Curs Ic - Ic Si Ci - Final - 11 - Nov 2013

Congestive Heart Failure
CHF
Prof Univ Dr Ion C.Tintoiu FESC

Centrul de Cardiologie al Armatei
Universitatea Titu Maiorescu
Clinical syndrome that can result from any

structural or functional cardiac disorder
that impairs the ability of the ventricle to
fill with or eject blood
Definition
The hearts inability to pump

enough blood to meet the bodys
oxygen and nutrient demands
Can be systolic or diastolic,

left- or right-sided, acute or
chronic
Definition-etiology
Heart failure is a clinical syndrome usually

due to left ventricular dysfunction,
resulting in acute or chronic symptoms of
cardiac pump failure.
The most common causes of heart failure
are coronary heart disease, hypertension,
alcohol abuse, and idiopathic dilated
cardiomyopathy
Other causes are valvular and pericardial
disease; or non-cardiac diseases causing
high-output cardiac failure, such as
anaemia, thyrotoxicosis, septicaemia,
Paget's disease of bone, and arteriovenous
fistulae.
HEART FAILURE
Modern clinical definition

ESC guideline
Typical symptoms
and signs of
heart failure
Response to
heart failure
treatment
Cardiac dysfunction
confirmed
(ECG, imaging modalities
Neurohumoral
aktivation confirmed
(BNP)
A normal heart pumps blood in a smooth and

synchronized way.
Heart Failure
Heart
A heart failure heart has a reduced ability to

pump blood.
Adaptation in heart failure

(Compensatory Mechanism)
Ventricular remodelling
LV mass, size, shape is altered

CHF Causes of CHF
Volume overload:
Regurgitate valve
High output status
Pressure overload:
Systemic hypertension
Outflow obstructionAS
Loss of muscles:
Post MI, Chronic ischemia

Connective tissue diseases
Infection, Poisons
(alcohol,cobalt,Doxorubicin)
Restricted Filling:
Pericardial diseases,
Restrictive cardiomyopathy
Tachyarrhythmia
Pathologic Progression of CV
Disease
Sudden
Death
Coronary artery
disease
Hypertension
Diabetes
Myocardial
injury
Pathologic
remodeling
Low ejection
fraction
Cardiomyopathy
Death
Pump
failure
Valvular disease
Neurohormonal
stimulation
Myocardial
toxicity
Adapted from Cohn JN. N Engl J Med. 1996;335:490498.
Symptoms:
Dyspnea
Fatigue
Edema
Chronic
heart
failure

CHF
Pathophysiology
Hemodynamic changes
Neurohormonal changes
Cellular changes
Hemodynamic changes
From hemodynamic stand point HF

can be secondary to systolic
dysfunction or
diastolic dysfunction
Cellular changes
Changes in Ca+2 handling.
Changes in adrenergic receptors:
Slight in 1 receptors
1 receptors desensitization followed by down
regulation
Changes in contractile proteins

Program cell death (Apoptosis)
Increase amount of fibrous tissue
Diagnosis of heart failure

Physical examination
X-ray, ECG,
Echo, SpiroErgometry
Medical history
Lab tests: BNP,
Cinical symptoms and

signs
Dyspnea- Orthopnea-Edema,Cough
Liver engorgement
fluid
dyspnoe
fatigue
retention

CHF
ORTHOPNEA
Jugular Venous Distention

not directly related to LVEF

CHF
EKG
Old MI or recent MI
Arrhythmia
Some forms of Cardiomyopathy are
tachycardia related
LBBBmay help in management
Heart Block

CHF
Rhythm problems leading to CHF

CHF
Chest X-ray
Look for Heart size

Pulmonary vascular markings
COPD, pneumonia, Pneumothorax, widened
mediastinum
Pleural effusions

CHF Echocardiogram
Function of both ventricles
Wall motion abnormality that may
signify CAD
Valvular abnormality
Intra-cardiac shunts
Pericardial effusion
Restrictive pericarditis
Pulmonary hypertension
DCM
HCM, HOCM
Restrictive CMP

CHF
Cardiac Catheterization
Coronary artery disease
Dilated ventricle
Hyperdynamic small ventricle
Wall motion abnormality that may
signify CAD
Valvular abnormality
Intra-cardiac shunts
Pulmonary hypertension

CHF
Lab Tests
Anemia
Hyperthyroid
Chronic renal insuffiency
Electrolyte abnormality-Na, K, Mag,
Calcium
Pre-renal azotemia
Hemochromatosis
BNP
TSH
HgA1c
Classifying Heart
Failure:
Terminology and
Staging
.
A Key Indicator for Diagnosing

Heart Failure
Ejection Fraction (EF)
Ejection Fraction (EF) is the
percentage of blood that is pumped
out of your heart during each beat
Systolic vs. Diastolic
Diastolic dysfunction
Systolic dysfunction
EF normal or increased
Hypertension
Due to chronic replacement
fibrosis & ischemia-induced
decrease in distensibility
EF < 40%
Usually from coronary disease
Due to ischemia-induced decrease
in contractility
Most common is a combination of

both

CHF Diastolic CHF
Impaired LV relaxation
Increase passive LV stiffness
Endocardial and pericardial disordersw
Microvascular flow
Myocardial turgor
Neurohormonal regulation

CHF
Diagnosis of diastolic CHF
Increased ventricular filling pressure with
normal systolic function
Incresed ventricular pressure with preserved
systolic function and normal ventricular
volumes
Increased left atrial and pulmonary capillary
wedge pressure
Clinical symptoms and signs.
Clinical Classifications
Acute
Chronic
sudden onset with associated signs and

symptoms
secondary to slow structural changes
occurring in the stressed myocardium
Acute Decompensated
sudden exacerbation or onset of

symptoms in chronic heart failure
39
Acute Heart Failure
Often precipitated by a myocardial

infarction.
Signs include:
Severe breathlessness
Frothy pink sputum
Cold clammy skin
Tachycardia
Low blood pressure
Lung crepitations
Raised jugular venous pressure
Third heart sound
Confusion
BACKWARD
FAILURE
:
Increased
pulmonary
venous pressure,
pulmonary edema
FORWARD FAILURE (Low

CardiacOutput):Decreased perfusion of the
brain (confusion).kidneys (impaired renal
function),
skin (cyanosis) etc.
Chronic Heart Failure
Making an accurate diagnosis of heart failure and

determining its cause can be difficult
Clinical diagnosis is confirmed to be accurate in
approximately half of cases when investigated by
echocardiography.
The likelihood of heart failure in the presence of
suggestive symptoms and signs is increased if there is a
history of myocardial infarction (MI) or angina, an abnormal
ECG, or a chest X-ray showing pulmonary congestion or
cardiomegaly.
Symptoms include:
Shortness of breath on exertion (sensitivity 66%, specificity 52%)

Decreased exercise tolerance (often simply 'fatigue')
Paroxysmal nocturnal dyspnoea (sensitivity 33%,
specificity 76%)
Orthopnoea (sensitivity 21%, specificity 81%)
Ankle swelling (sensitivity 23%, specificity 80%)
Acute vs. Chronic
Acutean emergency situation in

which a patient was completely
asymptomatic before the onset of
heart failure; seen in acute heart
injury such as MI
Chroniclong-term syndrome in
which a patient exhibits symptoms
over a long period of time, usually as
a result of a preexisting cardiac
Types
Systolic (pumping problem)inability of the

heart to contract to provide enough blood flow
forward
Diastolic (filling problem)inability of the left

ventricle to relax normally, resulting in fluid back
up into the lungs
Left-sidedinability of the left ventricle to pump

enough blood, causing fluid back up into the lungs
Right-sidedinefficient pumping of the right side

of the heart, causing fluid buildup in the abdomen,
legs, and feet
Left-Sided Heart Failure

Signs & Symptoms
Dyspnea
Unexplained cough
Pulmonary crackles
Low oxygen
saturation
Altered digestion
Dizziness and lightheadedness
Confusion
Restlessness and
anxiety
Fatigue and weakness
Third heart sound

Reduced urine output
Right-Sided Heart
Failure
Signs
&
Symptoms
Lower extremity
Abdominal pain
edema
Nausea
Weight gain
Weakness
Liver enlargement
Ascites
Anorexia
Classification of
stages of heart
failure
Stage A
At high risk of
heart failure
Hypertension
CHD
Diabetes
Metabolic sy.
Cardiotoxin
Stage B
Structural heart
disease without
symptoms
LV remodeling
LV hypertrophy
Valve disease
Stage C
Structural heart
disease
with symptoms
of heart failure
Stage D
Refractory
heart failure
Classification of HF:
Comparison Between
ACC/AHA HF Stage and
NYHA
Class
ACC/AHA HFFunctional
Stage
NYHA Functional
Class
1
None
A At high risk for heart failure but without

structural heart disease or symptoms
of heart failure (eg, patients with
hypertension or coronary artery disease)
B Structural heart disease but without
symptoms of heart failure
C Structural heart disease with prior or

current symptoms of heart failure
D Refractory heart failure requiring

specialized interventions
Asymptomatic
II Symptomatic with moderate exertion

III Symptomatic with minimal exertion
IV Symptomatic at rest
Hunt SA et al. J Am Coll Cardiol. 2001;38:21012113.
New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890897.
Current & Future

Perspectives in the
Treatment of Heart
Failure
Principles of Treatment
Systolic HF
Preload
Afterload
Ionotropy
Neurohumoral
activity
ACE-I, Betablockers, and

aldosterone
antagonist are the
mainstay of
treatment
Treatment of heart failure

Heart transplantation
Pharmacologic
treatment
Pozitv inotrop
Digitalis
Neurohumorlis
blokd: BB, ACEi
Diureticum
Vasodilator
Antiarrhythmis
Surgical/interventional
Revascularisation
Valve replacement
Aneurysm resection
Surgical remodeling
Stem-cell therapy
Non-pharmacologic treatment
Resynchronization (CRT)
ICD
IABP
Assist device
Drug Therapy

CHF Treatment of CHF
Correction of reversible causes
Medications
Diuretics, ACE inhibitors, beta blokers etc.
Ischemia
Arrhythmia: A fib, flutter, PJRT
Valvular heart disease
Thyrotoxicosis and other high output status
Shunts
Diuretics & ACEI reduces the number of

sacks on the wagon
Diuretics
symptoms, oedema, prognosis

only in case of fluid retention
RAAS activationadd ACEi or ARB!
Titrate, combine
Hyonatraemia, hypokalemia, volume
depletion, renal dysfunction
Diuretic resistance
Loop Diuretics
Agent
Initial
Daily Dose
Furosemid
e
20-40mg
qd or bid
Bumetanid 0.5-1.0 mg
e
qd or bid
Max Total
Daily Dose
600 mg
10 mg
Eliminatio
n: Renal
Met.
Duration
of Action
65%R35%M
4-6 hrs
62%R/38%
M
6-8 hrs
Torsemide
10-20 mg
qd
200 mg
20%R80%M
12-16 hrs
Ethacrynic
acid
25-50 mg
qd or bid
200 mg
67%R33%M
6 hrs
All available for oral or IV administration
56
Aldosterone antagonists
symptoms, prognosis, mortality

NYHA III, EF<35%
Renal dysfunction
Hyperkalaemia
ACEI and ARB

remodelling, myocardial fibrosis
starting dose, target dose
Hypotension
Hyperlakaemia, renal dysfunction
Cough
Angio-oedema
-Blockers
Limit the donkeys speed, thus saving energy

CHF
VasodilatorsHydralazine and Nitrates
Reduction of afterload by arteriolar
vasodilatation (hydralazin) reduce
LVEDP, O2 consumption,improve myocardial
perfusion, stroke volume and COP
Reduction of preload By venous

dilation
( Nitrate) the venous return the
load on both ventricles.
Usually the maximum benefit is achieved

by using agents with both action.
Digitalis Compounds
Like the carrot placed in front of the donkey
Cardiac glycosides in clinical use

are:
Digoxin,
Digitoxin
Ouabain.
Inotropic Agents
Like the carrot placed in front of the donkey

CHF
Inotropic Agents
These are the drugs that improve
myocardial contractility ( adrenergic
agonists, dopaminergic agents,
phosphodiesterase inhibitors),
Dopamine
Dobutamine
Milrinone,
Aamrinone
Several studies showed mortality with oral inotropic
agents
So the only use for them now is in acute sittings such as
cardiogenic shock

CHF CHF Management
Bi-Vv pacing if sxs CRT
Hydralazine/nitrate or ARB if
BP allows + sxs
Digoxin to reduce
hospitalizations
Aldosterone antagonists in
select patient
Diuretics for fluid retention
Beta Blocker
ACE-I (or ARB if ACE intolerant)
Regular exercise program
Sodium restriction
ICD
Device Therapy:
Biventricular
Pacing
Device Therapy
Implantable CardioverterDefibrillators (ICD)

Cardiac Resynchronization Therapy
(CRT)
Left Ventricular Assist Devices
(LVAD)
Biventricular Assist Devices
Intraaortic Baloon Pump

Increase the donkeys (heart) efficiency
Biventricular Pacing
Ventricular Dysynchrony
Abnormal ventricular conduction

resulting in a mechanical delay and
dysynchronous contraction
Overview of Device Therapy
69
Cardiac Resynchronization
Therapy
Indications Key Points
Moderate to severe CHF who have failed

optimal medical therapy
EF<30%
Evidence of electrical conduction delay
Timing of Referral Important
Patients often not on optimal Medical Rx

Patients referred too late- Not a Bail Out
Defibrillators
(ICDs)
How does a defibrillator

for sudden cardiac death
work?
Device
Shown:
Combinatio
n
Pacemaker
&
Defibrillato
r
Surgery
for
Heart Failure
VAD Issues
What is a VAD?
A single system device that is surgically
attached to the left ventricle of the
heart and to the aorta for left
ventricular support
For Right Ventricular support, the
device is attached to the right atrium and
to the pulmonary artery
Thoratec pVAD
Jarvik 2000 LVAD
Left Ventricular Assist

Devices (LVAD)
REMATCH Trial1 yr survival 52%

(LVAD) vs 24% (rx)
2 yr survival 23% vs
8%
End-Stage (Class IV)
HF pts ineligible for
transplant due to:
>65yo
DM with EOD
CRI
Newer Generation Artificial

Hearts
biventricular
CardioWest TAH
Surgery
Coronary Revascularization
Valvular Surgery
Ventricular Reconstruction for
Ischaemic Cardiomyopathy
Mitral Repair for Regurgitation

LV Aneurysm Plication/Resection
Ventricular Remodelling
Post-infarct VSD repair
SURGERY TREATMENT IN HF
LV Reconstruction (Dor)
LV Reconstruction by Patch Plasty

Jatene, Dor, Fontan
Bockeria et al. Eur J Cardio-thorac Surg

2006;29:S251-8S.
Novel Mechanical Anti-remodeling

Therapies in Heart Failure
ACORN
Myosplint
SURGERY TREATMENT IN HF
Area of previous infarct with rupture of

ventricular wall
Cardiac Transplant
It has become more widely used since the

advances in immunosuppressive
treatment
Survival rate
1 year 80% - 90%
5 years 70%
Christian Barnard
BorninSouthAfricain1922
Studiedheartsurgeryatthe
UniversityofMinnesotathen
returnedtosetupacardiacunit
inCapeTown.
December1967:transplantedthe
heartofaroadaccidentvictim
intoa59yearoldpatient
Patientonlysurvived18days
duetoinfectiouscomplications
Outpatient Therapy
92
THE END
Inca nu s-a terminat !!!
Ischemic Heart
Disease and
Myocardial
Infarction
Prof Univ Dr Ion C.Tintoiu
Coronary Arteries
Normal Anatomy
Coronary Angiography
Myocardial Ischemia:
Occurs when myocardial oxygen

demand exceeds myocardial oxygen
supply
MVO2 = Myocardial Oxygen Demand

MVO2 determined by:
-Heart Rate
--Contractility
-----Wall Tension
Coronary obstruction/Cardiac
pain/Cardiac Ischemia lesion
Obstruction:
Impediment.
Stenosis Narrowing of
blood vessle
: Pain
Cardiac lesions
Angina Pectoris
.Ischemia fibrosis
Pain :
Cardiac lesions
Narrow
lumen
I) Obstruction
II) Occlusion
Occlusion:
Closed
vessel
Infarct Pain
Closure
of the
lumen
.Infarct (necrosis)
Risk Factors
family History
cigarette smoking
diabetes mellitus
hypertension
hyperlipidemia
sedentary life-style
obesity
elevated homocysteine, LP-a ?
Screening and Diagnosis

Myocardial Ischemia
su
pp
ly
show s
Coronary
Angiography
g in
Narrow in
coronaries
Stress
Test
to
he
ar t
es
s
l
pu
im
blo
od
Electrocardiogram
me
asu
res
of
es
Sit
ele ctrical
ea
su
res
sp
ec
i fi
c
C
Angina
Pectoris
m
ISCHEMIC CHEST PAIN
EXERTIONAL ANGINA
* BRIEF EPISODES BROUGHT ON BY EXERTION AND
RELIEVED BY REST ON NTG
UNSTABLE ANGINA
* NEW ONSET
* CHANGE IN FREQUENCY/SEVERITY
* OCCURS AT REST
AMI
* SEVERE PERSISTENT SYMPTOMS
* ELEVATED TROPONIN
ISCHEMIC CHEST PAIN:

DIAGNOSIS
12 LEAD EKG
- Look for ST segment elevation (at
least
1mm in two contiguous leads)
- Look for ST segment depression
- Look for T wave inversions
- Look for Q waves
- Look for new LBBB
- Always compare to old EKGs
EKG CHANGES IN
ISCHEMIC HEART
DISEASE
ST SEGMENT
DEPRESSION
T WAVE
IINVERSIONS
ISCHEMIC CHEST PAIN:

DIAGNOSTIC TESTS
CARDIAC ENZYMES
- Myoglobin
* Will rise within 3 hours, peak within 4-9
hours, and return to baseline within 24 hrs.
- CKMB
* Will rise within 4 hours, peak within 12- 24
hours and return to baseline in 2-3 days
- TROPONIN I
* Will rise within 6 hours, peak in 12 hours
and return to baseline in 3-4 days
Coronary Artery
Angiography
Coronary Artery
Angiography
Echocardiograph
y
Ischemic Heart Disease
Stable Angina
Angina
Angina is a type
of chest
discomfort
caused by poor
blood flow
through the blood
vessels (coronary
vessels) of the
heart muscle
(myocardium).
Myocardial Blood Flow

Myocardial O2 Demands
Transient Myocardial
ischemia
Severe Chest pain
Angina Pectoris
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Types of Angina
1. Stable Angina.
2. Unstable Angina.
3. Variant Angina.
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1. Stable Angina . Symptom

The commonest cause is ADVANCED
ATHEROSCELEROSIS
Retrosternal pain
Radiating to left arm &
shoulder
Relieved by rest, NTG
Lasting less than 15 min.
HOME
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Stable Angina
Predisposing factors
Emotion
Heavy meals
Relieving
factors
Exertion
Rest
sublingual
nitroglycerin
Exposure to cold
weather
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Stable Angina
Anginal pain is often associated with Depression
of ST segment
Exercise ECG showing typical severe down sloping ST
segment :
Standing
1 min.
3 min.
7 min.
9 min.
In between attacks : ECG is entirely NORMAL

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Diagnosis
Exercise Treadmill Test
Management of Stable
Angina
1- General measures.
2- Drug Treatment.
3- Coronary artery
revascularization.
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General measures
Treat Hypertension ,
Hypercholestrolimia
and Diabetes
Stop smoking
AVOID
Severe
exertion
Reduce weight
Heavy meal
Emotions
Graduated exercise may open new

collaterals
Cold Weather
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Stable Angina Treatment
Risk factor modification (HMG Co-A

Reductase inhibitors = Statins)
AspirinDecrease thrombotic risc
Decrease MVO2
nitrates
beta-blockers
calcium channel blockers
ACE-inhibitors
Anti-oxidants (E, C, Folate, B6)?
What are the antianginal drugs?

Organic nitrates.
- adrenoceptor blockers.
Calcium channel blockers.
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NITRATES
Veins
Relaxation of smooth
muscles
Dilatation
Arteries
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Effect of Nitrates :
On Stable Angina :
1- Venodilatation
Preload
Arteriolar
dilatation
Afterload
Myocardial
Oxygen demand
2- Redistribution of coronary flow towards
subendocardium
3- Dilatation of coronary collateral vessels.
Preparations :
Short acting
For acute attacks
Nitroglycerin
(sublingual, buccal
spray)
Isosorbide
dinitrate(sublingual,
buccal spray)
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Long acting
For antianginal prophylaxis

Nitroglycerin
oral SR (6.25-12mg) 2-4
times/day
- 2% ointment (1-1.5
inch/4hrs)
- patches (1 patch=25mg)/day
Isosorbide dinitrate (oral) 1040mg t.d.s.

Isosorbide mononitrate (oral)
Duration of Action of Various Preparations of

Organic Nitrates
Duration of
action
Preparation
" Short-acting"
1-Nitroglycerin
a) Sublingual
b) Spray
10-30 min
10-30 min
2- Isosorbide dinitrate
a) Sublingual
b) Spray
Up to 60 min.
1.5 hours
1-Nitroglycerin
a) Oral; sustained release

b) Ointment
c) Transdermal patches
4-8 hours
3-6 hours
8-12 hours
2- Isosorbide dinitrate
3-Isosorbide mononitrate
Oral
Oral
4-6 hours
6-10 hours
" Long-acting"
Adverse Reactions :
1- Postural Hypotension &
Syncope
2- Tachycardia
3- Drug Rash
4- Facial Flushing
5- Throbbing Headache
6- Prolonged high dose

Methaemoglobinaemia
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-blockers are effective in STABLE & UNSTABLE

angina
In contrast they are not useful for

vasospastic angina (Variant) {Prinzmetal} &
may worsen the condition. This deleterious

effect is likely due to an increase in coronary
resistance caused by the unopposed effects of
catecholamines acting at -adrenoceptors.
Contraindications :
CHF
Peripheral
Vascular
disease
A-V block
Bronchial
asthma
Hypotension
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Used in treatment of all types of angina.

Verapamil (80-160 mg) /8 hr
Diltiazem
(60-120 mg) /8 hr
Dihydropyridine group
Nifedipine (10-40mg) /8 hr
Amlodipine
5mg/day
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Mechanism of anti-anginal action :

1 - Coronary artery dilatation and relief
of coronary spasm (variant angina)
2 -Decrease myocardial O2 demand due to:
Arteriolar
dilatation
Vascular
resistance
(Verapamil & Diltiazem)

Decrease HR.
Decrease contractility
Decrease AV conductivity
Afterload
Adverse reactions :
Dizziness
Flushing
Ankle
edema
Constipation
Headache
A-V block & HF only

with Verapamil &
Diltiazem
Hypotension
Reflex
Tachycardia
with Nifedipine
Contraindications of
Verapamil & Diltiazem:
2 - Sinus or A-V node

1 - HF
disease.
3 - Bradycardia.
Treatment of an acute attack of angina

Sublingual nitroglycerin (0.5 mg ) or isosorbide
dinitrate (5 mg ) or
Oral spray nitroglycerin (0.4 mg/metered
dose), isosorbide dinitrate(1.25 mg/metered
dose)
Persistence of pain
Relief within 1-3 min.
Repeat nitroglycerin at 5 min.

interval (3 tab. max.)
Relief
not relieved
Infarction
HOSPITALIZATION
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Coronary artery bypass grafting

(CABG)
Percutaneous Transluminal
coronary Angioplasty (PTCA)
For patients not responding to
adequate medical therapy
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Treatment of Stable Angina

-STENTS
Treatment (continued)
1) Stenting
a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the artery
the balloon is then inflated and causes the stent to
expand until it fits the inner wall of the vessel,
conforming to contours as needed
the balloon is then deflated and drawn back
The stent stays in place permanently, holding the vessel
open and improving the flow of blood.
Treatment
(continued)
2) Angioplasty
a balloon catheter is passed through the guiding catheter to
the area near the narrowing. A guide wire inside the balloon
catheter is then advanced through the artery until the tip is
beyond the narrowing.
the angioplasty catheter is moved over the guide wire until
the balloon is within the narrowed segment.
balloon is inflated, compressing the plaque against the artery
wall
once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.
TREATEMENT-CABG
Stable Angina - Treatment

Coronary Artery Bypass Grafting Surgery
(CABG)
Acute Coronary
Syndrome
Acute Coronary
Syndromes:
Terminology
Pathophysiology of all 3 is the same
Unstable Angina (UA)

ST depression, T Wave inversion or normal
No enzyme release
Non-Transmural Myocardial Infarction (NTMI or
SEMI)
ST depression, T Wave inversion or normal
No Q waves
CPK, LDH + Troponin release
Transmural Myocardial Infarction (AMI)
ST elevation
+ Q waves
CPK, LDH + Troponin release
The underlying cause is

Fissuring of atheroscelerotic plaques
Platelet aggregation
Thrombosis
Coronary artery spasm
Atheroscelerotic changes
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Unstable Plaque:
More Detail.
Cross section of a
complicated plaque
Acute Coronary
Syndrome
Ischemic Discomfort
Unstable Symptoms
No ST-segment
elevation
Unstable
angina
History
Physical Exam
ST-segment
elevation
Non-Q
AMI
Q-Wave
AMI
ECG
Acute
Reperfusion
Definition:
Definition: NSTEMI
NSTEMI
NSTEMI is an acute process of

myocardial ischemia with sufficient
severity and duration to result in
myocardial necrosis.
The initial ECG in patients with NSTEMI
does not show ST-segment elevation.
NSTEMI is distinguished from UA by the
detection of cardiac markers indicative
of myocardial necrosis in NSTEMI and
the absence of abnormal elevation of
such biomarkers in patients with UA.
ACC/AHA Guidelines
Screening and Diagnosis
su
pp
ly
sp
ec
i fi
c
show s
Coronary
Angiography
g in
Narrow in
coronaries
MARKERS
Test
to
he
ar t
es
s
l
pu
im
blo
od
Electrocardiogram
me
asu
res
of
es
Sit
ele ctrical
me
as
ur
es
MI - Types
Transmural
(STEMI)
Full thickness
Superimposed
thrombus in
atherosclerosis
Focal damage
Sub-endocardial (NSTEMI)
Inner 1/3 to half of ventricular

wall
Decreased circulating blood
volume( shock, Hypotension,
Lysed thrombus)
Circumferential
Heart - Pathology
TTC
Diagnosis of MI: Cardiac enzymes

Role of troponin i
Troponin I is highly
sensitive
Troponin I may be
elevated after
prolonged
subendocardial
ischemia
See examples below
Cardiac enzymes: overview
Legend: A. Early CPK-MB isoforms after acute MI

B. Cardiac troponin after acute MI
C. CPK-MB after acute MI
D. Cardiac troponin after unstable angina
EKG diagnosis of MI
ST segment
elevation
ST segment
depression
T wave inversion
Q wave formation
ACUTE INFERIOR MI
ST ELEVATION II, III, AVF
ACUTE ANTERIOR MI
ST SEGMENT ELEVATION V2-4
3. Variant Angina
(Prinzmetal)
Chest pain at rest due to
coronary artery spasm
ECG
changes:
The baseline ECG
With chest pain ,

marked ST segment
elevation
Acute elevation of ST
segment
Return of the ST segment to

the baseline after
nitroglycerin administration
161
BACK
MAIN
EXIT
INDEX
2. Unstable Angina .
Increased frequency, severity or duration
of pain in a patient of Stable Angina
N.B.
Pain occurs with less exertion
or at rest
Myocardial infarction may occur in 10-20% of patients.
162
BACK
MAIN
EXIT
INDEX
Treatment of Acute Myocardial

Infarction
aspirin, heparin, analgesia, oxygen

reperfusion therapy
thrombolytic therapy (t-PA, SK, n-PA, r- PA)

new combinations ( t-PA, r-PA + 2b / 3a inhib)
cath lab (PTCA, stent)
decrease MVO2
nitrates, beta blockers and ACE inhibitors

for high PCWP - diuretics
for low Cardiac Output - pressors (dopamine,
levophed, dobutamine; IABP; early
catheterization
Fibrinolytic
Therapy in
STEMI
Coagulation and
Tissue Plasminogen
Fibrinolysis
Activator
Coagulation Factors
Plasminogen
Fibrinogen
Plasmin
Fibrin
Fibrinolysis
Fibrinolysis
Aside: other Anti-thrombotic

drug types
Anti-platelet agents include:
Aspirin (acetylsalicylic acid)

clopidogrel
dipyridamole
ticlopidine
glycoprotein IIb/IIIa inhibitors
Thrombolytic (/fibrinolytic) drugs include:
tissue plasminogen activator - t-PA - alteplase

(Activase)
reteplase (Retavase)
tenecteplase (TNKase)
anistreplase (Eminase)
streptokinase (Kabikinase, Streptase)
urokinase (Abbokinase)
Thrombolytic Drugs
Streptokinase
It is a bacterial protein produced by group C (beta)hemolytic streptococci

Mechanism: It binds to plasminogen producing an
"activator complex" that lyses free plasminogen to
the proteolytic enzyme plasmin
Plasmin degrades fibrin clots as well as fibrinogen
and other plasma proteins (non-fibrin specific)
Pharmacokinetics:
The t of the activator complex is about 23 minutes
The complex is inactivated by anti-streptococcal
antibodies & by hepatic clearance
Thrombolytic Drugs
Alteplase (rt.PA)
It is a tissue plasminogen activator (t.PA)

produced by recombinant DNA technology of 527
amino acids
Cost per day is around 2200 $
Mechanism:
It is an enzyme which has the property of fibrinenhanced conversion of plasminogen to plasmin
It produces limited conversion of free plasminogen in
the absence of fibrin
When introduced into the systemic circulation it binds
to fibrin in a thrombus and converts the entrapped
plasminogen to plasmin followed by activated local
fibrinolysis with limited systemic proteolysis
Thrombolytic Drugs
Alteplase
Therapeutic Uses
Acute Myocardial Infarction in adults for the

improvement of ventricular function following AMI the
reduction of the incidence of congestive heart failure,
and the reduction of mortality associated with AMI
Acute Ischemic Stroke for improving neurological
recovery and reducing the incidence of disability.
Treatment should only be initiated within 3 hours after
the onset of stroke symptoms, and after exclusion of
intracranial hemorrhage
Pulmonary Embolism: Treatment of acute massive
pulmonary embolism
Reteplase & Tenectaplase

Reteplase is another human t-PA prepared
by recombinant mutation technology
It is fibrin-specific
It has longer duration than alteplase
Tenectaplase is another genetically
modified human t-PA prepared by
recombinant technology
It is more fibrin-specific & longer duration
than alteplase
Thrombolytic Drugs
Urokinase
It is an enzyme produced by the kidney,
and found in the urine
It is mainly used in the low molecular
weight form of urokinase obtained from
human neonatal kidney cells grown in
tissue culture
Mechanism: It acts on the endogenous
fibrinolytic system converting plasminogen
to the enzyme plasmin that degrades fibrin
clots as well as fibrinogen and some other
plasma proteins (Non-fibrin selective)
Thrombolytic Drugs
Urokinase
Urokinase administered by
intravenous infusion is rapidly cleared
by the liver with an elimination halflife for biologic activity of 12-20
minutes
Clinical Uses:
For the lyses of acute massive
pulmonary emboli
Contraindications to
Thrombolytic Therapy
Absolute contraindications include:
Recent head trauma or caranial tumor
Previous hemorrhagic shock
Stroke or cerebro-vascular events 1 year
old
Active internal bleeding
Major surgery within two weeks
Relative contraindications include:
Active peptic ulcer, diabetic retinopathy,
pregnancy, uncontrolled HTN
Fibrinolitic Therapy in
STEMI
90% of patients w/ acute STEMI have complete

occlusion of culprit artery
PCI preferred if performed w/in 90 minutes
of presentation or if transfer to
neighboring institution for PCI can occur
w/in 30-60 min.
Thombolytic therapy is the alternative
treatment
Not as effective in non-STEMI as the infarctrelated artery is not totally occluded in 60-85%
of cases
PCI after
thrombolytics???
This issue remains unresolved
3 possible scenarios
*Facilitated PCIlytic drug given prior to
planned PCI in attempt to achieve an open
infarct-related artery before arrival of cath
lab
*Adjunctive PCIPCI performed within hours
after thrombolysis
*Early elective PCIPCI performed within a
few days after thrombolysis
Angiogram in unstable angina:

eccentric, ulcerated plaque
Angiogram in unstable angina:

after stent deployment
PCI after
thrombolytics???
planned PCI in attempt to achieve an open
infarct-related artery before arrival of cath
lab
*Adjunctive PCIPCI performed within hours
after thrombolysis
*Early elective PCIPCI performed within a
few days after thrombolysis
Prehospital
Thrombolysis
Prehospital Thrombolysis
Project:
Acute inferolateral infarct
Heparin
And other current Parenteral
Anticoagulants
Unstable Angina
Anti-coagulant Therapy
Heparin
recommendation is based on
documented efficacy in many trials of
moderate size
meta-analyses (1,2) of six trials showed a
33% risk reduction in MI and death, but
with a two fold increase in major
bleeding
titrate PTT to 2x the upper limits of
normal
1. Circulation 1994;89:81-88
2. JAMA 1996;276:811-815
Unstable Angina
Anti-coagulant Therapy
Low-molecular-weight heparin
advantages over heparin:
better bio-availability
higher ratio (3:1) of anti-Xa to anti-IIa
activity
longer anti-Xa activity, avoid rebound
induces less platelet activation
ease of use (subcutaneous - qd or bid)
no need for monitoring
PCI after thrombolytics???

planned PCI in attempt to achieve an
open infarct-related artery before
arrival of cath lab
*Adjunctive PCIPCI performed within
hours after thrombolysis
*Early elective PCIPCI performed within
a few days after thrombolysis
Coronary Artery
Bypass Graft
Cardiogenic
Shock
Definition
<90 mmHg
<2.2 li/min.m2
>15 mmHg
Schematic
LVEDP elevation
Hypotension
Decreased coronary
perfusion
Ischemia
Further myocardial
dysfunction
Neurohormonal
activation
Vasoconstriction
Endorgan hypoperfusion
QUESTIONS ???
THE END
Bine ca s-a terminat !!!
Myosplint
Change in radius
R1
R2
Infarct in ventricular wall with loss of

muscle and scarring
QUESTIONS ???
Treatment of heart
failure
1. Hypertrophy &
Dilatation
E.D.V
Positive
Inotropi
cs
2. Sympathetic activity:
H.R.
V.C
vasodilator
s
Angiotensine
Diuretic
s
Aldosterone
ACE
inhibito
rs
Pharmacological Treatment
Diuretics
(loop diuretics, thiazide diuretics

and potassium sparing diuretics)
These act by promoting the renal excretion
of salt and water by blocking tubular
reabsorption of sodium and chloride. The
resulting loss of fluid reduces ventricular
filling pressures (preload), produces
consistent haemodynamic and symptomatic
benefits and rapidly improves dyspnoea and
peripheral oedema.
In therapeutic dose leads to partial inhibition of Na+/K+

ATPase enzyme
ca++
+
Na
K+
Na + /ca + +
ATPase
exchange
Na+
Na+ Na+
+
Na
Na+ Na+
+
Na
intracellular Na
ca++
ca++ca
ca++ ca++
++
resulting in:
ca++ca++ca++
ca++
++ ++
++ ca
ca++ caca
sarcoplasmic reticulum
troponin
Actin Myosin
Force Of Contractility
Acute heart failure (AHF) occurs with

the rapid onset of symptoms and
signs of heart failure secondary to
abnormal cardiac function, causing
elevated cardiac filling pressures.
This causes severe dyspnoea and
fluid accumulates in the interstition
and alveolar spaces of the lung
(pulmonary oedema).
SHOCK is a severe failure of tissue perfusion,

characterized by hypotension, a low cardiac output and
signs of poor tissue perfusion such as oliguria, cold
extremities and poor cerebral function. Cardiogenic
shock is commonly due to myocardial infarction, acute
massive pulmonary embolus, pericardial tamponade &
sudden-onset valvular regurgitation.
TREEATMENT: Patients require intensive care
General measures such as complete rest, continuous
60% oxygen administration and pain and anxiety relief
are essential.
The infusion of fluid is necessary if the pulmonary
capillary wedge pressure is below 18 mmHg.
Short-acting venous dilators such as glyceryl trinitrate
or sodium nitroprusside should be administered
intravenously if the wedge pressure is 25 mmHg or
more.
Cardiac inotropes to increase aortic diastolic pressure.
Emergency revascularization of occluded arteries
Pathophysiology of chronic heart failure.
Ramani G V et al. Mayo Clin Proc. 2010;85:180-195
2010 Mayo Foundation for Medical Education and Research
Modified Dor Procedure

CHF
Prof Univ Dr Ion C.Tintoiu FESC

Centrul de Cardiologie al Armatei
Universitatea Titu Maiorescu
Cardiac Transplant
It has become more widely used since the

advances in immunosuppressive
treatment
Survival rate
1 year 80% - 90%
5 years 70%
Christian Barnard
inCapeTown.
Outpatient Therapy
210

CHF
Predictors of Mortality Based on
Analysis of ADHERE Database
Classification and Regression Tree (CART) analysis of

ADHERE data shows:
Three variables are the strongest predictors of mortality in
hospitalized ADHF patients:
BUN
BUN>>43
43mg/dL
mg/dL
Systolic
Systolic blood
bloodpressure
pressure<<115
115 mmHg
mmHg
Serum
Serumcreatinine
creatinine>>2.75
2.75mg/dL
mg/dL
Fonarow GC et al. JAMA 2005;293:572-80.
Continuous Heart Transplant Perfusion
Starlings Law
Future Tech
Inotropes in Cardiac
Surgery
Basics
BEFORE INOTROPES
Fluid
Rhythm
Drains, CXR, Hb
Pneumothorax
CVP, BE, UO, temp, CXR, echo
Bleeding
ECG, SR, slow, fast, paced on ventricle, STs, ectopics
Tamponade
Bolus
Legs up
CXR, examine, vent alarms
Fight Ventilator
Paralyse, sedate or extubate
Which Inotrope
Ohms Law
V=I x R
BP=CO x SVR
Simple terms
Low or high cardiac output, what is the PA
pressure
Receptors
Atropine
Antimuscurinic ie causes tachycardia

Some pateints have muscurinic
receptors on ventricle as well ie
inotropic
Increases HR
CO=SV x HR
Ca
Inotrope and
vasoconstrictor
Short acting
Beware radial artery

patients
Warn patient if
awake
2+
Dopamine
Acts on dopamine
receptors on heart and
kidney
Causes a tachycardia
(CO=SV x HR)
Increases urine output in
some patients
Less metabolic side effects
compared with adrenaline
Beware patients with

tachycardia (give k+, Mg2+)
Dopexamine
Tachycardia
Increase splanchnic and renal blood
flow
VASODILATOR
Beware
Vasodilated patients
Dobutamine
Like dopamine
Has less effect on
pulmonary artery
pressure good for
mitral valve
patients
Adrenaline
Excellent inotrope but dirty
Increased heart rate and

inotropy (1-adrenoceptor
mediated)
Vasoconstriction in most
systemic arteries and veins
(postjunctional a 1 and a 2
adrenoceptors)
Vasodilation in muscle and liver

vasculatures at low
concentrations (b2adrenoceptor); vasoconstriction
at high concentrations (a1adrenoceptor mediated)
Adrenaline
Noradrenaline
Vasoconstrictor
Increased heart rate and

increased inotropy (1adrenoceptor mediated)
Vasoconstriction occurs in
most systemic arteries and
veins (postjunctional a 1 and
a 2 adrenoceptors)
Ask can I wake patient up to

avoid Norad
Must have a good cardiac

output
Noradrenaline
Isoprenaline
Causes tachycardia
and vasodilatation
Good in patients
with high PA
pressures
Beware vasodilated
patients
Enoximone
Phosphodiesterase Inhibitor
Good in patients with high PA pressure
2nd line when adrenaline having no
effect receptor dissociation
Aminophylline
Phosphodiesterase
inhibitor
Main effect on lung
compared to heart
Good in patients
who have hypoxic
vasoconstriction
short fat little
smoker with poor
urine output
Vassopresin
2nd line
vasoconstrictor
Most powerful
available
Associated with
organ ischaemia
Nitric Oxide
Medication
Drug treatments should be initiated

in the following order:
ACE inhibitor - with diuretic if needed for NYHA Grades I-IV.
Angiotensin-II receptor antagonist - if
intolerant of ACE inhibitor.
Beta-blocker - for NYHA Grades I-IV.
Spironolactone - for NYHA Grades III-IV.
Digoxin - for NYHA Grades II-IV.

CHF Antiarrhythmics
Most common cause of SCD in these patients is
ventricular tachyarrhythmia
Patients with h/o sustained VT or SCD ICD implant
Patients with CHF with an ejection fraction of less than
30% may receive ICD implant
Amiodarone for patients with frequent VPCs and at fib
Dranedone for patients with recurrent paroxysmal at fib.

CHF
VasodilatorsHydralazine and Nitrates
Reduction of afterload by arteriolar
vasodilatation (hydralazin) reduce
LVEDP, O2 consumption,improve myocardial
perfusion, stroke volume and COP
Reduction of preload By venous

dilation
( Nitrate) the venous return the
load on both ventricles.
Usually the maximum benefit is achieved

by using agents with both action.

CHF Anticoagulation
Atrial fibrillation
H/o embolic episodes
Left ventricular apical thrombus
Low LV ejection fraction

CHF
Inotropic Agents
These are the drugs that improve
myocardial contractility ( adrenergic
agonists, dopaminergic agents,
phosphodiesterase inhibitors),
Dopamine
Dobutamine
Milrinone,
Aamrinone
Several studies showed mortality with oral inotropic
agents
So the only use for them now is in acute sittings such as
cardiogenic shock

CHF
New Treatment Choices
Implantable ventricular assist devices
Biventricular pacing (only in patient
with LBBB & CHF)

Artificial Heart
Device Therapy:
Biventricular
Pacing

241
BiV Pacing
Therapy

EF<30%

Ventricular remodelling
Excitation-contraction
coupling
Electrical dyssynchrony
Mechanical dyssynchrony
Dysrhythmias !
Defibrillators
(ICDs)

Hearts
Future Tech
Heart Failure: Therapy
Stage A:
Stage B:
ACE/ARB/BB if appropriate
Stage C:
Control risk factors, treat underlying chronic disease

contributors
ACE?ARB, BB, diuretics

Other vasodilators as appropriate
Devices (bi-V pacing, Implantable defibrillators
Stage D:
Mechanical assist devices

Continuous infusion of inotropics
Heart transplant
Hospice
Experimental surgery or drugs
Devices and Surgical

Management
First option if the cause of heart failure can be

treated surgically
Several therapeutic options: pacing, an ICD, a

ventricular assist device, an artificial heart, or a
heart transplant
Pacing or resynchronization therapy is

recommended for patients with NYHA Class III
or IV with QRS prolongation who are
experiencing symptoms despite medications
Devices and Surgical

Management
An ICD may be used in patients with arrhythmias

to prevent sudden cardiac death
A left ventricular assist device may be used as a

bridge to transplant or destination therapy
End-stage heart failure patients may consider

heart transplant
ECG 12 leads
Chest X-ray
Lab tests (hyponatraemia!)
Biomarkers of HF: BNP, proBNP, CRP,
troponins
Echocardiography (systolic/diastolic
dysfunction, structural heart disease)
spiroergometry

Physical examination
X-ray, ECG,
Echo, SpiroErgometry
Medical history
Lab tests: BNP,
ACE inhibitors

remodelling, myocardial fibrosis
Hypotension
Hyperlakaemia, renal dysfunction
Cough
Angio-oedema
Betablockers

remodelling, dyssynchrony
SCD , antiarrhythmic effect
Hypotension
Fatigue
Bradycardia, block
Reduce dose in case of decompensation
Aldosterone antagonists

NYHA III, EF<35%
Renal dysfunction
Hyperkalaemia
Diuretics
symptoms, oedema, prognosis

only in case of fluid retention
RAAS activationadd ACEi or ARB!
Titrate, combine
Hyonatraemia, hypokalemia, volume
depletion, renal dysfunction
Diuretic resistance
Patients with acute heart failure

frequently develop chronic heart failure.
Patients with chronic heart failure
frequently decompensate acutely.
HEART FAILURE
MultiDisciplinary
Heart Failure
Management
260
Systolic:
Impaired ability of the heart to contract

Weakened muscle, enlarged heart size
Inability of heart to empty
Left ventricular ejection fraction (LVEF) < 4045%
Diastolic:
inability of the heart to relax is impaired

Stiff, thickened myocardial wall but normal size
Inability of heart to fill
LVEF 45%
261
Acute
Chronic
sudden onset with associated signs and

symptoms
secondary to slow structural changes
occurring in the stressed myocardium
Acute Decompensated
sudden exacerbation or onset of

symptoms in chronic heart failure
262
Heart Failure is a Symptomatic Disorder
New York Heart Association-Functional
Classification
Class I: No abnormal symptoms with activity
Class II: Symptoms with normal activity
Class III: Marked limitation due to symptoms
with less than ordinary activity
Class IV: Symptoms at rest and severe
limitations in functional activity
263
Heart Failure is a Progressive Disorder
ACC/AHA Stages of HF
Stage A--Presence of risk factors for heart failure
Stage B--Presence of structural heart disease but
no Symptoms
Stage C--Presence of structural heart disease
along with signs and symptoms
Stage D--Presence of structural heart diseases
and advanced signs and symptoms
264
ACC/AHA 2005
Guidelines
265
Cardiac Rhythm Management

Small improvements in
hemodynamics =significant
improvements in HF symptoms
symptoms.
Optimizing hemodynamics has
long been a target of
therapy in HF.
266
Cardiac Rhythm Management

Risk Reduction
CRT
Diagnostics
HR Trends
HR Variability
Patient Activity
Intrathoracic Impedance
Arrhythmias
Remote Monitoring
267
LV Reconstruction by Patch Plasty

Jatene, Dor, Fontan
Bockeria et al. Eur J Cardio-thorac Surg

2006;29:S251-8S.
Left Ventricular Assist Device
Types of Heart Failure
Systolic (or squeezing) heart failure
Decreased pumping function of the heart, which

results in fluid back up in the lungs and heart
failure
Diastolic (or relaxation) heart failure
Involves a thickened and stiff heart muscle

As a result, the heart does not fill with blood
properly
This results in fluid backup in the lungs and heart
failure
Risk Factors for Heart

Failure
Coronary
artery
disease
Hypertension (LVH)
Valvular heart
disease
Alcoholism
Infection (viral)
Diabetes
Congenital
heart defects
Other:
CAD=coronary artery disease; LVH=left ventricular hypertrophy.
Obesity
Age
Smoking
High or low hematocrit

level
Obstructive Sleep Apnea
Classifying Heart
Failure:
Terminology and
Staging
A Key Indicator for Diagnosing

Heart Failure
Ejection Fraction (EF)
Ejection Fraction (EF) is the percentage
of blood that is pumped out of your heart
during each beat
Classification of HF:
Comparison Between
ACC/AHA HF Stage and
NYHA
Class
ACC/AHA HFFunctional
Stage
NYHA Functional
Class
1
None
A At high risk for heart failure but without

structural heart disease or symptoms
of heart failure (eg, patients with
hypertension or coronary artery disease)
B Structural heart disease but without
symptoms of heart failure
C Structural heart disease with prior or

current symptoms of heart failure
D Refractory heart failure requiring

specialized interventions
Asymptomatic
II Symptomatic with moderate exertion

III Symptomatic with minimal exertion
IV Symptomatic at rest
Hunt SA et al. J Am Coll Cardiol. 2001;38:21012113.
New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890897.
How Heart Failure Is

Diagnosed
Medical history is taken to reveal symptoms

Physical exam is done
Tests
Chest X-ray
Blood tests
Electrical tracing of heart (Electrocardiogram or
ECG)
Ultrasound of heart (Echocardiogram or Echo)
X-ray of the inside of blood vessels (Angiogram)
Pathophysiology
Pathologic Progression of CV
Disease
Sudden
Death
Coronary artery
disease
Hypertension
Diabetes
Myocardial
injury
Pathologic
remodeling
Low ejection
fraction
Cardiomyopathy
Death
Pump
failure
Valvular disease
Neurohormonal
stimulation
Myocardial
toxicity
Adapted from Cohn JN. N Engl J Med. 1996;335:490498.
Symptoms:
Dyspnea
Fatigue
Edema
Chronic
heart
failure
Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone
System
Beta
Stimulation
CO
Na+
Renin + Angiotensinogen
Angiotensin I
ACE
Angiotensin II
Peripheral
Vasoconstriction
Kaliuresis
Aldosterone Secretion
Salt & Water Retention
Plasma Volume
Afterload
Cardiac Output
Heart Failure
Fibrosis
Preload
Cardiac Workload
Edema
Drug Therapy
Heart Failure
Treatments: Medication
Types What it
Type
ACE inhibitor
(angiotensin-converting
enzyme)
does
Expands blood vessels which
lowers blood pressure,
neurohormonal blockade
ARB (angiotensin
receptor blockers)
Similar to ACE inhibitor

lowers blood pressure
Betablocker
Reduces the action of stress

hormones and slows the heart
rate
Slows the heart rate and improves
the hearts pumping function (EF)
Digoxi
n
Diuretic
Aldosterone
blockade
Filters sodium and excess fluid from

the blood to reduce the hearts
workload
Blocks neurohormal activation and
Rational for Medications

(Why does my doctor have
me on so many pills??)
Improve Symptoms
Diuretics (water
pills)
digoxin
Improve Survival
Betablockers
ACE-inhibitors
Aldosterone
blockers
Angiotensin
receptor blockers
(ARBs)
Lifestyle Changes
What
Why
Eat a low-sodium, lowfat diet
Sodium is bad for high blood

pressure, causes fluid retention
Lose weight
Extra weight can put a

strain on the heart
Stay physically active
Exercise can help reduce

stress and blood pressure
Reduce or eliminate
alcohol and caffeine
Alcohol and caffeine can weaken

an already damaged heart
Quit Smoking
Smoking can damage blood vessels

and make the heart beat faster
Oral Medications to
Counteract..
RAAS Inhibitors:
SNS Inhibitors:
ACE I/ARBs
Aldosterone Antagonists
Beta Blockers
Beta Blockers
Vasodilator/Nitric Oxide Agonists:
Isorbide dinitrate/hydralzine
283
ACE Inhibitors
Inhibit the enzyme responsible for

converting Angiotensin I to Angiotensin
II; counteracts RAAS
Decrease Systemic Vascular Resistance
(SVR)
Enhance activity of kinins and kininmediated prostaglandin synthesis
Modify cardiac remodeling
Reduce BP; how low is too low?
284
Beta Blockers: Up to 35%

RR
Counteract activation of RAAS and SNS

SNS activation promotes catecholamine
toxicity on cardiomyocytes, increases LV
afterload and wall stress, promotes
myocardial ischemia and oxidative stress
Negative inotrope & Negative chronotrope
Rate control with arrhythmias
Controls HR and BP
285
Beta Blockers: 3
Indicated
Metoprolol XL ( beta 1 selective): MERIT HF

Carvedilol (beta 1, beta 2, alpha blockade)
COPERNICUS, COMET
Bisoprolol
(CIBIS II) ONLY
A Beta blocker is not a beta blocker is not.
Given to all post MI and/or with LV
dysfunction
Superiority with non-selective beta blockers
with some alpha blockade?
Comet trial
286
How to give Beta

Blockers
Start low; go slowunless switching

Patient should be euvolemic prior to
starting; neg. inotropic action, increased
preload can exacerbate fluid overload.
Titrate q 2 weeks; can go by dose
Titrate to highest tolerated dose/study dose;
HR in 60s signifies adequate b1 blockade
Few contraindications: high degree blocks,
true bronchospastic Asthmatic disease
Few side effects; can feel worse at first
287
The Adverse Impact of

Aldosterone
Myocardial
Myocardial
fibrosis
fibrosis
Prothrombotic
Prothrombotic
effects
effects
Adverse
Adverse effects
effects
of
of aldosterone
aldosterone
Endothelial
Endothelial
dysfunction
dysfunction
Adapted from McMahon. Curr Opin Pharmacol. 2001;1:190-196.

Korantzopoulos et al. Med Sci Monit. 2003;9:RA140-RA145.
Oxidative
Oxidative
stress
stress
Vascular
Vascular
inflammation
inflammation
288
Aldosterone
Antagonists
Aldosterone release influenced by Angiotension II

Promotes salt and water retention, K+ and Mg loss;
sympathetic stimulation and parasympathetic
inhibition, baroreceptor dysfunction, vascular
damage and impaired arterial compliance.
RALES: (Spironolactone): 30% risk reduction in
mortality and 35% reduction in HF admissions as
compared with placebo; Real world?? Few on Beta
Blockers
EPHESUS:Eplerenone (Inspra): post MI; 15% risk

reduction ON current therapy HF meds; more
specific; less S.E. (gynecomastia)
Must carefully monitor K+ levels

289
Nitric Oxide
Isosorbide dinitrate/hydralazine
(BiDil)
Regulates CV processes including
myocardial hypertrophy,
remodeling, substrate use, vascular
function, inflammation, and
thrombosis
290
Isosorbide
Dinitrate/Hydralazine
A-HeFT 1: Protective role of nitric oxide

Additional 43% reduction in mortality when added
to current standard therapy : (African Americans)
Decreased 1st hospitalization for HF by 33%
Improved QOL scores
How it works: Vasodilator: Balance of arterio and
venodilation
Hydralazine prevents degredation of n.o. and prolongs
vasodilatory effects of isosorbide
Should be given to AA with HF
A reasonable alternative for any patient who cannot
take ACE/ARBs
$$$$$$$$$
291
Symptom Relief
Digoxin:
Very mild positive inotrope, some

sympathoinhibitory neurohormonal
modulating effects.
No mortality data; data on decreased
hospitalizations
Rarely used for HF in Europe
Helpful for rate control with A-fib
Use 3rd line for symptom relief
Very Low dose
292
Diuretics: Fluid & Na+

Retention
No known impact on mortality

Useful and necessary adjunct to therapy for
congestive HF symptoms due to sodium
and water retention.
Do not maintain clinical stability as
monotherapy
Refractoriness & Renal Dysfunction
Inotropes: Still given in OP setting; for low
c.o. states; for sx relief; end stage HF only
293
MI?
PVCs, Nonsustained VT May
Not Help
Anderson KP, et al. J Am Coll Cardiol. 1995;26:489-496.
2 major types of VT
Type 1: Premature
ventricular
contraction (PVC)
initiates (6.6%)
Type 2: No PVC
(91.8%)
Cannot predict which

patients get Type 1 vs
Type 2
294
HFSA 2010
Comprehensive
Heart Failure
Practice
Guideline
Key
Recommendations
HFSA 2010 Practice Guideline (7.19)
Pharmacologic Therapy:
Hydralazine and Oral
Nitrates
A combination of hydralazine and

isosorbide dinitrate is
recommended as part of standard
therapy, in addition to betablockers and ACE-inhibitors, for
African Americans with HF and
reduced LVEF:
NYHA III or IV HF Strength of Evidence = A
NYHA II HF
Strength of Evidence = B
Diuretics
Diuretic therapy is recommended to

restore and maintain normal volume
status in patients with clinical evidence
of fluid overload, generally manifested
by:
Congestive symptoms
Signs of elevated filling pressures
Strength of Evidence = A
Loop diuretics rather than thiazidetype diuretics are typically necessary to

restore normal volume status in
patients with HF.
Strength of
Evidence = B
Loop Diuretics
Agent
Initial
Daily Dose
Furosemid
e
20-40mg
qd or bid
e
qd or bid
Max Total
Daily Dose
600 mg
10 mg
Eliminatio
n: Renal
Met.
Duration
of Action
65%R35%M
4-6 hrs
62%R/38%
M
6-8 hrs
Torsemide
10-20 mg
qd
200 mg
20%R80%M
12-16 hrs
Ethacrynic
acid
25-50 mg
qd or bid
200 mg
67%R33%M
6 hrs
298
Potassium-Sparing
Diuretics
Agent
Initial
Daily
Dose
Spironolacton 12.5-25
e
mg qd
Eplerenone
25-50 mg
qd
Amiloride
5 mg qd
Triamterene
50-75 mg
bid
Max Total Eliminatio

Daily
n
Dose
Duratio
n of
Action
50 mg
Metabolic
48-72
hrs
100 mg
Renal,
Metabolic
Unknow
n
Renal
24 hrs
Metabolic
7-9 hrs
20 mg
200 mg
299
Device Therapy:
Prophylactic ICD
Placement
Prophylactic
ICD placement should be

considered in patients with an LVEF 35% and
mild to moderate HF symptoms:
Ischemic etiology
Non-ischemic etiology
In
patients who are undergoing implantation of a

biventricular pacing device, use of a device that
provides defibrillation should be considered.
Decisions
should be made in light of functional

status and prognosis based on severity of
underlying HF and comorbid conditions, ideally
after 3-6 mos. of optimal medical therapy.
Strength of Evidence = C
Adapted from:
HFSA 2010 Practice Guideline (11.111.2)
HF with Preserved LVEF

Diagnosis
Careful attention to differential diagnosis is

recommended in patients with HF and
preserved LVEF.
Treatments may differ based on cardiac
disorder.
Evaluation for ischemic disease and inducible
myocardial ischemia should be included.
Recommended diagnostic tools:
Echocardiography
Electrocardiography
Stress imaging (via exercise or pharmacologic
means, using myocardial perfusion or
echocardiographic imaging)
Cardiac catheterization
Adapted from:
Diagnostic Algorithm
for HF with Preserved LVEF
HF with
Preserved LVEF
Dilated LV
Valvular disease
AR, MR
Non-dilated LV
No valvular dis.
High output HF
Increased
thickness
Normal or
increased QRS
Hypertrophic dis.
No aortic
valve disease
No hypertensive
history of PE
HCM, Fabry dis.
Low QRS voltage

Infiltrative
myopathy
Aortic valve dis.

Aortic stenosis
Hypertensive
history of PE
Hypertensive-HCM
Normal
Thickness
Right vent.
dysfunction
No mitral
obstruction
Pulmonary
hypertension
Pericardial dis.
Tamponade
Constriction
Isolated predominant RVMI
No pericardial
disease
No inducible ischemia, fibrotic, collagenInducible
ischemia
Vascular,
RCM, cardinoid,
diabetes,
Radiation
or chemotherapy induced
Intermittent/active
heart disease, infiltrative disease, coischemia
morbid conditions, reconsider diagnosis
of HF
Some patients with RV

dysfunction have LV
dysfunction due to
ventricular interaction.
Mitral obstruction
MS, atrial myxoma
HFSA 2010 Practice Guideline (12.3, Table 12.3)
Acute Decompensated Heart

Failure (ADHF)Treatment Goals
for Hospitalized Patients
Improve symptoms, especially congestion and lowoutput symptoms

Optimize volume status
Identify etiology
Identify precipitating factors
Optimize chronic oral therapy; minimize side effects
Identify who might benefit from revascularization
Education patients concerning medication and HF selfassessment
Consider enrollment in a disease management
program
HFSA 2010 Practice Guideline (12.5-12.20)
Overview of Treatment Options for

Patients with Acute
Decompensated HF
Fluid
and sodium restriction

Diuretics, especially loop diuretics
Ultrafiltration/renal replacement therapy
(in selected patients only)
Parenteral vasodilators *
(nitroglycerin, nitroprusside, nesiritide)
Inotropes * (milrinone or dobutamine)
*See recommendations for stipulations and restrictions.
Device Therapy:
Biventricular
Pacing
Implantable Cardiac
Defribrillators
EBM Therapies
Relative Risk
Reduction
Mortality
2 year
ACE-I
23%
27%
-Blockers
35%
12%
Aldosterone
Antagonists
30%
19%
ICD
31%
8.5%

307
BiV Pacing
Therapy

EF<30%

Defibrillators
(ICDs)
Heart Failure and Sudden

Cardiac Death
Sudden Cardiac Death (SCD)
Your heart suddenly goes into a very fast and chaotic

rhythm and stops pumping blood
Caused by an electrical problem in your heart
SCD is one of the leading causes of death in the U.S.

approximately 450,000 deaths a year
Patients with heart failure are 6-9 times as likely to

develop sudden cardiac death as the general
population
How does a defibrillator

for sudden cardiac death
work?
Device
Shown:
Combination
Pacemaker
&
Defibrillator
Who should Consider an

ICD? heart, New York
Patients with weakend
Heart Association (NYHA) Class II and
III heart failure, and measured left
ventricular ejection fraction (LVEF) <
35%
Patients who meet all current

requirements for a cardiac
resynchronization therapy (CRT) device
and have NYHA Class IV heart failure;
Other Therapies?
Transplant
Artificial hearts
New gadgets to help doctors
manage heart failure
Heart Transplantation
A good solution to the failing heart

get a new heart
Unfortunately we are limited by
supply, not demand
Approximately 2200 transplants are
performed yearly in the US, and this
number has been stable for the past
20 years.

Hearts
Future Tech
Intrathoracic Impedance
for Heart Failure
What have we
learned?
In Summary.
Heart failure is common and has high

mortality
Drug therapy improves survival
Newer device therapies are showing promise

for symptom relief and improved survival
Betablockers, ACE-I, aldosterone antagonists
Biventricular pacing, ICDs
Transplants remain rare, but technology for

mechanical assist devices continues to
improve- stay tuned!
Heart Failure:
Current
Guidelines in
Therapy
323
SBAR:
Navy Nuclear Submarine

Communications Model
Situation: Whats going on with the

patient
Background: Pertinent clinical

background
Assessment: What I think

Recommendation: What is needed &
time frame
324
Chronic Heart Failure:

Medications Rationale
Evidence-Based
Symptomatic Relief
325
Evidence-Based Medications
Counteract HF Compensatory
Mechanisms
Goals:
Prevent Remodeling and Progressive

Worsening of LV function
Decrease morbidity and mortality
326
Oral Medications to
Counteract..
RAAS Inhibitors:
SNS Inhibitors:
ACE I/ARBs
Beta Blockers
Beta Blockers
Vasodilator/Nitric Oxide Agonists:
Isorbide dinitrate/hydralzine
327
ACE Inhibitors
Inhibit the enzyme responsible for

converting Angiotensin I to Angiotensin
II; counteracts RAAS
Decrease Systemic Vascular Resistance
(SVR)
Enhance activity of kinins and kininmediated prostaglandin synthesis
Modify cardiac remodeling
Reduce BP; how low is too low?
328
Beta Blockers: Up to 35%

RR
Counteract activation of RAAS and SNS

SNS activation promotes catecholamine
toxicity on cardiomyocytes, increases LV
afterload and wall stress, promotes
myocardial ischemia and oxidative stress
Negative inotrope & Negative chronotrope
Rate control with arrhythmias
Controls HR and BP
329
Beta Blockers: 3
Indicated
Metoprolol XL ( beta 1 selective): MERIT HF

Carvedilol (beta 1, beta 2, alpha blockade)
COPERNICUS, COMET
Bisoprolol
(CIBIS II) ONLY
A Beta blocker is not a beta blocker is not.
Given to all post MI and/or with LV
dysfunction
Superiority with non-selective beta blockers
with some alpha blockade?
Comet trial
330
How to give Beta

Blockers
Start low; go slowunless switching

Patient should be euvolemic prior to
starting; neg. inotropic action, increased
preload can exacerbate fluid overload.
Titrate q 2 weeks; can go by dose
Titrate to highest tolerated dose/study dose;
HR in 60s signifies adequate b1 blockade
Few contraindications: high degree blocks,
true bronchospastic Asthmatic disease
Few side effects; can feel worse at first
331
The Adverse Impact of

Aldosterone
Myocardial
Myocardial
fibrosis
fibrosis
Prothrombotic
Prothrombotic
effects
effects
Adverse
Adverse effects
effects
of
of aldosterone
aldosterone
Endothelial
Endothelial
dysfunction
dysfunction
Adapted from McMahon. Curr Opin Pharmacol. 2001;1:190-196.

Korantzopoulos et al. Med Sci Monit. 2003;9:RA140-RA145.
Oxidative
Oxidative
stress
stress
Vascular
Vascular
inflammation
inflammation
332
Aldosterone
Antagonists
Aldosterone release influenced by Angiotension II

Promotes salt and water retention, K+ and Mg loss;
sympathetic stimulation and parasympathetic
inhibition, baroreceptor dysfunction, vascular
damage and impaired arterial compliance.
RALES: (Spironolactone): 30% risk reduction in
mortality and 35% reduction in HF admissions as
compared with placebo; Real world?? Few on Beta
Blockers
EPHESUS:Eplerenone (Inspra): post MI; 15% risk

reduction ON current therapy HF meds; more
specific; less S.E. (gynecomastia)
Must carefully monitor K+ levels

333
Nitric Oxide
Isosorbide dinitrate/hydralazine
(BiDil)
Regulates CV processes including
myocardial hypertrophy,
remodeling, substrate use, vascular
function, inflammation, and
thrombosis
334
Isosorbide
Dinitrate/Hydralazine
A-HeFT 1: Protective role of nitric oxide

Additional 43% reduction in mortality when added
to current standard therapy : (African Americans)
Decreased 1st hospitalization for HF by 33%
Improved QOL scores
How it works: Vasodilator: Balance of arterio and
venodilation
Hydralazine prevents degredation of n.o. and prolongs
vasodilatory effects of isosorbide
Should be given to AA with HF
A reasonable alternative for any patient who cannot
take ACE/ARBs
$$$$$$$$$
335
Symptom Relief
Digoxin:
Very mild positive inotrope, some

sympathoinhibitory neurohormonal
modulating effects.
No mortality data; data on decreased
hospitalizations
Rarely used for HF in Europe
Helpful for rate control with A-fib
Use 3rd line for symptom relief
Very Low dose
336
Diuretics: Fluid & Na+

Retention
No known impact on mortality

Useful and necessary adjunct to therapy for
congestive HF symptoms due to sodium
and water retention.
Do not maintain clinical stability as
monotherapy
Refractoriness & Renal Dysfunction
Inotropes: Still given in OP setting; for low
c.o. states; for sx relief; end stage HF only
337
MI?
PVCs, Nonsustained VT May
Not Help
Anderson KP, et al. J Am Coll Cardiol. 1995;26:489-496.
2 major types of VT
Type 1: Premature
ventricular
contraction (PVC)
initiates (6.6%)
Type 2: No PVC
(91.8%)
Cannot predict which

patients get Type 1 vs
Type 2
338
What is ICD Therapy?

Implantable Cardiac Defibrillator
(ICD) Therapy consists of pacing,
cardioversion, and defibrillation
therapies to treat brady and tachy
arrhythmias.
An external programmer is used to
monitor and access the device
parameters and therapies for each
patient.
339
Cardiac
Resynchronization
Therapy
Standard right atrial pace/sense lead

implanted to establish AV synchrony
Standard right ventricular
pace/sense/defibrillation lead and left
ventricular lead implanted to restore
ventricular synchrony with biventricular
pacing
Atrial lead
Right ventricular
lead
Left ventricular
lead
340
ACC/AHA 2005 Guidelines

for
CRT Therapy
Class I recommendation
Moderate to severe HF (NYHA Class III,

or ambulatory Class IV)
LVEF 35%
QRS duration >120 ms
For symptomatic patients despite optimal
medical therapy
Group at high risk of SCD from ventricular arrhythmia
Hunt SA, et al. J Am Coll Cardiol. 2005;46:e1-e82.
341
Stages
Recommended
Treatments
Stage
Treatment
High risk for developing

heart failure (HF)
No structural heart
disease or HF symptoms
Structural heart disease

with no signs or
symptoms of HF
Optimize drug therapy

ICD if LVEF 35% and 40 days postMI (Class IIa)
Structural heart disease

with prior or current
symptoms of HF

ICD (if LVEF 35%, 40 days post-MI;
reduced LVEF and Hx of SCA, VF or VT)
CRT (if QRS >120 msec, LVEF 35%)
Refractory end-stage HF
Therapeutic lifestyle changes

Aspirin, ACE inhibitors, statins, blockers, -blockers (carvedilol),
diabetic therapy

ICD (bridge to transplantation)
CRT
Other devices (LVAD, pericardial
restraint; Class IIa)
Hunt SA, et al. J Am Coll Cardiol. 2005;46:e1-e82.
342
Latest ACC/AHA
Treatment Guidelines
Take Home Summary:
Ace Inhibitors & Beta Blockers for all Systolic

HF (unless contraindicated) The writing
committee suggests that the benefits of beta
blockade are not a class effect and drugs
evaluated in clinical trials should be utilized.
New data supporting the use of Ace Receptor
Blockers in the management of systolic heart
failure.
The guidelines support the use of ICD in
patients with LVEF 0.35 regardless of etiology.
343
Take Home continued
Bi-ventricular pacers should be used in

patients with an EF 0.35, class III-IV
symptoms and a QRS > 120 mSec.
Aldosterone antagonists should be started
in patients with moderate-severe symptoms
and reduced LVEF as long as the patient
can be monitored for hyperkalemia.
Hydralazine and nitrates can be added on
to standard medical therapy in AfricanAmericans or others with residual
symptoms or used in patients with
intolerance to ACE-I or ARBs.
344
Back to the Case

Study..
What NYHA Class of HF?

What ACC / AHA Stage??
345
Prevention
Symptomatic HF - The Tip of
The Iceberg
Post-MI
Remodeling
Diastolic
Dysfunction
Asymptomatic
Left Ventricular
Dysfunction
Left Ventricular
Hypertrophy
Hypertension
Myocardial Ischemia
Diabetes
Dyslipidemia
Coronary Artery Disease
Other CVD Risk Factors
346
HFSA 2010
Comprehensive
Heart Failure
Practice
Guideline
Key
Recommendations
Hydralazine and Oral
Nitrates
A combination of hydralazine and

isosorbide dinitrate is
recommended as part of standard
therapy, in addition to betablockers and ACE-inhibitors, for
African Americans with HF and
reduced LVEF:
NYHA III or IV HF Strength of Evidence = A
NYHA II HF
Diuretics
Diuretic therapy is recommended to

restore and maintain normal volume
status in patients with clinical evidence
of fluid overload, generally manifested
by:
Congestive symptoms
Signs of elevated filling pressures
Loop diuretics rather than thiazidetype diuretics are typically necessary to

restore normal volume status in
patients with HF.
Strength of
Evidence = B
Loop Diuretics
Agent
Initial
Daily Dose
Furosemid
e
20-40mg
qd or bid
e
qd or bid
Max Total
Daily Dose
600 mg
10 mg
Eliminatio
n: Renal
Met.
Duration
of Action
65%R35%M
4-6 hrs
62%R/38%
M
6-8 hrs
Torsemide
10-20 mg
qd
200 mg
20%R80%M
12-16 hrs
Ethacrynic
acid
25-50 mg
qd or bid
200 mg
67%R33%M
6 hrs
350
Potassium-Sparing
Diuretics
Agent
Initial
Daily
Dose
Spironolacton 12.5-25
e
mg qd
Eplerenone
25-50 mg
qd
Amiloride
5 mg qd
Triamterene
50-75 mg
bid
Max Total Eliminatio

Daily
n
Dose
Duratio
n of
Action
50 mg
Metabolic
48-72
hrs
100 mg
Renal,
Metabolic
Unknow
n
Renal
24 hrs
Metabolic
7-9 hrs
20 mg
200 mg
351
Device Therapy:
Prophylactic ICD
Placement
Prophylactic
ICD placement should be

considered in patients with an LVEF 35% and
mild to moderate HF symptoms:
Ischemic etiology
Non-ischemic etiology
In
patients who are undergoing implantation of a

biventricular pacing device, use of a device that
provides defibrillation should be considered.
Decisions
should be made in light of functional

status and prognosis based on severity of
underlying HF and comorbid conditions, ideally
after 3-6 mos. of optimal medical therapy.
Adapted from:
Device Therapy:
Biventricular pacing therapy is

recommended for patients with all of the
following:
Sinus rhythm
A widened QRS interval (120 ms)
Severe LV systolic dysfunction (LVEF <
35%)
Persistent, moderate-to-severe HF
(NYHA III) despite optimal medical
therapy.
HFSA 2010 Practice Guideline (11.111.2)
HF with Preserved LVEF

Diagnosis

recommended in patients with HF and
preserved LVEF.
Treatments may differ based on cardiac
disorder.
Evaluation for ischemic disease and inducible
myocardial ischemia should be included.
Recommended diagnostic tools:
Echocardiography
Electrocardiography
Stress imaging (via exercise or pharmacologic
means, using myocardial perfusion or
echocardiographic imaging)
Cardiac catheterization
Adapted from:
Diagnostic Algorithm
for HF with Preserved LVEF
HF with
Preserved LVEF
Dilated LV
Valvular disease
AR, MR
Non-dilated LV
No valvular dis.
High output HF
Increased
thickness
Normal or
increased QRS
Hypertrophic dis.
No aortic
valve disease
No hypertensive
history of PE
HCM, Fabry dis.
Low QRS voltage

Infiltrative
myopathy
Aortic valve dis.

Aortic stenosis
Hypertensive
history of PE
Hypertensive-HCM
Normal
Thickness
Right vent.
dysfunction
No mitral
obstruction
Pulmonary
hypertension
Pericardial dis.
Tamponade
Constriction
Isolated predominant RVMI
No pericardial
disease
No inducible ischemia, fibrotic, collagenInducible
ischemia
Vascular,
RCM, cardinoid,
diabetes,
Radiation
or chemotherapy induced
Intermittent/active
heart disease, infiltrative disease, coischemia
morbid conditions, reconsider diagnosis
of HF
Some patients with RV

dysfunction have LV
dysfunction due to
ventricular interaction.
Mitral obstruction
MS, atrial myxoma
HFSA 2010 Practice Guideline (12.3, Table 12.3)
Acute Decompensated Heart

Failure (ADHF)Treatment Goals
for Hospitalized Patients
Improve symptoms, especially congestion and lowoutput symptoms

Identify etiology
Identify precipitating factors
Optimize chronic oral therapy; minimize side effects
Identify who might benefit from revascularization
Education patients concerning medication and HF selfassessment
Consider enrollment in a disease management
program
HFSA 2010 Practice Guideline (12.5-12.20)
Overview of Treatment Options for

Patients with Acute
Decompensated HF
Fluid
and sodium restriction

Diuretics, especially loop diuretics
Ultrafiltration/renal replacement therapy
(in selected patients only)
Parenteral vasodilators *
(nitroglycerin, nitroprusside, nesiritide)
Inotropes * (milrinone or dobutamine)
*See recommendations for stipulations and restrictions.
Predictors of Mortality
Based on Analysis of
ADHERE Database
Classification and Regression Tree (CART)

analysis of ADHERE data shows:
Three variables are the strongest predictors of
mortality in hospitalized ADHF patients:
BUN
BUN>>43
43 mg/dL
mg/dL
Systolic
Systolicblood
blood pressure
pressure<<115
115 mmHg
mmHg
Serum
Serumcreatinine
creatinine>>2.75
2.75mg/dL
mg/dL
Fonarow GC et al. JAMA 2005;293:572-80
Evidence-Based Treatment
Across the Continuum of
Systolic LVD and HF
Control Volume
Diuretics
Renal Replacement
Therapy*
Improve Clinical Outcomes

Aldosterone
ACEI
-Blocker Antagonist
or ARB
or ARB
CRT
an ICD*
HDZN/ISDN*
*In selected patients
Treat Residual Symptoms

Digoxin
Heart Failure
Management
Applying the
ACC/AHA Chronic
Heart Failure
Guidelines
The Core
Basic management
Refractory HF
Stage C
Stage D
Beta blockers
Transplantation
ACE inhibitors
Subgroups
ARB
HF with normal LVEF
Aldosterone blocker
Diuretics
Digoxin
Hydralazine/Nitrate
Devices
Inotropic agents
The Core
Congestive Heart
Failure
Objectives
Definition and Epidemiology

Pathophysiology
Diagnosis and Classification
Treatment of Systolic Dysfunction
Medical Therapy
Device Therapy
What is CHF?
Definition
Abnormality of cardiac function that leads
to the inability of the heart to pump blood
to meet the bodys basic metabolic
demands or when it can do so only with
an elevated filling pressure
Epidemiology
Prevalence
Cost
Effects 1-2% of patient from 50-59-years-old and 10% of patient over

the age of 75
Frequency
Annual direct cost in >10 billion dollars
Incidence increased with age
Affects nearly 5 million Americans currently, >500,000 new cases

diagnosed each year
It is the most common inpatient diagnosis in the US for patients over

65 years of age
Visits to their family practitioner on average 2-3 times per year
Gender
Men> women in those between 40 and 75 years of age

The sexes are equal over 75 years of age
Pathophysiology of Heart
Failure
Hemodynamic Model
Neurohumoral Adaptations
double-edged swords
Renin-Angiotensin-Aldosterone System
Sympathetic Nervous System
Antidiuretic Hormone
Atrial and B-type Natriuretic Peptides
Endothelin
Help initially
Vasoconstriction
Redistributes blood to vital organs
Restoration of Cardiac Output

Increased myocardial contractility and
heart rate
Expansion of the extracellular fluid
volume
Neurohumoral-RAAS
Hurt long-term
Precipitating Causes
Common
CAD (70%)
Systemic
Hypertension
Idiopathic
Less Common
Diabetes Mellitus
Valvular Disease
Rare
Anemia
Connective Tissue Disease
Viral Myocarditis
Hemochromatosis
HIV
Hyper/Hypothyroidism
Hypertrophic
Cardiomyopathy
Infiltrative Disease including
amyloidosis and sarcoidosis
Mediastinal radiation
Peripartum cardiomyopathy
Restrictive pericardial
disease
Tachyarrhythmias
Toxins
Trypanosomiasis (Chagas
disease)
Systolic vs. Diastolic
Systolic dysfunction
EF normal or increased
Hypertension
Due to chronic replacement
fibrosis & ischemia-induced
decrease in distensibility
EF < 40%
Usually from coronary disease
Due to ischemia-induced decrease
in contractility
Most common is a combination of

both
Subtypes of Systolic
Heart Failure
High output
Severe anemia
AV malformations
hyperthyroidism
Low cardiac
output
Right Heart Failure
Left Heart Failure
Peripheral edema
Pulmonary
congestion
Biventricular
Failure
Systemic and
pulmonary
congestion
Evaluation
History: risk factors for ischemic

heart disease, family history
Physical exam: S3, JVD more specific
signs of HF than rales, peripheral
edema
Exam
Major Criteria
Paroxysmal
nocturnal dyspnea
Neck Vein Distention
Rales
Cardiomegaly
Pulmonary Edema
S3 Gallop
Hepatojugular
Reflex
Minor Criteria
Ankle edema
Nocturnal Cough
Dyspnea on
ordinary exertion
Hepatomegaly
Pleural Effusion
Tachycardia
>120bpm
Confirming the Presence

of Heart Failure
CXR-cardiomegaly and pulmonary
edema; Kerleys B Lines
Laboratory Values
BNP
Maybe inc by age, female gender, CRI,

pulm disease, hyperthyroid, obesity,
steroid use
Electrocardiogram/ECHO
Anterior Q waves, LBBB, LVH
Negative Prognostic
Factors
Clinical
Laboratory
Hyponatremia, Elevated neurohormones
Hemodynamic
Increased Age, Diabetes, Smoking
Reduced EF, Increased Pulm Cap Wedge

Pressure
Electrophysiological
A-fib, A-flutter, Ventricular ectopy, V-tach
Classification of Heart Failure: ACC/AHA Stage vs NYHA Class
Principles of Treatment
Systolic HF
Preload
Afterload
Ionotropy
Neurohumoral
activity
ACE-I, Betablockers, and

aldosterone
antagonist are the
mainstay of
treatment
Treatment of Systolic
Heart Failure
ACE InhibitorsWorks to inhibit the over stimulation of the

RAS that leads to myocardial hypertrophy and
fibrosis
Causes balanced vasodilation
Decrease the rate of morbidity & mortality in
all pts with systolic heart failure
-If treating acute HF, can start after BP tolerates
and pulmonary edema is relieved
ACE-I
CONSENSUSEnalapril 2.5-40mg
(188 days) vs placebo
Pts were already
taking digoxin and
diuretics
253 Patient with
NYHA Class IV
Dec mortality at:
6 months -40%
1 Year 27%
SOLVD-Enalapril
20mg/day (41 mo)
2569 Patients with
and EF <35%
Earlier stages of HF
even asymptomatic
NYHA Class II-III
All cause mortality

dec by 16%
Morality rate from
HF dec by 16%
Angiotensin-Receptor
Blockers
Comparable to ACE inhibitors
Reduce all-cause mortality
Suitable alternative for patient with
adverse events (angioedema, cough,
hyperkalemia) occur with ace-i
Beta-Blockers
34% reduction in all mortality

with use of beta-blockers
Decrease Cardiac Sympathetic

Activity
Use in stable, chronic disease (start
as early as discharge-IMPACT-HF)
Titrate slowly
Contraindications-bradycardia, heart
block or hemodynamic instability
Mild asthma was not a
contraindication
Work irrespective of the etiology of
the heart failure
Betablocker therapy-which to
pick?
Three beta-blockers :
Bisoprolol (Zebeta) -Trial CIBIS-II

Metoprolol (Toprol XL) Trial MERIT-HF (sustained release)
Carvedilol (Coreg) Trial-COPERNICUS
6 RCTs with > 9,000 pts already taking ACE-I showed a

significant reduction in total mortality and sudden death (NNT
24, and 35 over 1-2 years) regardless of severity
Carvedilol vs. Metoprolol (COMET 2003)

3029 pts; carvedilol 25mg bid vs. metoprolol 50 mg bid
Patient with NYHA Classes II-IV
Carvedilol greater reduction in mortality (NNT, 18 over 5
years) and cardiovascular mortality (NNT, 16 over 5 years)
than metoprolol but hypotension was greater in carvedilol (14
vs 11 percent)
Spironolactone (Aldactone; RALES 1999)
Pts 1,663 Class III/IV, ACE, Loop,Dig, EF < 35%

Decreased all cause mortality of 30%, NNT=10
Hyperkalemia, gynecomastia
Eplerenone (Inspra; EPHESUS 2003)
Pts 6,642 asym LV dysfunction, DM, or after MI

Dec CV mortality of 13%, NNT=43
Newer more selective inhibitor; fewer side
effects
More pts on beta-blockers
Hydralazine (Apresoline)
and isosorbide dinitrate
(Sorbitrate)
Hydralazine
Reduces systemic vascular resistance by
preferentially dilating arterioles
Isosorbide Dinitrate
Preferential Venodilator-reduces ventricular
filling pressure and treat pulmonary congestion
Reduces mortality upto 28%
Poor tolerability->30% drop out of study
flushing, headaches, gi upset, less frequently can
cause positive ANA titers and lupus-like
syndrome
Hydralazine (Apresoline)
and isosorbide dinitrate
(Sorbitrate)
African-American Heart Failure Trial

(A-HeFT)
advanced HF and a fixed dose of
isosorbide dinitrate and hydralazine
Added to Standard B-blocker/Ace-I
therapy
Some survival improvement
Digoxin
May relieve symptoms, does not

reduce mortality
Pts taking digoxin are less likely to
be hospitalized (25% reduction)
More admissions for suspected
digoxin toxicity
Loop Diuretics
Mainstay of symptomatic treatment

Improve fluid retention
Increase exercise tolerance
No effects on morbidity or mortality
Antiplatelet Therapy and

Anticoagulation
Increased risk of Thromboembolic

events, 1.6-3.2% per year
Antiplatelet therapy (aspirin) in not
useful in patient in sinus rhythm
Coumadin for patient with atrial
fibrillation or a previous
thromboembolic event
Nesiritide (Natrecor)
Recombinant form of human BNP

Causes venous and arterial
vasodilation
has been shown to improve dyspnea
and global assessments at 3 hours after
initiation in pts with Acute HF.
Risks- deleterious effect on renal
function and decreased 30 day survival
Nonpharmacological
Management
Sodium Restriction to 2g/day

Risk Factor Management
Exercise
Decreases mortality (NNT=4)

Decreases hospitalizations (NNT=5)
Multidisciplinary, Disease-Management Approach
CHAMP Cardiovascular Hospital Atherosclerosis

Management Program
ASA, beta-blocker, Nitrates, ACE-I, Statin, Exercise,
Smoking Cessation, Dietary counseling (use increased
by 80%)
Device Therapy
Implantable CardioverterDefibrillators (ICD)

(CRT)
Left Ventricular Assist Devices
(LVAD)
ICD
SCD-HeFT (sudden cardiac death)

2521 patients with depressed LV systolic
function and Class II-III HF
Randomized to standard therapy vs.
standard therapy plus ICD vs. standard
therapy plus amiodarone
23% reduction in mortality with ICD
No difference in mortality with amiodarone
Results did not vary based on etiology of LV
dysfunction
ICD
Recommended in pts with EF<30%

and mild to moderate symptoms of
HF
Survival with good functional
capacity is anticipated for > 1 year
Left Ventricular Assist

Devices (LVAD)
REMATCH Trial1 yr survival 52%

(LVAD) vs 24% (rx)
2 yr survival 23% vs
8%
End-Stage (Class IV)
HF pts ineligible for
transplant due to:
>65yo
DM with EOD
CRI
Diastolic Dysfunction
Acute Management is the SAME

Chronic Management is
CONTROVERSIAL
Diuretics-dec fluid volume

CCB-promote left ventricular relaxation
ACE-I-promote regression of left ventricular
hypertrophy
Beta-blockers/antiarrhytmic agents-control
heart rate or maintain atrial contraction
Pathophysiology of chronic heart failure.
Ramani G V et al. Mayo Clin Proc. 2010;85:180-195
2010 Mayo Foundation for Medical Education and Research
Heart Failure
Treatment.
Directions in Heart Failure

Therapy
Blocking the RAAS and Sympathetic

Nervous system
Blocking several neurohormonal /
cytokine systems
Enhancing compensatory mechanisms in
acute heart failure; BNP
Blocking metabolic pathways
Treating concomitant problems
Devices and mechanical support
Surgical reconstruction
Pharmacogenomics

Therapy

Nervous system
cytokine systems
Pharmacogenomics
DoesinhibitionofBNPdegradation(whencoupledtoACE
inhibition)withomapatrilatimprovesurvival?
OVERTURE: ACE/NEP Inhibitors

in Heart Failure
% Event Free Survival
1.0
0.8
0.6
0.4
0.2
0.0
P=0.187
Omapatrilat
Enalapril
0
12
Months
15
18
21
24
Packer et al, Circulation 2002
Etanercept Survival Study (RENEWAL)

Primary End-Point (Death or CHF Hospitalization)
Event-free survival %
100
80
60
40
Placebo
Etanercept biw + tiw
20
(n=1500)
(n=1500)
RR = 1.10
95% CI: 0.91-1.33
P = 0.33
0
0
4 8 12 16 20 24 26 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96
Weeks
Mann et al, HFSA 2002
ENABLE I & II: bosentan (ETA+ ETB Antagonist) I

n Heart Failure (n=1,613)
% of Patients (Event-Free from death/HF hosp)
100
90
80
70
60
50
40
30
Bosentan
20
Placebo
Log rank p-value: 0.8986
10
0
Weeks from
0 13 26 39 52 65 78 91 104 117 130 Randomization
No. at Risk: 804 680 615 573 542 502 393 238 123 16
0
807
0
723
655
613
577
512 388 229 113 19

Packer et al, ACC Late-Breaking Trials 2002

Therapy

Nervous system
cytokine systems
Pharmacogenomics
Natriuretic Peptides:
The Heart as a Secretory
Organ
Atrial/ventricular stretch
receptors link blood volume
to renal function
Distension of a balloon catheter in
atria of dogs resulted in diuresis
Henry, et al. (1956)
Secretory granules discovered in
the atria
Kisch (1956)
Jamieson and Palade (1964)
de Bold, et al (1981) report
natriuresis
in rats after injection of atrial
extracts
BNP was characterized by amino
Jamieson and Palade J Cell Biol 1964;23:151
acid sequence and DNA clones
(Sudoh, et al. 1988 and
Family of Natriuretic Peptides

1
ANP
BNP
H2N Ser
Ser
Pro
Pro
CNP
Lys
Lys
1
H2N Ser
Ser
Leu
Leu
5
Arg
Arg
Gly
Met
Gly
Met
Gly
Asp
Gly
Asp
Ser
Ser
Phe
Ser
Ser Phe
Cys
Cys 7
Phe
Phe
Arg
Arg
Tyr
HOOC Tyr
28
25
Ser
Ser
Ile
Ile
Gly
Gly
Ala
Ala
Leu
Leu
Gin
Gin
Gly
Gly Ser
Ser
20
15
Ser
Ser
Lys
Arg
Arg Lys
Met
Met
Gly
Gly
Asp
Asp
Phe
Gly
Gly Phe
Cys
Cys 10
Arg
Cys
Cys 23
Asn
Asn Gly
Gly
Ser
Ser
Gly
Gly
Arg
Arg
Ile
Ile
Cys
Cys 26
Ser
Ser
Lys
Lys Gly
Gly
Ser
Ser
Val
Leu
Leu
Ser
Ser
25
20
Gly
Gly Ser
Ser
Leu
Leu
Arg
Arg
Arg
Arg
10
Leu
Leu
15
Gin
Gin
n a Di u
tri ret
ur i c
et
ic
Arg
Arg
H2N Gly
Gly
Val
Val
10
Arg
Arg
Met
Met
LysLeu
Leu
LeuLys
Leu
Gly
Gly
Lys
Lys
Asp
Asp
Phe
Gly
Gly Phe
Arg
Arg
Cys
Cys 6
Ile
Ile
Cys 22
HOOC Cys
Gly
Gly
Gly
15
Ser
Ser
Leu
Leu
Met
Met
Gly
Gly Ser
20
5
30
His
HOOC His
32
Diuretic
Natriuretic
Vascular relaxation
Inhibition of RAAS, SNS
Atria
Same actions as ANP

In atria and ventricles
Longer 1/2 life
Excellent marker
Used as therapy
No natriuresis
or diuresis
Potent vasodilator
B-Type Natriuretic
Peptide (nesiritide) as Therapy
1
H2N Ser
Ser
Pro
Pro
ANP
H2N Ser
Ser
Leu
Leu
Arg
Arg
Ser
Ser
Phe
Phe
Arg
Arg
Tyr
HOOC Tyr
25
Gin
Gin
Gly
Gly
Ile
Ile
Gly
Gly
Ala
Ala
Leu
Leu
Gin
Gin
Gly
Gly Ser
Ser
20
ee
NN
Ser
Ser
15
Arg
Arg
10
Leu
Leu
15
Ser
Ser
Lys
Arg
Arg Lys
Met
Met
Gly
Gly
Asp
Asp
Arg
Arg
Ile
Ile
Cys
Cys 26
Ser
Ser
Lys
Lys Gly
Gly
Ser
Ser
Val
Leu
Leu
Ser
Ser
25
20
Gly
Gly Ser
Ser
Leu
Leu
Arg
Arg
CNP
1
H2N Gly
Gly
Phe
Gly
Gly Phe
Cys
Cys 10
Arg
Cys
Cys 23
Asn
Asn Gly
Gly
BNP
NN
Val
Val
Arg
Arg
Gly
Met
Gly
Met
Gly
Asp
Gly
Asp
Ser
Ser
Phe
Ser
Ser Phe
Cys
Cys 7
Met
Met
10
Arg
Arg
28
Lys
Lys
n a Di u
tri ret
ur i c
et
ic
LysLeu
Leu
LeuLys
Leu
Gly
Gly
Lys
Lys
Asp
Asp
Phe
Gly
Gly Phe
Arg
Arg
Cys
Cys 6
Ile
Ile
Cys 22
HOOC Cys
Gly
Gly
Gly
15
Ser
Ser
Leu
Leu
Met
Met
Gly
Gly Ser
20
5
30
His
HOOC His
32
Diuretic
Natriuretic
Vascular relaxation
Inhibition of RAAS, SNS
Atria
Same actions as ANP

In atria and ventricles
Longer 1/2 life
Excellent marker
Used as therapy
No natriuresis
or diuresis
Potent vasodilator
B-Type Natriuretic
Peptide
90
1
H2N H
H
PP L
10
L G
G SS P
P G
G SS A
A SS
propro-BNP
70
YY T
T LL
76
R
R A
A PP
R
R
R I
D
D R I SS
M
M
SS
K
K
R
R
C
C
FF
C
C
G
G
SS
80
G
G
Q
Q
VV
M
M
K
K
P
SS P
SS
SS
G
G
L
C
C L 100
C
CK
K V
V L
L
R
R
R
R
108
H
HCOOH
Cleavage
R II SS
D
D R
M
M
SS
K
K
SS
R
R
SS
C
C
G
G
FF
NTBNP
NT-proBNP
L
C
C
C
C L
C
CK
1
10
70
76
G
K V
SS G
G
V L
G
Q
L
Q
H2N H
YY TT LL R
H PP LL G
G SS PP G
G SS A
A SS
R A
A PP R
R COOH
VV
R
R
M
M
R
R H COOH
K
K
PP
H
H2N S
S
Biologically Inactive
NT-proBNP: Roche /
Dade-Behring
Biologically Active
BNP: Biosite, Bayer, Abbott,

Beckman-Coulter
Nesiritide in Heart Failure: VMAC

P
Pulmonary Capillary Wedge Pressure (absolute and change)
U
( mHg)
Mean Observed
L Value (mmHg) Mean Change m
M
30
-1
28
26
24
22
#*
-4
#*
#*
-7
20
18
BL 15m30m 1hr
2hr
# p < .05 versus placebo

p*< .05 versus nitroglycerin
3hr
-10
#*
#*
#
#*
#*
Placebo
Nitroglycerin
Nesiritide
BL 15m 30m 1hr
2hr
3hr
Primary End Point: PCWP through 3 Hours

Young et al, JAMA 2002
Heart Failure
Prof Univ Dr Ion C.Tintoiu
Centrul de Cardiologie al
Armatei
Universitatea Titu
Maiorescu
New Diuretics- Adenosine Receptor

Modulators
Adenosine1 receptor antagonists - afferent arteriole flow
BG9719 (CVT-124)
250
Sodium Excretion
(mEq)
200
150
100
50
0
Furosemide Placebo
BG9719
Gottlieb et al, Circulation 2002
Conivaptan andTolvaptan:
New Aquaretic Agents
Conivaptan - an AVP-1 and AVP-2 receptor

blocker; promotes an aquaresis, corrects
hyponatremia, and has vasodilator activity
(reduces pulmonary capillary wedge
pressure and raises cardiac output).
Tolvaptan an AVP-1 receptor blocker that
corrects hyponatremia in edematous patients
with hyponatremia via an aquaresis
survival study underway (EVEREST)
Francis and Tang, JAMA 2004

Therapy

Nervous system
cytokine systems
Pharmacogenomics
Partial Fatty Acid Oxidation (pFOX) Inhibition

Ranolazine, Trimetazidine, and Etomoxir
Fatty
Inhibit fatty acid oxidation only

Acids
at high fatty acid concentrations
Permit normal fatty acid oxidation rates
at physiologic fatty acid concentrations
Preserve high-energy phosphates
pFOX
and contractile function
Inhibition
Reduce accumulation of lactic
acid and maintains tissue pH
Delay or prevent onset of
biochemical myocardial ischemia
Allow more energy to be produced from
each O2 molecule consumed
Glucose
Pyruvate
Lactic
acid ( )
H+ ( )
Krebs
Cycle
Oxidative Phosphorylation
Energy ATP

Therapy

Nervous system
cytokine systems
Pharmacogenomics
Anemia in Ambulatory Heart

Failure
Tang et al. ACC Presentation 2003
Erythropoietin in Heart Failure
Double blind, randomized, placebocontrolled study evaluating the safety

and efficacy of erythropoietin in the
treatment of patients with heart
failure and anemia
Darbepoetin
(Amgen): STAMINA-HeFTexercise study; HIPOCRATES -survival

study
Concerns about thrombosis

Therapy

Nervous system
cytokine systems
Pharmacogenomics
Pipeline Drug Development in Heart

Failure:
some winners and losers
Selective Aldosterone Antagonists
Phosphodiesterase-3
Phosphodiesterase-3
Inhibitor
Eplerenone (4E, EPHESUS)
Endothelin Receptor Antaginst (ERA)
Bosentan (REACH-1, ENABLE-1 & -2)

Tesozantan (RITZ-1 to -5)
Darusentan (EARTH)
Enrasentan (ENCOR)
Immune Modulators
Vasopeptidase Inhibitors (VPI)
Omapatrilat (OVERTURE, OCTAVE,

OPERA)
Natriuretic Peptides
Moxonidine (MOXCON, MOXSE)
Calcium Sensitizers
Etanercept (RENAISSANCE,
RECOVER)
Infliximab (ATTACH)
Immune modulator, VAS-991
(ACCLAIM)
Miscellaneous
Nesiritide (PRECEDENT, VMAC,

FUSION1,2)
Imidazoline-1 Rececptor Antagonist
Enoximone (EMPOWER,
ESSENTIAL, EMOTE)
Levosimendan (LIDO, RUSSLAN, REVIVE)
AGE cross-link breaker, ALT711 (DIAMOND, SAPPHIRE,

SILVER)
Nebivolol (SENIORS)
BiDil (A-HeFT)
darbepoetin (STAMINA-HeFT,
HIPOCRATES)
Slide courtesy of G. Francis
Nonpharmacologic
Management
and Health Care
Maintenance
in Patients with
HFSA 2010
Chronic
Heart
Recommendations
Failure
HFSA 2010 Practice

Guideline
NonpharmacologicDiet and Nutrition
Recommendation 6.1
Dietary instruction regarding sodium

intake
is recommended in all
patients with HF.
Patients with HF and diabetes,
dyslipidemia or severe obesity should
be given specific dietary instructions.
HFSA 2010 Practice

Guideline
NonpharmacologicDietary Sodium
Recommendation 6.2
Dietary sodium restriction (2-3 g

daily) is recommended for patients
with the clinical syndrome of HF
and preserved or depressed LVEF.
Further restriction (< 2 g daily)

may be considered in
moderate to severe HF.
HFSA 2010 Practice

Guideline
NonpharmacologicFluid Intake
Recommendation 6.3
Restriction of daily fluid intake to < 2

liters:
Is recommended in patients with
severe hyponatremia (serum sodium
< 130 mEq/L)
Should be considered for all patients
demonstrating fluid retention that is
difficult to control despite high doses
of diuretic and sodium restriction.
HFSA 2010 Practice

Guideline
NonpharmacologicNutrition in
HF
RecommendationAdvanced
6.4
It is recommended that specific attention be
paid to nutritional management of patients
with advanced HF and unintentional weight
loss or muscle wasting (cardiac cachexia).
Measurement of nitrogen balance, caloric
intake, and prealbumin may be useful in
determining appropriate nutritional
supplementation.
Caloric supplementation is recommended.
Anabolic steroids are not recommended for
cachexic patients.
HFSA 2010 Practice

Guideline
NonpharmacologicVitamins
Recommendation 6.5
Patients with HF, especially those on

diuretic therapy and restricted diets,
should be considered for
daily multivitamin-mineral
supplementation to ensure adequate
intake of the recommended daily value
of essential nutrients.
Evaluation for specific vitamin or nutrient

deficiencies is rarely necessary.
HFSA 2010 Practice

Guideline
NonpharmacologicNutraceuticals
Recommendation 6.6
Documentation of the type and dose of naturoceutical

products utilized by patients with HF is
recommended.
Naturoceutical use is not recommended for relief of
symptomatic HF or for the secondary prevention of
cardiovascular events.
Patients should be instructed to avoid using
natural or synthetic products containing ephedra
(ma huang), ephedrine or its metabolites because
of an increased risk of mortality and morbidity.
Products should be avoided that may have
significant drug interactions with digoxin,
vasodilators, beta blockers, antiarrhythmic drugs
and anticoagulants.
Strength of
Evidence = B
HFSA 2010 Practice

Guideline
NonpharmacologicCPAP
Recommendation 6.7
Continuous positive airway

pressure to improve daily
functional capacity and quality of
life is recommended in patients
with HF and obstructive sleep
apnea documented by approved
methods of polysomnography.
HFSA 2010 Practice

Guideline
NonpharmacologicOxygen
Recommendation 6.8
Supplemental oxygen, either at night

or during exertion, is not
recommended for patients with HF in
the absence of an indication due to
underlying pulmonary disease.
Patients with resting hypoxemia or
oxygen desaturation during exercise
should be evaluated for residual fluid
overload or concomitant pulmonary
disease.
HFSA 2010 Practice

Guideline
NonpharmacologicInsomnia
Recommendation 6.9
The identification of treatable

conditions, such as sleep-disordered
breathing, urologic abnormalities,
restless leg syndrome and depression
should be considered in patients with
HF and chronic insomnia.
Pharmacologic aids to sleep induction may

be necessary.
Agents that do not risk physical dependence
are preferred.
HFSA 2010 Practice

Guideline
NonpharmacologicDepression
Recommendation 6.10
It is recommended that screening for

endogenous or prolonged reactive
depression in patients with HF be conducted
following diagnosis and at periodic intervals
as clinically indicated.
For pharmacologic treatment, selective
serotonin receptor uptake inhibitors (SSRIs)
are preferred over tricyclic antidepressants,
because the latter have the potential to
cause ventricular arrhythmias, but the
potential for drug interactions should be
considered.
HFSA 2010 Practice

Guideline
NonpharmacologicStress
Recommendation 6.11
Nonpharmacologic techniques
for stress reduction may be
considered as a useful adjunct
for reducing anxiety in patients
with HF.
HFSA 2010 Practice

Guideline
NonpharmacologicSexual Dysfunction
Recommendation 6.12
It is recommended that treatment

options for sexual dysfunction be
discussed openly with both male and
female patients with HF.
The use of phosphodiasterase-5 (PDE5)
inhibitors such as sildenafil may be
considered for use for sexual dysfunction
in patients with chronic stable HF.
These agents are not recommended in

patients taking nitrate preparations.
HFSA 2010 Practice

Guideline
NonpharmacologicSmoking & Alcohol
Recommendation 6.13
It is recommended that patients with HF

be advised to stop smoking and to limit
alcohol consumption to 2 standard
drinks per day in men or 1 standard
drink per day in women.
Patients suspected of having an alcoholinduced cardiomyopathy should be advised
to abstain from alcohol consumption.
Patients suspected of using illicit drugs
should be counseled to discontinue such
use.
Strength of Evidence
=B
Phisical examination
ECG 12 leads
Chest X-ray
Lab tests (hyponatraemia!)
Biomarkers of HF: BNP, proBNP,
CRP, troponins
Echocardiography (systolic/diastolic
dysfunction, structural heart disease)
spiroergometry
HFSA 2010 Practice

Guideline
NonpharmacologicVaccinations
Recommendation 6.14
Pneumococcal vaccine and annual

influenza vaccination are
recommended in all patients with
HF in the absence of known
contraindications.
HFSA 2010 Practice

Guideline
NonpharmacologicEndocarditis
Prophylaxis
Recommendation 6.15
Endocarditis prophylaxis is not recommended based on

the diagnosis of HF alone. Consistent with the AHA
recommendation, prophylaxis should be given for only
specific cardiac conditions, associated with the highest
risk of adverse outcome from endocarditis:
prosthetic cardiac valves

previous infective endocarditis
congenital heart disease (CHD) such as: unrepaired cyanotic
CHD, including palliative shunts and conduits
completely repaired congenital heart defect with prosthetic
material or device, whether placed by surgery or by catheter
intervention, during the first six months after the procedure
repaired CHD with residual defects at the site or adjacent to
the site of a prosthetic patch or prosthetic device (which
inhibit endothelialization)
cardiac transplantation recipients who develop cardiac
valvulopathy.
HFSA 2010 Practice

Guideline
NonpharmacologicNSAIDs
Recommendation 6.16
NSAIDs, including COX-2

inhibitors, are not recommended
in patients with chronic HF.
The risk of renal failure and fluid

retention is markedly increased in
the setting of reduced renal function
or ACE inhibitor therapy.
HFSA 2010 Practice

Guideline
NonpharmacologicEmployability
Recommendation 6.17
It is recommended that patients with

new or recent-onset HF be assessed for
employability following a reasonable
period of clinical stabilization.
An objective assessment of functional
exercise capacity is useful in this
determination.
Strength of
Evidence = B
HFSA 2010 Practice

Guideline
NonpharmacologicEmployability
Recommendation 6.18
It is recommended that patients with chronic

HF who currently are employed and whose job
description is compatible with their
prescribed activity level be encouraged to
remain employed, even if a temporary
reduction in hours worked or task performed
is required.
Retraining should be considered and
supported for patients with a job demanding a
level of physical exertion exceeding
recommended levels.
Strength of
Evidence = B
HFSA 2010 Practice

Guideline
NonpharmacologicExercise
Training
Recommendation 6.19 (NEW in 2010)
It is recommended that patients with HF

undergo exercise testing to determine suitability
for exercise training (patient does not develop
significant ischemia or arrhythmias). If deemed
safe, exercise training should be considered for
patients with HF in order to:
Facilitate understanding of exercise
expectations (heart rate ranges and appropriate
levels of exercise training)
Increase exercise duration and intensity in a
supervised setting
Promote adherence to a general exercise goal of
30 minutes of moderate activity/exercise, 5 days
per week with warm up and cool down exercises
Drill of the
Month
Developed
by Michael Lindsay
An Overview of Ventricular
Assist Devices
&
Pre Hospital Management
Student Objectives
At the conclusion of this Drill

Students will be able to:
Define Heart Failure

Define Ventricular Assist Device (VAD) and their use in
treating Heart Failure
Identify types of Ventricular Assist Devices
Explain the difference between Pulsatile and
Nonpulsatile flow
Identify hemodynamic differences in patients with a VAD
List VAD related complications
Demonstrate how to assess a patient with a VAD
Describe how to treat VAD complications
Identify VAD resources that can be utilized when caring
for these patients.
Heart Failure
* Heart failure is a condition where the heart
cannot pump enough blood throughout the body.
* It develops over time as the pumping action of
the heart grows weaker.
* Most cases involve the left side where the heart
cannot pump enough oxygen-rich blood to the
rest of the body.
* With right sided failure, the heart cannot
effectively pump blood to the lungs where the
blood picks up oxygen.
Ventricular Assist Device

(VAD)
A mechanical pump that is surgically attached

to one of the hearts ventricles to augment or
replace native ventricular function
Can be used for the left (L VAD), right (R VAD),
or both ventricles (Bi VAD)
Are powered by external power sources that
connect to the implanted pump via a
percutaneous lead (driveline) that exits the
body on the right abdomen
Pump output flow can be pulsatile or
nonpulsatile
Why Do We Need VADs?
Heart disease is the leading cause of death in

the Western world
~5 million people in the US have congestive

heart failure (CHF)
250,000 are in the most advanced stage of

CHF
~500,000 new cases each year
~50,000 deaths each year
only effective treatment for end stage CHF is

heart transplant
Why Do We Need VADs?
But, in 2008:
7318
people were waiting for a heart
2210
received one
623
died waiting
~1200-1500
VAD implanted in 2008
Indications for VAD
Bridge to transplant
(BTT)
most common
allow rehab from
severe CHF while
awaiting donor
Bridge to recovery
(BTR)
unload heart, allow
reverse remodeling
can be short- or longterm
Destination therapy (DT)

permanent device,
instead of transplant
currently only in
transplant-ineligible
patients
Bridge to candidacy
(BTC)/
Bridge to decision (BTD)
when eligibility unclear
at implant
not true indication
but true for many pts
Types of VADs
Pulsatile
and
Non Pulsatile
Pulsatile
Ventricle-like pumping sac device.

Blood enters via the inflow cannula and fills a flexible
pumping chamber.
Electric motor or pneumatic (air) pressure collapses
the chamber and forces blood into systemic
circulation via the outflow cannula.
Can be LVAD, RVAD, or BiVAD
First-generation devices (in use since early 1980s)
Patients will have a palpable pulse and a measurable

blood pressure. Both are generated from the VAD
output flow.
Pulsatile VAD Key

Parameters
Pump Rate:
How fast the VAD is pumping (filling &
emptying)
Can be set at a fixed rate or can automatically
adjust
Pulsatile VADs are loud and the rate can be
assessed by listening
Output:
The amount of blood ejected from the VAD
Measured is liters per minute
Is dependent upon preload, afterload, and
pump rate
Non-Pulsatile
Continuous-flow devices
Impeller (spinning turbine-like rotor blade) propels blood
continuously forward into systemic circulation.
Axial flow: blood leaves impeller blades in the same direction as
it enters (think fan or boat motor propeller).
Most implanted devices are LVADs only
Are quite and cannot be heard outside of the patients body.

Assess VAD status by auscultation over the apex of the LV. The
VAD should have a continuous, smooth humming sound.
The Patient may have a weak, irregular, or non-palpable pulse
The Patient may have a narrow pulse pressure and may not be
measurable with automated blood pressure monitors. This is due
to the continuous forward outflow from the VAD.
The Mean Arterial Pressure is the key in monitoring

hemodynamics. Ideal range is 65-90 mmHg.
Non Pulsatile VAD Key

Parameters
Flow:
Measured in liters per minute
Correlates with pump speed (speed=flow,
speed=flow)
Dependent on Preload and Afterload
Speed:
How fast the impeller of the internal pump
spins
Measured in revolutions per minute (rpm)
Flow speed is set and determined by VAD
clinical team and usually cannot be
manipulated outside of the hospital

Parameters
Power:
The amount of power the VAD consumes to
continually run at a set speed
Sudden or gradual sustained increases in the
power can indicate thrombus inside the VAD
Pulsatility Index (PI):

A measure of the pressure differential inside
the internal VAD pump during the native
hearts cardiac cycle
Varies by patient
Indicates volume status, right ventricle
function, and native heart contractility

Parameters
The device parameters are displayed

numerically on the VAD console or Controller
Will vary with each individual patient and VAD

device
VAD Parameters
Parameters for pulsatile and non pulsatile

devices vary with each device model
Patients and their care givers know the

expectable parameter ranges and goals
for their specific device
Contact the VAD Coordinator at the

implanting medical center, they will be
your best resource when treating a VAD
patient.
Basic VAD Management
ALL VADs are:

Preload-dependent
EKG-independent
Afterload-sensitive
Anticoagulated
Prone to:
infection
bleeding
thrombosis/stroke
mechanical malfunction
Key differences depend on pulsatile vs. nonpulsatile device
VADs commonly seen in the

community
Thoratec VAD (pVAD/iVAD)
Pneumatic, external(pVAD) or internal (iVAD),

pulsatile pump(s)
right-, left-, or bi-ventricular support

(RVAD/LVAD/BiVAD)
up to ~7.2 lpm flow
Short- to medium-term use (up to ~1-2 years)
bridge to recovery
bridge to transplant
hospital discharge possible
iVAD
pVAD
Thoratec pVAD
HeartMate XVE LVAS
Internally implanted, electric pulsatile pump
left heart support only
up to 10 lpm flow
Medium- to long-term therapy (months to

years)
destination therapy (only FDA-approved DT

device)
HeartMate II LVAS
Internally implanted, axial-flow (non-pulsatile) device
speed: 8000-15000 rpm
flow: ~3-8 lpm
Medium- to long-term therapy (months to years)
bridge to transplant (FDA-approved)
destination therapy (investigational)
Jarvik 2000 LVAD
Axial-flow (non-pulsatile)
pump
electric, intraventricular
Speed: 8000-12000 rpm
Medium- to long-term therapy

flow: ~3-5 lpm
(months to years)
(investigational)
Jarvik 2000 LVAD
VAD Issues
Problems/Complications
Major VAD Complications
Bleeding
Thrombosis
Infection
sepsis is leading cause of death in long-term VAD

support
RV dysfunction/failure
Suckdown (low preload causes a nonpulsatle VAD to

collapse the ventricle)
Device failure/malfunction (highly variable by device

type)
Other Common Issues
Arrhythmias
A patient can be in a lethal arrhythmia and be

asymptomatic. Treat the patient not the monitor.
Do not cardiovert/ defib. unless the patient is

unstable with the arrhythmia.
Do not initiate chest compressions unless

instructed by a physician or VAD coordinator.
Chest compressions can disrupt the implanted
equipment causing bleeding and death
Electrical shock from cardiovert/ defib. will not

damage any of the VAD equipment
Other Common Issues
Hypertension
High afterload can limit VAD flow/ output
Do not administer antihypertensive medications

or nitrates unless instructed by a physician or
VAD Coordinator
Hypotension/ loss of Preload
All VADs are preload dependent. A loss or

reduction in preload will compromise VAD
function and limit flow/ output
Other Common Issues
Depression/ Adjustment Disorders
Living with a VAD is difficult to management for a

lot of patients.
A large percentage of patients experience

symptoms of depression
Portability/ Ergonomics
The external VAD equipment is heavy and

cumbersome limiting a patients mobility and
greatly impacting their quality of life.
Bleeding & Thrombosis

Careful control of anticoagulation is
imperative
Patients
are often on both anticoagulants

and platelet inhibitors
Device thrombosis
rare in pulsatile devices
typically revealed by increased power and
signs and symptoms of hemolysis
Alarms
All VAD devices typically have two

distingue alarms to indicate a
problem and its severity
Advisory Alarms
Critical/ Hazardous Alarms
Alarms
Advisory Alarms are intermittent

beeping sounds that have a
corresponding YELLOW light that
illuminates on the system controller
Not critical but the device requires
attention
Likely due to low battery, cable
disconnected, or device not functioning
properly.
Alarms
Hazardous or Critical alarms are a loud,

continuous, shrill sound that have a
corresponding RED light that illuminates
on the system controller
Indicating the device needs immediate
attention
Often because the pump has stopped or a
problem is detected with the system
controller
Most likely intervention required is to
change out the system controller
Field Management
All VADs are dependant on adequate

preload in order to maintain proper
functioning
Volume resuscitation in an unstable
VAD patient is the first line of
therapy before vasopressors but be
cautious with fluid as to not over load
the right ventricle in L VADs only.
Field Management
Nitrates can be detrimental to a VAD

patient because of the reduction in
preload
Results in decreased pump efficiency
Consult with medical control before
administering nitrates per protocol
Field Management
Initiate IV therapy with all VAD

patients if possible
Use aseptic technique due to the

patients increased risks of infection
Field Management
VAD patients are susceptible to

other injuries unrelated to the VAD
Contact the VAD Coordinator, they
are your most valuable resource
when encountering these patients
Consult with medical control about
transport
A, B, C, D, Es of
the
Management of
Nanette
Kass
Wenger,
MD
Heart
Failure
Emory University School of
Medicine
Grady Memorial Hospital
Atlanta, Georgia
Objectives
Understand the cornerstones of
therapy
angiotensin-converting enzyme
inhibitors, diuretics, and digitalis
review the role of other therapies:
pharmacotherapeutic as well as
nonpharmacotherapeutic
approaches
Epidemiology
4.7 million patients in the United

States are estimated to have heart
failure
470,000 new cases recognized annually
Each year, 875,000 hospitalized
patients have a primary diagnosis of
heart failure. It is the major hospital
discharge diagnosis for patients in the
Medicare age group.
Epidemiology
heart failure increases with age

half of all heart failure
hospitalizations occur in
individuals > age 65 years.
In the United States, the estimated
costs for the management of
patients with heart failure exceed
$10 billion annually.
Treatment objectives
Decrease symptoms
Improve exercise capacity
Enhance quality of life
Decrease morbidity
Retard the progression of heart
failure
Improve survival
Cornerstones of Therapy
Angiotensin converting enzyme

(ACE) inhibitors
diuretics
digitalis
guidelines for the severity-based
therapy of heart failure.
Asymptomatic Patients
For asymptomatic patients with
left ventricular dysfunction
(NYHA class I), typically those
with an ejection fraction below
40%,
ACE inhibitors are
recommended
Symptomatic Patients
NYHA class II
NYHA class III
ACE inhibitors, mild diuretics, and

digoxin, with or without the use of Bblocker therapy
add loop diuretics
NYHA class IV
consider positive inotropic agents
surgical therapies may also be applied
Angiotensin Converting
Inhibitors physiologic
benefits
Arteriovenous Vasodilatation
pulmonary arterial diastolic

pressure
pulmonary capillary wedge pressure
left ventricular end-diastolic
pressure
systemic vascular resistance
systemic blood pressure
maximal oxygen uptake (MVO2)
Inhibitors
physiologic benefits
LV function and cardiac output

renal, coronary, cerebral blood flow
No change in heart rate or myocardial
contractility
no neurohormonal activation
resultant diuresis and natriuresis
Inhibitors
clinical benefits
Increases exercise capacity

improves functional class
attenuation of LV remodeling post MI
decrease in the progression of chronic
HF
decreased hospitalization
enhanced quality of life
improved survival
Asymptomatic Patients
Enalopril
SOLVD Prevention Trial
EF<35%
HF progression, hospitalization
Captopril
SAVE, GISSI-3, ISIS-4
Post MI, EF <40%
overall mortality, re-infarction
hospitalization, HF progression
Hydralazine + Isosorbide dinitrate
VHeFT-I
mortality, improved functional class
as compared with use of digoxin and
diuretics
VHeFT-II
proved less effective than enalopril
Enalopril + digoxin + diuretics
SOLVD Treatment Trial
EF<35%, FC III-IV
mortality, hospitalization
CONSENSUS-II
FC IV
mortality (40%), symptoms,
hospitalization
improved functional class
Losartan (AT-II inhibitor)
ELITE Trial
losartan improved the survival of elderly
heart failure patients treated compared with
captopril therapy
Guidelines to ACE Inhibitor

Therapy
Contraindications
Renal artery stenosis

Renal insufficiency (relative)
Hyperkalemia
Arterial hypotension
Cough
Angioedema
Alternatives
Hydralazine + ISDN, AT-II inhibitor
Guidelines to ACE Inhibitor

Therapy
It is important to titrate to the

dosage regimen used in the clinical
trials in the absence of symptoms
or adverse effects on end-organ
perfusion
in very severe heart failure,
hydralazine and nitrates added to
ACE inhibitor therapy can further
improve cardiac output
Anticoagulant Therapy
Recommended for
patients with NYHA III-IV and EF <30% or

ventricular aneurysm or very dilated LV
Indicated for
patients with heart failure who have atrial

fibrillation, a prior embolic episode,
identified intracardiac thrombus, left
ventricular aneurysm, thrombophlebitis,
or prolonged bed rest
titrate INR to 2 to 3
Arrhythmias
Sudden death occurs in
about 50% of patients with
heart failure
Amiodarone
Randomized clinical trials

CHF-STAT
NYHA II-III patients with ischemic
cardiomyopathy - amiodarone had no
affect on survival
GESICA
NYHA III-IV patients with more nonischemic cardiomyopathy - open
labeled amiodarone decreased
mortality
AICD
Randomized clinical trials
AVID
amiodarone vs implantable defibrillator
showed the AICD group had lower mortality
AICD should be considered for patients

with ventricular fibrillation or prior
sudden death
Beta-blockers or amiodarone may be
appropriate for patients with sustained
VT, with or without symptoms
Assist Devices
a bridge to cardiac transplantation

candidates must meet the inclusion
and exclusion criteria for cardiac
transplantation
-blocking Drugs
Physiologic benefits
increase the density of -1 receptors
inhibit catecholamine toxicity
decrease neurohormonal activation
decrease heart rate
provide antihypertensive, antianginal,
and antiarrhythmic effects
antioxidant and antiproliferative
effects
-blocking Drugs
Clinical benefits
decrease symptoms of HF
improve left ventricular function
improve exercise tolerance
-blocking Drugs - Clinical

Trials
BHAT ( -Blocker Heart Attack Trial)

propranolol decreased
cardiovascular mortality, sudden
death, and reinfarction in post-MI
patients
benefit is greatest in patients who
also had left ventricular dysfunction

Trials
SAVE (Survival and Ventricular

Enlargement)
post-MI patients with an EF <40%
- blockers reduced mortality both
in the ACE inhibitor and the placebo
group
lowest mortality occurred in
patients receiving both ACE and blocking therapy

Trials
MDC (Metoprolol in Dilated

Cardiomyopathy)
NYHA II-III with dilated
cardiomyopathy
no decrease in mortality
significant decrease in symptoms
significant increase in exercise
tolerance, LV ejection fraction,
quality of life

Trials
MOCHA (Multicenter Oral Carvedilol

Heart Failure Assessment Trial )
NYHA II-III heart failure
quadruple therapy (+ACE, diuretic,
digoxin)
49% decrease in the combined
endpoints of mortality and
hospitalization
no improvements in exercise tolerance

Trials
PRECISE
(Prospective Randomized
Evaluation of Carvedilol on
Symptoms and Exercise)
decrease in mortality from 8% to 3%
40% decrease in hospitalization
decrease in symptoms
improvement in LV ejection fraction
no affect on exercise tolerance
Calcium Channel Blocking

Drugs
Potential benefit:
Adverse effect:
anti-ischemic and vasodilatory

effects
negative inotropic properties
MDPIT / SPRINT trials
diltiazem, verapamil, and nifedipine

are not recommended for patients
with HF
Calcium Channel Blocking

Drugs
PRAISE-1 (Prospective Randomized

Amlodipine Survival Evaluation)
NYHA III-IV heart failure
ACE, digoxin, diuretics amlodipine
no change in total mortality
no survival benefit in ischemics
improved survival in non-ischemics
no change in exercise tolerance
Coronary Revascularization
80% of patients with heart failure

have coronary disease
Patients should be evaluated for the
presence of myocardial ischemia and
the potential benefit of
revacularization
Survival was improved by
revascularization compared with
medical therapy, even in the absence
of angina pectoris (Duke database)
Cardiac Transplantation
Survival of 60%-90% at 1-yr, 70% at 5-yr

Inclusion Criteria:
must first exclude remediable myocardial

ischemia
heart failure refractory to optimal medical Rx
left ventricular ejection fraction <20%
VO2 max 14 mL/kg/min
Problems:
rejection, graft atherosclerosis, neoplasia,

cost/availability
Cardiomyoplasty
Cardiac Reduction Surgery
currently considered
experimental
Diet
Traditional approach nonpharmacologic management is

sodium and water restriction
Sodium excess is the main reason
for heart failure exacerbation
Restrict sodium to 2 to 3 grams / day
Diuretics
sodium and water retention

symptoms of volume overload
thiazide diuretics are not active with
GFR <30 mL/min
in resistant edema, loop diuretics,
K+-sparing diuretics, and metolazone
are indicated
Digitalis
Beneficial hemodynamic effects

cardiac output
left ventricular ejection fraction
left ventricular diastolic pressure
exercise tolerance
natriuresis
neurohormonal activation
Digitalis - Clinical Trials
DIG (Digitalis Investigation Group)

NYHA class I-IV heart failure
no change in mortality compared
with placebo therapy
combined endpoint of
hospitalizations and death
serious arrhythmia and MI
RADIANCE (Randomized Assessment of
the effect of Digoxin on Inhibitors of

ACE)
ejection fraction <35%
ACE, diuretics, digoxin
associated with exercise tolerance in
patients with normal sinus rhythm
withdrawal of digoxin resulted in
exercise tolerance, and in
hospitalization
PROVED (Prospective Randomized
Study of Ventricular Function and

Efficacy of Digoxin)
mild-to-moderate HF with EF <35%
in NSR and not on ACE inhibitor
therapy
withdrawal of digoxin resulted in
exercise tolerance and in
hospitalization
Dobutamine
-1 receptor agonist
low-dose dobutamine (2-3 ug/kg/min)
myocardial contractility and cardiac
output, arteriovenous dilatation
high-dose dobutamine (5-15 ug/kg/min)
tachycardia, arrhythmia, splanchnic
and renal vasoconstriction
associated with symptomatic benefit
continuous home pump infusion
Exercise Training
AHCPR
Cardiac Rehabilitation Guidelines
Exercise training in patients with HF
decrease symptoms
improves exercise tolerance
benefit additive to that attained
with ACEI
no worsening of left ventricular
function
Exercise Training
Clinical Trials on exercise following
MI
EAMI (Exercise and Anterior MI)

ELVD (Exercise in LV Dysfunction)
both interventional groups showed
improvement in functional capacity and
decrease in symptoms
ELVD also showed an improvement in
ejection fraction
Conclusion
Effects of Heart Failure
Therapies
Improve in survival
ACE inhibitors
-blocking drugs (selective)
Increased mortality
positive inotropic agents
calcium channel blocking drugs (?)
Neutral on survival
digitalis
Conclusion
Effects of Heart Failure
Therapies
Prevention of ischemia
-blocking drugs (selective)
coronary revascularization
anticoagulant therapy
Hemodynamic improvement
ACEI, digitalis, diuretics,
hydralazine/ISDN
Prevention of sudden death
amiodarone and AICD
Evaluation and
Management of
Acute
Decompensated
2010 HFSA
Heart
Failure
Recommendations
HFSA 2010 Practice

Guideline
Acute HFDiagnosis
Recommendation 12.1
The diagnosis of ADHF should be based primarily on

signs and symptoms.
When the diagnosis is uncertain, determination of

BNP or NT-proBNP concentration is recommended
in patients being evaluated for dyspnea who have
signs and symptoms compatible with HF.
Strength
of Evidence = A
The natriuretic peptide concentration should not be

interpreted in isolation, but in the context of all
available clinical data bearing on the diagnosis of
HF, and with the knowledge of cardiac and noncardiac factors that can raise or lower natriuretic
peptide levels.
1 of 3
HFSA 2010 Practice

Guideline
Acute HFHospital Admission
Recommendation 12.2
Hospital admission is recommended

for patients presenting with ADHF
when the clinical circumstances listed
in Table 12.1.a are present.
Patients presenting with ADHF
should be considered for hospital
admission when the clinical
circumstances listed in Table 12.1.b
are present.
Evidence = C
Strength of
2 of 3
HFSA 2010 Practice

Guideline
Table 12.1.(a) Hospitalization recommended in

the presence of:
Evidence of severely decompensated HF, including:
Dyspnea at rest
Typically reflected by resting tachypnea

Less commonly reflected by oxygen saturation < 90%
Hemodynamically significant arrhythmia
Including new onset of rapid atrial fibrillation

Acute coronary syndromes
Strength of
Evidence = C
Hypotension
Worsening renal failure
Altered mentation
3 of 3
HFSA 2010 Practice

Guideline
Table 12.1.(b) Hospitalization should be considered in

the presence of:
Worsened congestion
Signs and symptoms of pulmonary or systemic

congestion
Even without dyspnea
Even in the absence of weight gain
Major electrolyte disturbance

Associated comorbid conditions
Pneumonia, pulmonary embolus, diabetic ketoacidosis,

symptoms suggestive of TIA or stroke
Repeated ICD firings

Previously undiagnosed HF with signs and symptoms of
systemic or pulmonary congestion
1 of 2
HFSA 2010 Practice

Guideline
Acute HFTreatment Goals
Recommendation 12.3
It is recommended that patients

admitted with ADHF be treated
to achieve the goals listed in
Table 12.3.
=C
HFSA 2010 Practice

Guideline
Acute HFTreatment Goals
Table 12.3 Treatment Goals for Patients Admitted

for ADHF
Improve symptoms, especially congestion and low output

symptoms
Restore normal oxygenation
Identify etiology
Identify and address precipitating factors
Optimize chronic oral therapy
Minimize side effects
Identify patients who might benefit from
revascularization or device therapy
Identify risk of thromboembolism and need for
anticoagulant therapy
Educate patients concerning medications and self
assessment of HF
Consider and, where possible, initiate a disease
management program
HFSA 2010 Practice

Guideline
Acute HFPatient Monitoring
Recommendation 12.4
Patients admitted with ADHF

should be carefully monitored.
It is recommended that the items
listed in Table 12.4 be assessed
at the stated frequencies.
HFSA 2010 Practice

Guideline
Acute HFTable 12.4. Patient

Frequenc Value
Specifics
Monitoring*
y
At least
daily
Weight
Determine after voiding in the morning

Account for possible increased food intake
due to improved appetite
At least
daily
Fluid
intake and
output
More than
daily
Vital signs
Orthostatic blood pressure, if indicated

Oxygen saturation daily until stable
At least
daily
Signs
Edema, ascites, pulmonary rales,

hepatomegaly, increased jugular venous
pressure, hepatojugular reflux, liver
tenderness
At least
daily
Symptoms
Orthopnea, paroxysmal nocturnal dyspnea or

cough, nocturnal cough, dyspnea, fatigue,
lightheadedness
At least
daily
Electrolyte
s
Potassium, sodium
At least
Renal
BUN, serum creatinine
HFSA 2010 Practice

Guideline
Acute HFFluid Overload and

Diuretics
Recommendation
12.5
It is recommended that patients

admitted with ADHF and
evidence of fluid overload be
treated initially with loop
diureticsusually given
intravenously rather than orally.
HFSA 2010 Practice

Guideline
Acute HFDiuretic Dosing
Recommendation 12.6
It is recommended that diuretics be

administered:
at doses needed to produce a rate of diuresis sufficient

to achieve optimal volume status with relief of
signs and symptoms of congestion

(edema, elevated JVP, dyspnea)
without inducing an excessively rapid reduction

in:
intravascular volume, which may result in symptomatic

hypotension and/or worsening renal function
or serum electrolytes, which may precipitate arrhythmias or
muscle cramps.
HFSA 2010 Practice

Guideline
Acute HFDiuretics & Assessment
Recommendation 12.7
Careful repeated assessment of

signs and symptoms of
congestion and changes in body
weight is recommended, because
clinical experience suggests it is
difficult to determine that
congestion has been adequately
treated in many patients.
HFSA 2010 Practice

Guideline
Acute HFDiuretics &Monitoring
Recommendation 12.8
Monitoring of daily weights, intake, and

output
is recommended to assess
clinical efficacy of diuretic therapy.
Routine use of a Foley catheter is not
recommended for monitoring volume status.
However, placement of a catheter is
recommended when close monitoring of
urine output is needed or if a bladder outlet
obstruction is suspected of contributing to
worsening renal function.
1 of 2
HFSA 2010 Practice

Guideline
Acute HFDiuretic Side Effects
Recommendation 12.9 (1 of 2)
Careful observation for development of a

variety of side effects, including renal
dysfunction, electrolyte abnormalities,
symptomatic hypotension, and gout
is recommended in patients treated with
diuretics, especially when used at high
doses and in combination.
Patients should undergo routine laboratory
studies and clinical examination as dictated
by their clinical response.
Strength of
Evidence = C
2 of 2
HFSA 2010 Practice

Guideline
Acute HFDiuretic Side Effects
It is recommended that serum potassium

and magnesium levels be monitored at
least daily and maintained in the normal
range. More frequent monitoring may be
necessary when diuresis is rapid.
Overly rapid diuresis may be associated

with severe muscle cramps. If indicated,
treatment with potassium replacement
should be considered.
Strength of
Evidence = C
HFSA 2010 Practice

Guideline
Acute HFDiuretics & Renal

Dysfunction
Recommendation
12.10
Careful observation for the
development of renal dysfunction is
recommended in patients treated with
diuretics.
Patients with moderate to severe renal
dysfunction and evidence of fluid
retention should continue to be treated
with diuretics.
In the presence of severe fluid
overload, renal dysfunction may
improve with diuresis.
Strength of
Evidence = C
HFSA 2010 Practice

Guideline
Acute HFDiuretic Alternatives
Recommendation 12.11
When congestion fails to improve in response to
diuretic therapy, the following options should be
considered:
Re-evaluating presence/absence of congestion,

Restricting sodium and fluid,
Increasing doses of loop diuretic,
Continuous infusion of a loop diuretic,
Or addition of a second type of diuretic orally
(metolazone or spironolactone) or intravenously
(chlorothiazide).
Another option, ultrafiltration, may be

considered.
HFSA 2010 Practice

Guideline
Acute HFSodium
A low sodium diet (2 g daily) is

recommended for most hospitalized
patients.
In patients with recurrent or
refractory volume overload, stricter
sodium restriction may be
considered.
HFSA 2010 Practice

Guideline
Acute HFFluid Restriction
Fluid restriction (<2 liters/day):
Is recommended in patients with moderate

hyponatremia (serum sodium < 130 mEq/L)
Should be considered to assist in treatment of
fluid overload in other patients.
In patients with severe (serum sodium

< 125 mEq/L) or worsening
hyponatremia, stricter fluid restriction
may be considered.
Strength of Evidence =
HFSA 2010 Practice

Guideline
Acute HF--Oxygen
Routine administration of
supplemental oxygen:
Is recommended in the presence of
hypoxia.
Is not recommended in the
absence of hypoxia.
=C
HFSA 2010 Practice

Guideline
Acute HF--NIV
Recommendation 12.15 (NEW in 2010)
Use of non-invasive positive

pressure ventilation may be
considered for severely
dyspneic patients with clinical
evidence of pulmonary edema.
=C
HFSA 2010 Practice

Guideline
Acute HFVT Prophylaxis
Recommendation 12.16 (NEW in 2010) 1 of 2
Venous thromboembolism prophylaxis

with low dose unfractionated heparin,
low molecular weight heparin, or
fondaparinux to prevent proximal
deep venous thrombosis and
pulmonary embolism is recommended
for patients who are admitted to the
hospital with ADHF and who are not
already anticoagulated and have no
contraindication to anticoagulation.
HFSA 2010 Practice

Guideline
Acute HFVT Prophylaxis
Recommendation 12.16 (NEW in 2010) 2 of 2
Venous thromboembolism prophylaxis

with a mechanical device (intermittent
pneumatic compression devices or
graded compression stockings ) to
prevent proximal deep venous
thrombosis and pulmonary embolism
should be considered for patients who
are admitted to the hospital with ADHF,
who are not already anticoagulated, and
who have a contraindication to
anticoagulation.
HFSA 2010 Practice

Guideline
Acute HFIV Vasodilators
In the absence of symptomatic hypotension,
intravenous nitroglycerin, nitroprusside or
nesiritide may be considered as an addition to
diuretic therapy for rapid improvement of
congestive symptoms in patients admitted
with ADHF.
Frequent blood pressure monitoring is recommended

with these agents.
These agents should be decreased in dosage or
discontinued if symptomatic hypotension or
worsening renal function develops.
Strength of
Evidence = B
Reintroduction in increasing doses may be
considered once symptomatic hypotension is
resolved. Strength of Evidence = C
HFSA 2010 Practice

Guideline
Intravenous vasodilators
(intravenous nitroglycerin or
nitroprusside) and diuretics are
recommended for rapid symptom
relief in patients with acute
pulmonary edema or severe
hypertension.
HFSA 2010 Practice

Guideline
Intravenous vasodilators may be

considered in patients with ADHF
who have persistent severe HF
despite aggressive treatment with
diuretics and standard oral
therapies.
Nitroprusside
Nitroglycerine, nesiritide
Strength of
Evidence = C
1 of 3
HFSA 2010 Practice

Guideline
Acute HFIV
Recommendation
12.20 (1 of Inotropes
3)
Intravenous inotropes (milrinone or

dobutamine) may be considered to relieve
symptoms and improve end-organ function in
patients with advanced HF characterized by:
LV dilation
Reduced LVEF
And diminished peripheral perfusion or end-organ
dysfunction
(low output syndrome)
Particularly if these patients:
Have marginal systolic blood pressure (<90 mm Hg),

Have symptomatic hypotension despite adequate
filling pressure,
Or are unresponsive to, or intolerant of, intravenous
vasodilators.
2 of 3
HFSA 2010 Practice

Guideline
Acute HFIV Inotropes
These agents may be considered in similar patients

with evidence of fluid overload if they respond
poorly to intravenous diuretics or manifest
diminished or worsening renal function.
When adjunctive therapy is needed in other

patients with ADHF, administration of vasodilators
should be considered instead of intravenous
inotropes (milrinone or dobutamine).
Intravenous inotropes (milrinone or dobutamine)

are not recommended unless left heart filling
pressures are known to be elevated or cardiac
index is severely impaired based on direct
measurement or clear clinical signs.
Strength
of Evidence = C
3 of 3
HFSA 2010 Practice

Guideline
Acute HFIV Inotropes
It is recommended that administration of

intravenous inotropes (milrinone or
dobutamine) in the setting of ADHF be
accompanied by continuous or frequent
blood pressure monitoring and
continuous monitoring of cardiac rhythm.
If symptomatic hypotension or worsening

tachyarrhythmias develop during
administration of these agents,
discontinuation or dose reduction should
be considered.
HFSA 2010 Practice

Guideline
Acute HFHemodynamic Monitoring
The routine use of invasive

hemodynamic monitoring in
patients with ADHF is not
recommended.
Strength of
Evidence = A
HFSA 2010 Practice

Guideline
Acute HFHemodynamic Monitoring

Invasive hemodynamic monitoring should be
considered in a patient:
Who is refractory to initial therapy

Whose volume status and cardiac filling pressures
are unclear
Who has clinically significant hypotension
(typically SBP < 80 mm Hg) or worsening renal
function during therapy
Or who is being considered for cardiac transplant
and needs assessment of degree and reversability
of pulmon. hypertension
Or in whom documentation of an adequate
hemodynamic response to the inotropic agent is
necessary when chronic outpatient infusion is
being considered
HFSA 2010 Practice

Guideline
Acute HFEvaluation for Precipitating

Factors
It is recommended that patients admitted

with ADHF undergo evaluation for the
following precipitating factors:
Atrial fibrillation or other arrhythmias (e.g.,

atrial flutter, other SVT or VT)
Exacerbation of hypertension
Myocardial ischemia/infarction
Exacerbation of pulmonary congestion
Anemia, thyroid disease
Significant drug interactions
Other less common factors
HFSA 2010 Practice

Guideline
Acute HFPatient Education
It is recommended that every

effort be made to utilize the
hospital stay for assessment and
improvement of patient adherence
via patient and family education
and social support services.
HFSA 2010 Practice

Guideline
Acute HFDischarge Criteria
It is recommended that criteria in

Table 12.7 be met before a patient
with HF is discharged from the
hospital.
In patients with advanced HF or
recurrent admissions for HF,
additional criteria listed in Table 12.7
should be considered.
Strength of
Evidence = C
HFSA 2010 Practice

Guideline
Acute HFTable 12.7. Discharge

Recommended Exacerbating factors addressed
Criteria
Near optimal volume status observed
for all HF
patients
Transition from intravenous to oral diuretic

successfully completed
Patient and family education completed, including
clear discharge instructions
Near optimal pharmacologic therapy achieved,
including ACEI and BB (for patients with reduced
LVEF) or intolerance documented
Follow-up clinic visit scheduled, usually for 7-10
days
Should be
considered for
patients with
advanced HF
or recurrent
admissions for
HF
Oral medication regimen stable for 24 hours

No intravenous vasodilator or inotropic agent for 24
hours
Ambulation prior to discharge to assess functional
capacity after therapy
Plans for post-discharge management (scale
present in home, visiting nurse or telephone follow
up generally no longer than 3 days after discharge)
Referral for disease management, if available
HFSA 2010 Practice

Guideline
Acute HFDischarge Planning
Discharge planning is recommended as part of the
management of patients with ADHF. Discharge
planning should address the following issues:
Details regarding medication, dietary sodium

restriction and recommended activity level
Follow-up by phone or clinic visit early after
discharge to reassess volume status
Medication and dietary compliance
Alcohol moderation and smoking cessation
Monitoring of body weight, electrolytes and renal
function
Consideration of referral for formal disease
management
Heart Failure
and VADs
Bridges for Broken

PriyaHearts
Gaiha MD MBA
May 26th 2010
University of Kentucky
Grand Rounds
Objectives
What is the pathophysiology of heart failure?
Why is heart failure relevant?
What is the history of mechanical circulatory

support?
What are the various types of ventricular assist

devices (VADs)?
How and when are VADs used?
What is the next generation of VADs?
Etiologies of cardiac
failure

Idiopathic cardiomyopathy
Peripartum cardiomyopathy
Dilated cardiomyopathy
Ischemic cardiomyopathy
Acute valvular disease
Arrhythmia (supraventricular or ventricular)
Myocarditis
Congenital heart disease
Drug induced
Diabetes mellitus
Hypertension
Pathogenesis of Heart
Failure
Mann, D. Circulation 1999;100;999-1008
NYHA classes
Class
PatientSymptoms
ClassI(Mild)
Nolimitationofphysicalactivity.Ordinaryphysical
activitydoesnotcauseunduefatigue,palpitation,or
dyspnea(shortnessofbreath).
ClassII(Mild)
Slightlimitationofphysicalactivity.Comfortableat
rest,butordinaryphysicalactivityresultsinfatigue,
palpitation,ordyspnea.
ClassIII
(Moderate)
Markedlimitationofphysicalactivity.Comfortable
atrest,butlessthanordinaryactivitycausesfatigue,
palpitation,ordyspnea.
ClassIV(Severe)
Unabletocarryoutanyphysicalactivitywithout
discomfort.Symptomsofcardiacinsufficiencyat
rest.Ifanyphysicalactivityisundertaken,
discomfortisincreased.
www.americanheart.org
Relevance
Options for Advanced

CHF
Transplant ($$$$$$)
Assist Device ($$$)
Die($)
Preceded by 6-12 months of medical
therapy
Multiple hospital re-admissions
Hospice ($$$)
Transplant
John Gibbon
Born in 1903 in Philadelphia

4th generation physician
1931: watched a young
woman postop from
cholecystectomy die from PE
Worked for 20 years on dogs
to refine bypass machine
Received financial and
technical support from
Thomas Watson of IBM
1953: first successful use of
machine on patient during
ASD repair
Christian Barnard
inCapeTown.
Short term Device

options
ECMO
IABP
Tandem Heart
Bridge to recovery
Bridge to decision
Centrimag
AbioMed 5000
Impella
Circulation 112 (3): 438
Intraaortic Balloon Pump

(IABP)
Developedinlate1960s
CounterpulsationissynchronizedtotheEKGor
arterialwaveforms
Increasecoronaryperfusion
Decreaseleftventricularstrokeworkand
myocardialoxygenrequirements
Mostwidelyusedformofmechanicalcirculatory
support
Indicationsforitsuseinclude
Failuretoweanfromcardiopulmonarybypass
CardiogenicshockafterMI
Heartfailure
Refractoryventriculararrhythmiaswith
ongoingischemia
Bridge to bridge:
ECMO
Immediately stabilize
Immediately stabilize
circulation
Improve end organ perfusion
Overall survival comparable
between ECMO + LVAD versus
LVAD alone
Clinical indicators of poor
outcome after ECMO: consider
VAD implantation carefully
Elevated blood lactate levels
Elevated LFTs
Pagani et al. Ann Thorac Surg 2000; 70:1977-8
Centrifugal pumps
Acute hemodynamic
support
Continuous flow
Extracorporeal
LV, RV or biventricular
support
Wide availability
Ease of use
Relatively low cost
Limited duration of support
Bridge to recovery
Bridge to decision
Hoy et al. Ann Thorac Surg 2000; 70:1259
Tandem
hearts
Acute hemodynamic support

Centrifugal pump
Percutaneous placement
LV support via transseptal
cannula
Used in high risk cardiac
catheterization procedures
Risk of vascular injuries due
to cannula size
Abiomed 5000
Extracorporeal
Pneumatic pulsatile
pumps
Uni- or biventricular
support
Easy to insert and
operate so used in
community hospitals
Flows 6L/min
Circulation. 2005;112:438-448.
Long term Device

options
Heartmate XVE
Jarvik 2000
Heartmate II
Thoratec
CardioWest TAH
Circulation 112 (3): 438
Thoratec
Pneumatic pump
LVAD, RVAD or
biventricular support
Durable
Can be used in
smaller patients
Flows 7L/min
Bridge to recovery
Circulation. 2005;112:438-448.
Heartmate
XVE
Pneumatic or vented
electric plates
Textured internal surfaces
Only left-sided support
Flows 10L/min
First device to be
approved for destination
therapy
Need BSA>1.5
Limited durability: half life
18 months
Infection risk with
percutaneous drive line
Circulation. 2005;112:438-448.
Heartmate
II
Axial flow
LV support
Flows 10L/min
Long term durability
Approved January 2010
for destination therapy
Over 4000 devices
implanted to date
Implantation of device
N Engl J Med 2007;357:88596
Implantation
Device complications
Early
Bleeding
Right sided heart failure
Progressive multiorgan system failure
Late
Infection
Nosocomial
Device related
Thromboembolism
Failure of device
Cellular benefits of VADs
Normalization of fiber orientation

Regression of myocyte hypertrophy
Reduction in contraction band necrosis
Reverse ventricular dilation
Improvement in EDPVR
Improved efficiency of myocardial

mitochondria
Reduction in abnormalities along
neurohormonal and cytokine pathways
Circulation. 1998;98:2367-2369.
Indicators of poor
clinical outcome
Advanced age
Independent predictor of poor survival

Independent predictor of poor bridge to transplant
37% post 30-day LVAD mortality
Age limit? >65 yo contraindication to transplant
Female
Independent predictor of poor survival

Independent predictor of poor bridge to transplant
Higher mortality
Longer waiting time to transplant due to size criteria
Increased operative mortality
Smaller BSA
Impaired wound healing
JCTS 2005:130;5: 1302-1311
Indicators of poor
clinical outcome
Diabetes mellitus
4-fold increased risk of early death

Associated with end organ failure
Renal failure
Increased allograft vasculopathy after transplant

Type I DM is contraindication to transplant
Low preoperative serum albumin
Surrogate measure of nutritional status

Increased infections and impaired wound healing
For every 1 mg/dL increase in albumin, had 19.2 times
increased likelihood for bridge to transplant
JCTS 2005:130;5: 1302-1311
Myocardial
recovery
Certain proportion of
idiopathic dilated
cardiomyopathy patients
have potential for
complete cardiac
recovery: 15-20%
Younger age
Shorter history of heart
failure
Faster and more complete
restoration of pump
function
Diminished fibrosis seen in
myocyte biopsies
Ann Thorac Surg 2001; 71:S109-13
Congestive Heart
Failure
Jarrod Eddy, PGY2
Internal Medicine
Sub-I Lecture Series
Clinical presentation of disease

NOT a diagnosis in and of itself
Differential includes
Underlying cardiovascular disease
Precipitating factors
Predisposing Cardiac
Diseases
Myocardial infarction
Chronic ischemia
Cardiomyopathy
Arrhythmias
Valvular diseases
Aortic Stenosis
Mitral Stenosis
Mitral Regurgitation
Cardiac Physiology
(remember this?)
CO = SV x HR
HR: parasympathetic and

sympathetic tone
SV: preload, afterload, contractility
Preload
Def: Passive stretch of muscle prior to

contraction
Measurement: Swan-Ganz
Really a function of LVEDV

Affected by compliance
LVEDP
Low compliance = higher LVEDP @ lower

LVEDV
False high estimate of preload
Frank-Starling right?
Afterload
Def: Force opposing/stretching

muscle after contraction begins
Measurement: SVR
Really a function of:
SVR
Chamber radius (dilated
cardiomyopathies)
Wall thickness (hypertrophy)
Contractility
Def: Normal ability of the muscle to

contract at a given force for a given
stretch, independent of preload or
afterload forces
In other words:
How healthy is your heart muscle?
Ischemia, Hypertrophy (?), Muscle loss
Classifying Heart Failure
Anatomically
Physiologically
Left versus Right
Systolic versus Diastolic
Functionally
How symptomatic is your patient?
Left versus Right Failure

Left Heart Failure
- Dyspnea
- Dec. exercise
tolerance
- Cough
- Orthopnea
- Pink, frothy
sputum
Right Heart
Failure
- Dec. exercise
tolerance
- Edema
- HJR / JVD
- Hepatomegaly
- Ascites
Systolic versus Diastolic
Systolic cant
pump
Aortic Stenosis
HTN
Aortic Insufficiency
Mitral Regurgitation
Muscle Loss
Ischemia
Fibrosis
Infiltration
Diastolic- cant
fill
Mitral Stenosis
Tamponade
Hypertrophy
Infiltration
Fibrosis
Clinical Data
CXR
Kerleys lines : A and B
Pulmonary Edema
Cephalization
Pleural Effusions (bilateral)
EKG
Left atrial enlargement
Arrhythmias
Hypertrophy (left or right)
Cardiomyopathy
Pulmonary Edema
Clinical Data
HEART SOUNDS!!!
Systolic Murmurs
Mitral Regurg
Aortic Stenosis
Diastolic Murmurs
Mitral Stenosis
Aortic Insufficiency
S3: Rapid filling of a diseased ventricle
Clinical Data
Laboratory Data
Chemistry
Renal Function: Be Wary
BNP
Used in ER departments the world over

Good negative correlation
Need baseline for positivity
Pulmonary versus cardiac dyspnea
Treatment of CHF
Treat Precipitating Factor(s)!!!!
Adjust Heart Rate

Decrease Preload
Decrease Afterload
Increase Contractility
Increase Oxygenation
Treatment of CHF
Oxygen nasal, BiPAP, intubation

Morphine
Preload Reduction
Loop diuretics
Nitrates
ACEi / ARB
Morphine
Heart
Failure
Amanda Ryan, D.O.
Cardiology Fellow
February 14th, 2008
Learning Objectives
Following
this presentation, the

participant should be able to:
1. Recognize the magnitude of heart failure epidemic and its public

health implications
2. Distinguish the different classifications and stages of heart failure
3. Review underlying pathophysiology of heart failure
4. Discuss signs and symptoms of heart failure exacerbation
5. Identify current practice guidelines for treatment of acute

decompensated heart failure
What is Heart Failure
Heart failure occurs when the heart

cannot pump enough blood fast
enough to meet the metabolic needs
of the body.
No longer use the term congestive
because all heart failure does not
result in clinically apparent volume
overload
It is an Epidemic
Estimated that over 5 million Americans have

heart failure
Estimated 500,000 new cases per year
Within 5 years, half of those diagnosed will be
dead
Over 1 million hospitalizations per year with HF
as primary diagnosis
Most common reason for hospitalization in those
>65 years old
85% of HF cases are in adults 65 and older
Heart failure is 4th in a list of quality of care
initiatives in vulnerable older adults
Costs of Heart Failure
It is the leading cause of hospitalization in patients older than 65 years

of age and is a primary hospital discharge diagnosis in 1.1 million
people of all ages each year.
It is one medical condition for which mortality continues to increase.

From 1994 to 2004, the overall death rate declined 2.0% in the United
States, but deaths from HF increased 28% in the same time period.
According to the National Heart, Lung, and Blood Institute, the

estimated direct and indirect costs associated with HF care in the US is
$33.2 billion yearly.
The majority of the costs approximately two-thirds are attributable to

the management of episodes of acute HF decompensation (i.e.,
hospitalization).
Different Ways to Define

HF
Dilated (congestive) cardiomyopathy is a group of heart

muscle disorders in which the ventricles enlarge but are
not able to pump enough blood for the body's needs,
resulting in heart failure. (Example - CAD, myocarditis,
EtOH, HIV)
Hypertrophic cardiomyopathy includes a group of heart
disorders in which the walls of the ventricles thicken
(hypertrophy) and become stiff, even though the
workload of the heart is not increased. (Example
congenital HOCM, or acquired)
Restrictive (infiltrative) cardiomyopathy includes a group
of heart disorders in which the walls of the ventricles
become stiff, but not necessarily thickened, and resist
normal filling with blood between heartbeats. (Example
radiation, amyloidosis)

HF
Diastolic Versus Systolic Heart Failure
A. Systolic cardiac (heart) dysfunction (or systolic

heart failure) occurs when the heart muscle
doesn't contract with enough force, so there is
not enough oxygen-rich blood to be pumped
throughout the body.
B. Diastolic cardiac dysfunction (or diastolic heart
failure) occurs when the heart contracts
normally, but the ventricle doesn't relax
properly so less blood can enter the heart.

HF
Clinically, patients are classified as

having HF of ischemic or
nonischemic etiology based on a
history of myocardial infarction (MI)
or based on objective evidence of
coronary artery disease (CAD) such
as angiography or functional testing.
Controversial Definitions
Staging of Heart Failure
New York Heart Association
Class I: No obvious symptoms, no limitations on patient

physical activity (35 percent).
Class II: Some symptoms during or after normal activity,

mild physical activity limitations (35 percent).
Class III: Symptoms with mild exertion, moderate to

significant physical activity limitations (25 percent).
Class IV: Significant symptoms at rest, severe to total

physical activity limitations (5 percent).
Causes of Heart Failure

Problems with the heart muscle itself [known
as cardiomyopathy (myocarditis, etc)]
Hypertension
Problems with any of the heart valves
Abnormal heart rhythms (also called
arrhythmias)
Toxic substances (EtOH, cocaine)
Congenital heart disease
Diabetes
Thyroid problems
HIV
Diastolic HF
Diastolic heart failure is defined as a condition caused by increased resistance

to the filling of one or both ventricles; this leads to symptoms of congestion from
the inappropriate upward shift of the diastolic pressure-volume relation.
40% of patients
Increasing incidence with age
More common in women
HTN and cardiac ischemia are most common causes
Common precipitating factors include volume overload; tachycardia; exercise;

hypertension; ischemia; systemic stressors (e.g., anemia, fever, infection,
thyrotoxicosis); arrhythmia (e.g., atrial fibrillation, atrioventricular nodal block);
increased salt intake; and use of nonsteroidal anti-inflammatory drugs.
More About Diastolic

Dysfunction
Alterations involve relaxation and/or

filling and/or distensibility.
Arterial hypertension associated to
LV concentric remodelling is the main
determinant of DD but several other
cardiac diseases, including
myocardial ischemia, and extracardiac pathologies also possible.
Stages of Diastole
1. Isovolumetric relaxation, period occurring between the end of LV

systolic ejection (= aortic valve closure) and the opening of the mitral
valve, when LV pressure keeps going its rapid fall while LV volume
remains constant.
2. LV rapid filling, which begins when LV pressure falls below left
atrial pressure and the mitral valve opens. During this period the blood
has an acceleration which achieves a maximal velocity, direct related
to the magnitude of atrio-ventricular pressure, and stops when this
gradient ends.
3. diastasis, when left atrial and LV pressures are almost equal and
LV filling is essentially maintained by the flow coming from pulmonary
veins with left atrium representing a passive conduit with an
amount depending of LV pressure, function of LV "compliance".
4. atrial systole, which corresponds to left atrial contraction and ends
at the mitral valve closure. This period is mainly influenced by LV
compliance, but depends also by the pericardial resistance, by the
atrial force and by the atrio-ventricular synchronicity (= ECG PR
interval).
Patient Differences
HF
is a hemodynamic disorder but there is a

poor relationship between measures of
cardiac performance and patient symptoms
For example, pts with very low EF may be
asymptomatic while someone with preserved
EF may be severely disabled with symptoms
Body Compensatory
Mechanisms
Epinephrine and norepinephrine release which increases heart rate and

contractility which increased myocardial work load
Decrease salt and water excretion from kidneys which helps maintain
BP by increasing blood volume, this leads to stretching of hearts
chambers which can impair ability to contract
Hypertrophy and thickening of heart muscle which initially increases
contractility but over time leads to stiff chambers and can impair
contractility
HF patients have higher levels of epinephrine, norepinephrine,
aldosterone, angiotensin II, endothelin, inflammatory cytokines, and
vasopressin which contribute to heart remodeling, progression of HF,
and higher levels are associated with increased mortality
Potential Reasons
Alternation in ventricular distensibility

Valvular regurgitation
Pericardial restraint
Cardiac rhythm
Conduction abnormalities
RV function
Also several non-cardiac factors including
peripheral vascular fxn, reflex autonomic
activity, renal sodium handling, etc.
HF Risk Factors - History
Smoking
EtOH use
DM
HTN
Dyslipidemia
Thyroid disorder
Chemotherapy
Radiation
Cardiotoxic drugs
Fam Hx of sudden
death, CAD,
conduction
problems, HCM
HIV status
Cardiovascular Medical
Hx
Hx of heart failure
Angina
MI
CABG
PCI
Pacemaker/ICD
Embolic events
arrhythmias
CVA
PVD
Rheumatic Dx
Other valvular hx
Congenital
Signs and Symptoms of

HF
Dyspnea
PND
Orthopnea
Cough
Exercise intolerance
Edema
Fatigue
Nausea
Abdominal Fullness
Rales
S3
Pulmonary edema
JVD
Tachycardia
Cardiomegaly
Hepatojugular reflex
Peripheral Edema
Hepatomegaly
HF Diagnosis and
Assessment
Remains primarily a clinical

diagnosis but additional information
via other diagnostics can be
beneficial
Evaluation depends on if this is first
presentation, change in clinical
symptoms, certainty of diagnosis, etc
Chronic Congestive Heart

Failure
Evolution of Clinical Stages
NORMAL
Asymptomatic
LV Dysfunction
Compensated
CHF
Decompensated
CHF
Refractory
CHF
No symptoms
Normal exercise
Normal LV fxn
No symptoms
Normal exercise
Abnormal LV fxn
No symptoms
Exercise
Abnormal LV fxn
Symptoms
Exercise
Abnormal LV fxn
Symptoms not controlled

with treatment
Ventricular Remodeling
in CHF
Jessup, NEJM 2003
Symptoms of HF
Fatigue
Activity
decrease
Cough (especially supine)
Edema
Shortness of breath
DIET Approach to the

Patient With Heart
Failure
Diagnose
Educate
Etiology
Severity (LV
dysfunction)
Initiate
Diuretic/ACE
inhibitor
-blocker
Spirololactone
Digoxin
Diet
Exercise
Lifestyle
CV Risk
Titrate
Optimize ACE
inhibitor
Optimize -blocker
Therapy of CHF
Clinical Approach to CHF:

Consider etiology
Identify triggers
Exclude ischaemia
General measures
Symptomatic therapy
Prognostic therapy
See Guide for HF Management Check-list
Symptoms & Signs of HF:
Fatigue (low cardiac out-put)

SOB
JVP
Rales
S3
Edema
Radiologic congestion
Cardiomegaly
Obtain CXR to r/o non-cardiac causes e.g.

interstitial lung disease & PPH
BNP in the Diagnosis of HF

The role of natriuretic peptides
ANP-atrial natriuretic peptide
BNP-brain natriuretic peptides
Produced in ventricles in response to volume and

pressure overload
CNP-central nervous system and endothelium
Produced in atria in response to wall stress
Produced in response to endothelial stress
Produced as prohormones and cleaved to active

molecule (ANP/BNP)and inactive NT forms

ANP/BNP elevated in
Heart failure
Systemic and pulmonary hypertension
Hypertrophic and restrictive cardiomyopathy
Pulmonary embolism
COPD
Cor pulmonale
AMI Cirrhosis
Renal Failure

Higher levels of BNP correlate with
higher PCW pressures
larger LV volumes
lower ejection fractions
in compensated and decompensated patients
in symptomatic HF patients
BNP study (Circ 2002;106: 416-422)
BNP sensitivity 90% and specificity 73% for

HF
BNP Diagnostic Cut Points

for CHF
JACC 2001;37(2):379-85.
BNP > 400 pg/L acute CHF present

BNP 100 pg/L 400 pg/L
Diagnostic of CHF with
Sensitivity 90%
Specificity 76%
Predictive accuracy 83%
R/O pulmonary embolism, LV dysfunction
without acute CHF or cor pulmonale
BNP < 100 pg/L 98% negative predictive

accuracy
Identify triggers
Acute-sudden
onset
Ischaemia
Arrhythmia
Infection
Pulmonary
embolism
Acute valvular
pathology
Chronic-gradual
onset
Anemia
Thyrotoxicosis
Non-compliance
Diet
Rx e.g. NSAIDs
Non-Invasive Evaluation of the

Heart Failure Patient-Implications
of LV Ejection Fraction
To know where you

are going you must
know where you
are coming from
Evaluate LV
function
clinical
echo
gated study
Ejection fraction
(obtain echo or LV gated study)
LVEF 40% = systolic dysfunction

LVEF 40-55% = mixed systolic and
diastolic dysfunction
LVEF 55% = diastolic dysfunction
identify triggers
treat underlying disorder
(HPT/ischaemia/pericardial
constriction/restrictive
CM/infiltrative disorders)
Echocardiographic
Evaluation
of CHF
LV function
(EF),chamber size,wall
motion
Segmental dysfunctioncoronary disease
MS-severity, valve area
AS- valve gradient,
valve area
AR/MR severity
TR- RV systolic
pressure = PA pressure
RV function
R/O IHSS, HCM
R/O Pericardial
Disease
R/O rare causes e.g.
myxoma, infiltrative
disorders- restrictive
cardiomyopathy
Diastolic function
Hyperdynamic states
Diastolic Dysfunction
30-50% of elderly HF patients have

reserved LV systolic function
Diastolic dysfunction may induce
dyspnea on exertion
Frank congestion usually has
identifiable precipitant
Clinical Implications of
LV Dysfunction in Heart
Failure
Calculated EF by
echo unreliable in
remodeled LV
Visual estimate of EF
semi-quantitative
(CCN LV function
scale)
Grade I LV EF 50%
Grade 2 LVEF 35-49%
Grade 3 LVEF 20-34%
Grade 4 LVEF< 20%
LVEF Entry Criteria in

ACE inhibitor and
-blocker Trials
SOLVD treatment an
prevention 35%
SAVE (post MI) 40%
U.S. Carvedilol HF Trials
Program LVEF 35%
Merit-HF LVEF 40%
CIBIS II LVEF 40%
Consider etiology
Ischemic- Cardiomyopathy (CM)

HPT-CM
Valvular HD-CM (AS/AR/MR)
Metabolic:
Toxins:
/ thyroid/hemochromatosis/
pheochromocytoma
Anthracyclines/Etoh/cocaine/amphetamines
Viral CM
Idiopathic Dilated CM
Other:
Treatment
General Measures
General
measures:
Correct triggers and

precipitants of acute
and chronic HF
Low sodium diet
Fluid restriction
Regular exercise/
Activity HR Rx
Treat ischemia
Control
hypertension
D/C Smoking
Treat lipid
abnormalities
Treat and control
diabetes
Identify & Rx
depression
HF Management
Algorithm
Is it Heart Failure?
Symptoms & Signs
YES
Diagnostic Tests:
CXR/ECG/BNP
Additional Tests
Specific Tx
Cath
CABG
Valve Sx
YES
Echo/RNA/MRI:
Etiology/Severity
Systolic HF:
MedicalSx/Device
Life Style +
Patient Education
HF Clinics F/U
Diastolic HF:
Rx causeReferral
Primary Targets of
Treatments
in CHF
Jessup, NEJM 2003
Symptoms
Prognosis & Symptoms
Assess LV Function (echo, gated RNA)

EF < 40%-systolic dysfunction
EF 40-55%-systolic/diastolic dysfunction
EF >55%-diastolic dysfunction
Assess Volume Status
Signs and Symptoms of

Fluid Retention
Loop Diuretic
+/- Thiazide
(titrate to euvolemic state)
Add Digoxin for

symptom control
No Signs and Symptoms

of Fluid Retention
ACE inhibitor/ARB if ACE intolerant

Combination Rx if HF, hospitalization or -blocker intolerant
-blocker (NYHA II-IV)

Spironolactone
(NYHA Class III-IV CHF/EF<35%/Cr<200/K<5)
Heart Failure
Therapeutic Goal
Mild-Moderate Heart Failure

Primary goal = Reduce mortality
-blockers + ACE inhibitors
Prevent progression to
symptoms
Prevent progressive LV
dysfunction
Heart Failure
Therapeutic Goal
Moderate-Severe Heart Failure

Primary goal = Reduce
symptoms
Improve quality of life (QOL)
Reduce hospitalizations
Prevent sudden death
General Rx Strategies in
HF
Asymptomatic
Mild/Mod
Severe
Refractory
Inotropes, mitral repair, VAD, Tx
Correct Cause:
Arrhythmias
Ischemia
Pressure Load
Tailored Rx
Digoxin
Diuretics (Spironolactone)
Carvedilol/ -Blockers
Angiotensin Converting Enzyme Inhibitors

No Added Salt
Activity as Tolerated
Modified from Warner-Stevenson, ACC HF Summit
2 gm Na
Customized Ex Training
Severity of Heart
Failure
Modes of Death
NYHA II
12%
24%
64%
NYHA III
CHF
CHF
Other
26%
Sudden
Death
59%
15%
n = 103
Other
Sudden
Death
n = 103
NYHA IV
33%
11%
56%
CHF
Other
Sudden
Death
n = 27
MERIT-HF Study Group. LANCET

1999;353:2001-07.
Therapies Provided by
Todays
Dual-Chamber ICDs
Atrium
AT/AF tachyarrhythmia
detection
Antitachycardia pacing
Cardioversion
Ventricle
Atrium &
Ventricle
VT/ VF detection
Bradycardia sensing
Antitachycardia pacing
Bradycardia pacing
Cardioversion
Defibrillation
Cardiac
Resynchronization
Therapy
(CRT)
Atrial-biventricular
stimulation
Electrical
synchronization
narrower QRS
Mechanical
synchronization
reverse
remodeling
Stages of Heart Failure
At Risk for Heart Failure:

STAGE A High risk for developing HF
STAGE B Asymptomatic LV dysfunction
Heart Failure:
STAGE C Past or current symptoms of HF
STAGE D End-stage HF
Acute heart failure

AHF: The rapid onset of symptoms and signs secondary to
abnormal cardiac function.
(reduced CO, tissue hypoperfusion + congestion, increase in PCWP)
1.
2.
3.
With or without previous cardiac disease.

The cardiac dysfunction can be related:
a) to systolic or diastolic dysfunction
b) to abnormalities in cardiac rhythm
c) to preload and afterload mismatch
Often life threatening and requires urgent treatment.
The Task Force on Acute Heart Failure of the European Society of Cardiology
BACKWARD
FAILURE
:
Increased
pulmonary
venous pressure,
pulmonary edema
FORWARD FAILURE (Low Cardiac Output):

Decreased perfusion of the brain (confusion).
kidneys (impaired renal function),
skin (cyanosis) etc.
Acute heart failure

Epidemiology
1.
2.
Increase of pts with CHF (aging of population +

improved survival) = increase in the number of
hospitalisations for the decompensated heart failure .
Poor prognosis: AMI + SHF: 30% annual mortality
APO: 40% annual mortality
12% in-hospital mortality
CAD: 60-70% (particularly in elderly population)
Dilated cardiomyopathy, arrhythmia, congenital or VHD or
myocarditis: in youmger subjects.
Acute Heart Failure :

Classification
Can present itself as:
Acute de novo (new onset of AHF in a

patient without previously known
cardiac dysfunction).
or
Acute decompensation of chronic
heart failure.
*PHARMACOLOGICAL STRATEGIES :
New drugs.
Pharmacogenetics.
Metabolic modulation.
Immunomodulation.
*Nonpharmacological Strategies:
Myocardial repair and regeneration by:
Stem cell&| progenetorcells
Tissue engineering
*Gene therapy.
*DEVICE THERAPY:
CRT
NEW VAD
*INTERVENTION.
New drugs
NEW ENOTROPICS.
AQUARETICS &NATRIURETICS.
ENDOTHELIN ANTAGONISTS.
NEW B-BLOCKERS.
BROMOCRIBTIN.
Adaptation in HF-Sympathetic
nervous system is activated
Heart rate
Force of contraction
Dilatation of coronary
arteries
Perif. vascular resistance

Redistribution (renal blood
supply)
Direct cytotoxic effect
Apoptosis
Activation of the RAAS
Adaptation-Activation of
the RAAS
Blood pressure
Perfusion of the
juxtaglom. appartus
renin
SA activation
Sodium and water retention
Vasoconstriction
Aldosterone
ADH (vasopressin)
Myocardial hypertrophy
Myocardial fibrosis
Endothel dysfunction
Coagulation

Curs Ic - Ic Si Ci - Final - 11 - Nov 2013

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Congestive Heart Failure

Prof Univ Dr Ion C.Tintoiu FESC

Clinical syndrome that can result from any

The hearts inability to pump

Can be systolic or diastolic,

Heart failure is a clinical syndrome usually

Modern clinical definition

A normal heart pumps blood in a smooth and

A heart failure heart has a reduced ability to

Adaptation in heart failure

LV mass, size, shape is altered

Congestive Heart Failure

Post MI, Chronic ischemia

Adapted from Cohn JN. N Engl J Med. 1996;335:490498.

Congestive Heart Failure

From hemodynamic stand point HF

Changes in contractile proteins

Diagnosis of heart failure

Lab tests: BNP,

Cinical symptoms and

Congestive Heart Failure

Jugular Venous Distention

Congestive Heart Failure

Congestive Heart Failure

Congestive Heart Failure

Look for Heart size

Congestive Heart Failure

Congestive Heart Failure

Congestive Heart Failure

A Key Indicator for Diagnosing

Systolic vs. Diastolic

Most common is a combination of

Congestive Heart Failure

Congestive Heart Failure

sudden onset with associated signs and

sudden exacerbation or onset of

Acute Heart Failure

Often precipitated by a myocardial

FORWARD FAILURE (Low

Chronic Heart Failure

Making an accurate diagnosis of heart failure and

Shortness of breath on exertion (sensitivity 66%, specificity 52%)

Acute vs. Chronic

Acutean emergency situation in

Systolic (pumping problem)inability of the

Diastolic (filling problem)inability of the left

Left-sidedinability of the left ventricle to pump

Right-sidedinefficient pumping of the right side

Left-Sided Heart Failure

Dizziness and lightheadedness

Fatigue and weakness

Third heart sound

A At high risk for heart failure but without

C Structural heart disease with prior or

D Refractory heart failure requiring

II Symptomatic with moderate exertion

Hunt SA et al. J Am Coll Cardiol. 2001;38:21012113.

Current & Future

ACE-I, Betablockers, and

Treatment of heart failure

Congestive Heart Failure

Diuretics & ACEI reduces the number of

symptoms, oedema, prognosis