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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

Congestive Heart Failure


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

Congestive 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

Congestive Heart Failure


CHF
ORTHOPNEA

Jugular Venous Distention


not directly related to LVEF

Congestive Heart Failure


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

Congestive Heart Failure


CHF
Rhythm problems leading to CHF

Congestive Heart Failure


CHF
Chest X-ray

Look for Heart size


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

Congestive Heart Failure


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

Congestive Heart Failure


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

Congestive Heart Failure


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

Congestive Heart Failure


CHF Diastolic CHF

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

Congestive Heart Failure


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

Congestive Heart Failure


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

symptoms, prognosis, mortality


remodelling, myocardial fibrosis
starting dose, target dose
Hypotension
Hyperlakaemia, renal dysfunction
Cough
Angio-oedema

-Blockers
Limit the donkeys speed, thus saving energy

Congestive Heart Failure


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

Congestive Heart Failure


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

Congestive Heart Failure


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

Cardiac Resynchronization Therapy


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

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
Ischemic Heart Disease
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
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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???
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

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???


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

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

Congestive Heart Failure


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

BorninSouthAfricain1922

Studiedheartsurgeryatthe
UniversityofMinnesotathen
returnedtosetupacardiacunit
inCapeTown.

December1967:transplantedthe
heartofaroadaccidentvictim
intoa59yearoldpatient

Patientonlysurvived18days
duetoinfectiouscomplications

Outpatient Therapy

210

Congestive Heart Failure


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.

Congestive Heart Failure


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.

Congestive Heart Failure


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.

Congestive Heart Failure


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

Congestive Heart Failure


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

Congestive Heart Failure


CHF
New Treatment Choices
Implantable ventricular assist devices
Biventricular pacing (only in patient

with LBBB & CHF)


Artificial Heart

Device Therapy:
Biventricular
Pacing

Biventricular Pacing
Ventricular Dysynchrony

Abnormal ventricular conduction


resulting in a mechanical delay and
dysynchronous contraction

Overview of Device Therapy

241

BiV Pacing

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

Ventricular remodelling

Excitation-contraction
coupling
Electrical dyssynchrony
Mechanical dyssynchrony
Dysrhythmias !

Defibrillators
(ICDs)

Newer Generation Artificial


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

Diagnosis of heart failure

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

Diagnosis of heart failure


Physical examination

X-ray, ECG,
Echo, SpiroErgometry

Medical history

Lab tests: BNP,

ACE inhibitors

symptoms, prognosis, mortality


remodelling, myocardial fibrosis
starting dose, target dose
Hypotension
Hyperlakaemia, renal dysfunction
Cough
Angio-oedema

Betablockers

symptoms, prognosis, mortality


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

Aldosterone antagonists

symptoms, prognosis, mortality


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

Clinical Classifications

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

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
262

Clinical Classifications
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

Clinical Classifications
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

HFSA 2010 Practice Guideline (7.23)

Pharmacologic Therapy:
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

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

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

All available for oral or IV administration

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

Strength of Evidence = A
Strength of Evidence = B

In

patients who are undergoing implantation of a


biventricular pacing device, use of a device that
provides defibrillation should be considered.
Strength of Evidence = B

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

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
Strength of Evidence = C
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
Strength of Evidence = C

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%

Biventricular Pacing
Ventricular Dysynchrony

Abnormal ventricular conduction


resulting in a mechanical delay and
dysynchronous contraction

Overview of Device Therapy

307

BiV Pacing

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)

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.

Newer Generation Artificial


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
Aldosterone Antagonists
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

Optimize drug therapy


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


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

Optimize drug 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

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

HFSA 2010 Practice Guideline (7.23)

Pharmacologic Therapy:
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

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

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

All available for oral or IV administration

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

Strength of Evidence = A
Strength of Evidence = B

In

patients who are undergoing implantation of a


biventricular pacing device, use of a device that
provides defibrillation should be considered.
Strength of Evidence = B

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 (9.7)

Device Therapy:
Biventricular Pacing

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.
Strength of Evidence = A

HFSA 2010 Practice Guideline (11.111.2)

HF with Preserved LVEF


Diagnosis
Careful attention to differential diagnosis is

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
Strength of Evidence = C
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
Strength of Evidence = C

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

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

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)

Aldosterone Antagonists

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)


Cardiac Resynchronization Therapy
(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

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

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

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

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

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

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

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

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

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

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.

Strength of Evidence = B

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.
Strength of Evidence = C

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.
Strength of Evidence = C

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.
Strength of Evidence = C

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.
Strength of Evidence = C

HFSA 2010 Practice


Guideline

NonpharmacologicNutraceuticals

Recommendation 6.6

Documentation of the type and dose of naturoceutical


products utilized by patients with HF is
recommended.
Strength of Evidence = C
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.
Strength of Evidence = B

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.
Strength of Evidence = B

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.
Strength of Evidence = C

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.
Strength of Evidence = B

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.
Strength of Evidence = C

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.
Strength of Evidence = C

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

Diagnosis of heart failure

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.
Strength of Evidence = B

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.

Strength of Evidence = C

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.
Strength of Evidence = B

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
Strength of Evidence = B

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

Non Pulsatile VAD Key


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

Non Pulsatile VAD Key


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)

bridge to transplant

destination therapy (only FDA-approved DT


device)

HeartMate II LVAS

Internally implanted, axial-flow (non-pulsatile) device

left heart support only

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

left heart support only

Speed: 8000-12000 rpm

Medium- to long-term therapy


flow: ~3-5 lpm
(months to years)

bridge to transplant
(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)

Problems/Complications

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

Problems/Complications

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

Problems/Complications

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.

Problems/Complications

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)

Angiotensin Converting
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

Angiotensin Converting
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

Symptomatic Patients
Hydralazine + Isosorbide dinitrate
VHeFT-I
mortality, improved functional class
as compared with use of digoxin and
diuretics
VHeFT-II
proved less effective than enalopril

Symptomatic Patients
Enalopril + digoxin + diuretics
SOLVD Treatment Trial
EF<35%, FC III-IV
mortality, hospitalization
CONSENSUS-II
FC IV
mortality (40%), symptoms,
hospitalization
improved functional class

Symptomatic Patients
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

-blocking Drugs - Clinical


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

-blocking Drugs - Clinical


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

-blocking Drugs - Clinical


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

-blocking Drugs - Clinical


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

Digitalis - Clinical Trials

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

Digitalis - Clinical Trials

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.
Strength of Evidence = C

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

Acute HFHospital Admission

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

Acute HFHospital Admission

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

Strength of Evidence = C

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.

Strength of Evidence
=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
Optimize volume status
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.

Strength of Evidence = C

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.
Strength of Evidence = B

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.

Strength of Evidence = C

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.

Strength of Evidence = C

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.

Strength of Evidence = C

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

Recommendation 12.9 (2 of 2)

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.
Strength of Evidence = C

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.

Strength of Evidence = C

HFSA 2010 Practice


Guideline
Acute HFSodium

Recommendation 12.12

A low sodium diet (2 g daily) is


recommended for most hospitalized
patients.
Strength of Evidence = C
In patients with recurrent or
refractory volume overload, stricter
sodium restriction may be
considered.
Strength of Evidence = C

HFSA 2010 Practice


Guideline
Acute HFFluid Restriction

Recommendation 12.13

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.
Strength of Evidence = C

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

Recommendation 12.14

Routine administration of
supplemental oxygen:
Is recommended in the presence of
hypoxia.
Is not recommended in the
absence of hypoxia.

Strength of Evidence
=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.
Strength of Evidence
=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.
Strength of Evidence = B

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.
Strength of Evidence = C

HFSA 2010 Practice


Guideline

Acute HFIV Vasodilators

Recommendation 12.17
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.
Strength of Evidence = B

Frequent blood pressure monitoring is recommended


with these agents.
Strength of Evidence = B
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
Acute HFIV Vasodilators

Recommendation 12.18

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

Strength of Evidence = C

HFSA 2010 Practice


Guideline
Acute HFIV Vasodilators

Recommendation 12.19

Intravenous vasodilators may be


considered in patients with ADHF
who have persistent severe HF
despite aggressive treatment with
diuretics and standard oral
therapies.

Nitroprusside
Strength of Evidence = B
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.
Strength of Evidence = C

2 of 3

HFSA 2010 Practice


Guideline
Acute HFIV Inotropes

Recommendation 12.20 (2 of 3)

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.
Strength of Evidence = C

When adjunctive therapy is needed in other


patients with ADHF, administration of vasodilators
should be considered instead of intravenous
inotropes (milrinone or dobutamine).
Strength of Evidence = C

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

Recommendation 12.20 (3 of 3)

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.
Strength of Evidence = C

If symptomatic hypotension or worsening


tachyarrhythmias develop during
administration of these agents,
discontinuation or dose reduction should
be considered.
Strength of Evidence = C

HFSA 2010 Practice


Guideline

Acute HFHemodynamic Monitoring

Recommendation 12.21

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


Recommendation 12.22
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
Strength of Evidence = C

HFSA 2010 Practice


Guideline

Acute HFEvaluation for Precipitating


Factors

Recommendation 12.23

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

Strength of Evidence = C

HFSA 2010 Practice


Guideline
Acute HFPatient Education

Recommendation 12.24

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.

Strength of Evidence = B

HFSA 2010 Practice


Guideline

Acute HFDischarge Criteria

Recommendation 12.25

It is recommended that criteria in


Table 12.7 be met before a patient
with HF is discharged from the
hospital.
Strength of Evidence = C
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

Recommendation 12.26
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
Strength of Evidence = C

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

Coronary artery disease


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

BorninSouthAfricain1922

Studiedheartsurgeryatthe
UniversityofMinnesotathen
returnedtosetupacardiacunit
inCapeTown.

December1967:transplantedthe
heartofaroadaccidentvictim
intoa59yearoldpatient

Patientonlysurvived18days
duetoinfectiouscomplications

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
Bridge to transplant
Easy to insert and
operate so used in
community hospitals
Flows 6L/min

Circulation. 2005;112:438-448.

Long term Device


options
Heartmate XVE

Bridge to transplant

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
Bridge to transplant

Circulation. 2005;112:438-448.

Heartmate
XVE

Pneumatic or vented
electric plates
Textured internal surfaces
Only left-sided support
Flows 10L/min
Bridge to transplant
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
Bridge to transplant
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

Congestive Heart Failure

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
Diastolic dysfunction
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)

Different Ways to Define


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.

Different Ways to Define


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

Coronary artery disease


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

BNP in the Diagnosis of HF


ANP/BNP elevated in

Heart failure
Systemic and pulmonary hypertension
Hypertrophic and restrictive cardiomyopathy
Pulmonary embolism
COPD
Cor pulmonale
AMI Cirrhosis
Renal Failure

BNP in the Diagnosis of HF


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.

The Task Force on Acute Heart Failure of the European Society of Cardiology

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.
The Task Force on Acute Heart Failure of the European Society of Cardiology

*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