different than in dogs. The Ataxia
common signs are vomiting, collapse or syncope, Coma
asthma-like syndrome, coughing, sudden death, Circling
and occasionally central nervous system signs. Syncope
Signs occur most often early in the infection and
again when young adult worms arrive in the pul-
monary arteries. Severe pulmonary complications *From severe pulmonary thromboembolism or heartworm
and death are most likely to occur whenever one occlusion of main pulmonary artery.
or more adult worm dies, either spontaneously or Pulmonary infiltrates of eosinophilia.
Congestive heart failure.
as a result of Immiticide administration.
Modified from Calvert C. Feline heartworm disease. In Fox PR,
Asthmatic signs are a common manifestation and ed: Canine and feline cardiology, New York, 1988, Churchill
often occur about 3 to 4 months post-infection. A Livingstone.
strong antibody response at this time may destroy
the developing larvae. If not, then a period of
quiescence occurs only to have asthma-like signs
recur in some cats 7 to 8 months post-infection. direct smear or a concentration test (modified Knott
Vomiting is a common, sporadic sign. It often