Download Heart Failure

Heart Failure
Michael W.Tempelhof, M.D.
Duke University Medical Center
I.
II.
III.
IV.
V.
VI.
VII.
VIII.
Index
Define
Prevalence/Incidence/Demographics/Mortality
Pathophysiology
Heart Failure Types
Etiology of Heart Failure
Clinical Manifestations
Drugs, Devices and Transplant for Heart Failure
Management of Heart Failure
I. Definition Of Heart Failure
A. General
B. Framingham Data
C. NYHA
D. ACC/AHA
A. General Definition of Heart Failure



Clinical syndrome resulting from inadequate systemic perfusion
from any structural or functional disorder that impairs the ability of
the ventricle to fill with or eject blood.
The classic syndrome of heart failure is dyspnea, fatigue, and fluid
retention.
Classified as Systolic or Diastolic Heart Failure.
B. Framingham Definition of Heart Failure
Major Criteria
Paroxysmal nocturnal dyspnea
Neck vein distention
R a le s
Radiographic cardiomegaly
Acute pulmonary edema
S3 gallop
Central venous pressure > 16 cmH2O
Circulation time ≥ 25 sec
Hepatojugular reflux
Pulmonary edema
Visceral congestion
Cardiomegaly at autopsy
Weight loss ≥ 4.5 kg in 5 days in response to treatment of heart failure

Minor Criteria
Bilateral ankle edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
30% decrease in baseline vital capacity
Tachycardia

C. New York Heart Association (NYHA)
Definition of Heart Failure

Classification System based upon Symptomology.
NYHA I: No symptoms with ordinary activity.
NYHA II: Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue,
palpitation, dyspnea, or angina.
NYHA III: Marked limitation of physical activity. Comfortable at
rest, but less than ordinary physical activity results in
fatigue, palpitation, dyspnea, or anginal pain.
NYHA IV: Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency
present at rest.
D. ACC/AHA Classification of Chronic Heart
Failure

Classification System based on structural and symptomatic stages of the
syndrome.
Stage 1: patients at risk of developing heart failure but who have no structural
heart disease at present.
Stage 2: patients with structural heart disease but no symptoms.
Stage 3: patients with structural heart disease and symptomatic heart failure.
Stage 4: patients with severe refractory heart failure.
D. ACC/AHA Classification of Heart Failure:
Stage 1

Patients “at Risk”:
Hypertension
Diabetes mellitus
Coronary artery disease
Exposure history to cardiac toxins:


History of cardiotoxic drug therapy.
History of alcohol abuse.
Familial history of cardiomyopathy
D. ACC/AHA Classification of Heart Failure:
Stage 2
Patients WITH structural disease, but NO history of
signs or symptoms of Failure.

Left ventricular hypertrophy
Myocardial Fibrosis
Left ventricular dilation or dysfunction
Asymptomatic valvular heart disease
Previous myocardial infarction
D. ACC/AHA Classification of Heart Failure:
Stage 3
Underlying structural heart disease AND symptoms
of Heart Failure.

Dyspnea or fatigue due to left ventricular systolic dysfunction.
Asymptomatic patients receiving treatment for prior symptoms of
HF.
D. ACC/AHA Classification of Heart Failure:
Stage 4
Despite maximal medical therapy, symptoms of HF at rest
and advanced structural heart disease.
Awaiting heart transplant
Requiring continuous inotropic or mechanical
Hospice management of HF

II. Prevalence, Incidence, Demographics and
Mortality.
Prevalence/Incidence:
 5.0 million persons in the United States have heart failure: 1.5%


of the population.
550,000 new cases diagnosed each year.
Patients with heart failure account for about 1,000,000 hospital
admissions annually: 30% will be re-admitted within 90 days for
decompensation.
II. Demographics

Prevalence of heart failure increases with age; 1 to 2 percent of persons aged 45 to 54
years and increases to 10 percent of individuals older than 75 years.

Americans over age 40, have a life-time risk for developing heart failure of 21 percent.
II. Dollars and Mortality


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The cost of hospitalizations for heart failure is twice that for all
forms of cancer and myocardial infarctions combined.
Annual cost of $38.1 billion or 5.4% of all healthcare dollars.
Overall 20% annual mortality.
30-60% of mortality is related to arrhythmia, sudden death.
III. Pathophysiology
Inadequate cardiac output and systemic perfusion results in a dichotomous
neurohormonal pathway activation.
1. In an effort to increase forward output the sympathetic nervous system increases heart
rate and myocardial contractility.
2. Circulating catecholamines create arteriolar vasoconstriction in non-essential vascular
beds.
3. Catecholamines also stimulate secretion of renin from the juxtaglomerular apparatus of
the kidney.
III. Pathophysiology: Cardiac
Catecholamines: worsen ischemia by increasing HR and contractility, potentiate
arrhythmias, promote cardiac remodeling, and are toxic to myocytes.
Left ventricular chamber dilatation: causes increased wall tension, worsens
subendocardial myocardial perfusion, and may provoke ischemia in patients with coronary
atherosclerosis. Left ventricular chamber dilatation results in separation of the mitral leaflets
and mitral regurgitation leading to pulmonary congestion.
High LV diastolic pressures: (diastolic dysfunction), increase left atrial pressures
increasing the hydrostatic and oncotic pressures in the pulmonary vasculature resulting in
pulmonary edema.
III. Pathophysiology: Vascular
Arteriolar vasoconstriction stimulates the renal secretion of renin and the
hypothalamic secretion of vasopressin.
Renin and Vasopressin stimulate salt and water reabsorbtion and retention.
Vascular Endothelin levels are elevated promoting endolethial growth and
cardiac apoptosis.
III. Pathophysiology: Renal
Renin-angiotensin system activation: results in sodium and water retention,
and release of aldosterone.
Aldosterone: increases sodium and water retention and increases vascular
resistance and organ fibrosis.
IV. Heart Failure Types
A. Systolic vs. Diastolic
B. Acute vs. Chronic
C. Low Output vs. High Output
A. Systolic vs. Diastolic
Systolic: heart failure abnormality in contractility function leading to a defect
in the forward expulsion of blood. End-Systolic AND Diastolic Volumes are
elevated.
Diastolic: heart failure abnormality in relaxation function leading to a defect in
ventricular filling.
Systolic Heart Failure
History
-Older pt.
-Ischemia, valvular disease
Physcial Exam findings
-JVP,
-Edema
-S3 and soft heart sounds
Studies
-Cardiomeagly
-LVH
-Chamber Enlargement
-Reduced Ejection Fraction
Diastolic Heart Failure
History
-Younger pt.
-Hypertension history, PND symptoms
Physical Exam findings
-Less evidence of fluid overload ie less edema
-S4
Studies
-NO Cardiomeagly
-Pulmonary congestion
-Very prominent LVH with NORMAL Ejection Fraction
B. Acute vs. Chronic
Acute:
Marked reduction in cardiac output resulting in inadequate tissue perfusion
with acute vascular congestion.
 Chronic:
Gradual reduction in cardiac output with adaptive counter- mechanisms of
vascular remodeling and neurohormonal activation.

C. Low Output vs. High Output

Low Output:
Multiple etiologies:
congenital, valvular, rheumatic, hypertensive, coronary, and cardiomyopathic
abnormalities.
-Cold, pale and/or cyanotic extremities with systemic vasoconstriction.
-LOW Mixed venous oxygen often low (<50ml/liter)

High Output:
Etiologies;
-thyrotoxicosis, arteriovenous fistulas, beriberi, Paget disease of bone, and anemia.
-Warm well perfused extremities with a widened pulse pressure.
-NORMAL to HIGH Mixed venous Oxygen
V.
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
Etiology of Heart Failure
Ischemic: accounts for 60% of cases.
Non-ischemic
hypertension
 valvular
 alcohol
 pregnancy
 myocarditis
 high output states
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congenital
infiltrative diseases
drug toxicity (doxorubicin and ETOH)
inflammatory diseases
1.
2.
3.
VI. Clinical Manifestations
Patients History and Symptoms
Physical Exam Findings
Findings On Workup
1. Patients History and Symptoms
Symptoms of pulmonary congestion:
cough, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
Symptoms of low cardiac output:
fatigue, effort intolerance, cachexia, and renal hypoperfusion and therefore
fluid retention.
Symptoms of Right sided failure:
pulsating neck, peripheral edema, early satiety, abdominal
discomfort/fullness and constipation.
2. Physical Exam Findings
Findings of pulmonary congestion:
rales, hypoxia, tachypneia, tachycardia.
Findings of low cardiac output:
S3, S4, cold extremities, pitting edema, pale/diaphoretic.
Symptoms of Right sided failure:
ascites, hepatosplenomegaly, elevated JVP, peripheral edema.
3. Findings On Workup
Chest radiographic:
cardiomegaly, pulmonary vascular redistribution, kerley B lines, and pleural
effusion.
Electrocardiogram: (no definitive, only suggestive findings)
Left ventricular hypertrophy, left bundle branch block, intraventricular
conduction delay, chamber enlargement, non-specific ST segment and T wave
changes.
Echocardiogram:
Asses and grade systolic vs diastolic dysfunction.
Asses for other etiologies: valvular heart disease, cardiac tamponade, pericardial
constriction, and infiltrative or restrictive cardiomyopathies.
Serum Electrolytes:
1. Hypervolemic hyponatremia: secondary to increases in extracellular fluid volume and
a normal total body sodium.
2. Secondary hyperaldosteronism: contributing to mild hypokalemia with mild
hypernatremia.
Hematologic Indices
1.
2.
3.
4.
Anemia (20% of Heart failure patients, multiple etiologies)
hemodilutional from increased plasma volume.
decreased red cell mass from low EPO levels in setting of chronic renal insufficiency.
bone marrow suppression by activated proinflammatory cytokines
Renal Indices: (from secondary to reduced renal blood flow and GFR)
1.
2.
3.
Proteinuria
Elevated urine specific gravity
Elevated BUN, creatinine
Hepatic Function:
(from congestive hepatomegaly)
1. Elevated AST, ALT, LDH
2. Cirrhosis
BNP:
1. Best utilized to differentiate heart failure vs. pulmonary disease as etiology to dyspnea.
2. BNP levels correlate with heart failure severity and correlate with disease progression.
Metabolic exercise testing:
1. To further characterize pulmonary vs. cardiac.
2. Peak oxygen consumption <14 ml/kg/min indicates cardiac etiology and predicts a poor
prognosis.
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2.
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5.
6.
7.
8.
VII. Drugs/Devices for Heart Failure
Diuretics
Beta-Blockers
Vasodilators
Inotropic Agents
Cardiac Resynchronization Therapy
Defibrillator Therapy
Left Ventricular Assist Devices (LVAD)
Cardiac Transplantation
VII. Drugs for Heart Failure
1. Diuretics
1. Loop diuretics
2. Thiazide diuretics
3. Potassium Sparing diuretics
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Provide symptomatic relief.
Slows the progression of ventricular remodeling by reducing ventricular
filling pressure and wall stress.
No survival benefit and may cause azotemia, hypokalemia, metabolic
alkalosis and elevation of neurohormones.
Loop Diuretics
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Furosemide, bumetanide, ethacrynic acid and torsemide.
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Inhibit the Na+/K+/2Cl- symporter.

Furosemide IV has direct vasodilatory effect.

Providing additional blood pressure reduction.
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Relaxes pre-contracted pulmonary venules: beneficial for treatment of
Pulmonary Edema.
Thiazide Diuretics
 Inhibit the Na+/Cl- co transporter in the distal convoluted tube.

Recommended for management of chronic heart failure.
Potassium Sparing Diuretics
 Spironlactone, amiloride and triamterene.
 Inhibit principal cells in the distal convoluted tubule and cortical
collecting duct.
 Inhibits Na reabsorbtion and Potassium secretion.
 Significant side effect of Hyperkalemia.
VII. Drugs for Heart Failure
2. Beta-Blockers
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ONLY: Metoprolol, Carvedilol and Bisoprolol have FDA
approval.
Blockade of compensatory sympathetic stimulation creates an
arrhythmic, ischemic, remodeling, and apoptotic benefit.
Used as monotherapy or combined with conventional heart failure
management, beta-blockers reduce the combined risk of morbidity
and mortality.
Initiate low starting dosing and titrate up to tolerated target doses.
VII. Drugs for Heart Failure
3. Vasodilators
a. ACE-I
b. Hydrazaline/Nitrates
ACE-I

Afterload reduction and neurohormonal modulation.

Improve mortality, symptoms, exercise tolerance, left ventricular ejection
fraction, and rate of hospitalizations.

10-20% rate of intolerance from drug induced cough.

Other uncommon side effects include angioedema and acute renal failure
(bilateral renal artery stenosis).
Hydrazaline/Nitrates
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For ACE-intolerant patients, hydralazine and nitrates in combination are
effective afterload and preload reducing agents.
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ACE inhibitors do have mortality benefit over hydralazine and nitrates.
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Hydralazine and nitrates may be added to ACE inhibitors when additional
vasodilation is necessary or pulmonary hypertension is present.
VII. Drugs for Heart Failure
4. Inotropic Agents
a.
b.
c.
d.
Digoxin
Dobutamine
Dopamine
Milrinone
Digoxin

Inhibits Na,K+-ATPase resulting in an increase in intracellular Na+,
extracellular Ca2+ exchange increasing the velocity and extent of
sarcomere shortening.
 ACC/AHA recommend Digoxin for symptomatic patients with left
ventricular systolic dysfunction.
 Digoxin reduces the rate of hospitalization for heart failure, but has NO
benefit on mortality.
Dobutamine
 Activates beta-1 receptors resulting in enhanced cardiac
contractility.
 Long-term dobutamine infusions are arrhythmogenic and
increase mortality.
Dopamine
 Unique dose dependent Mechanism of Action.
 At low doses: (≤2 µg/kg/min), selective dilation of splanchnic and
renal arterial beds. assists in increasing renal perfusion.
 At intermediate doses: (2 to 10 µg/kg/min), increased

norepinephrine secretion results in increased cardiac contractility,
heart rate and peripheral vascular resistance.
At higher doses: (5 to 20 µg/kg/min), direct alpha-adrenergic
receptor stimulation increases systemic vascular resistance.
Milrinone

Phosphodiesterase-III inhibitor that enhances contractility by
increasing intracellular cyclic adenosine monophosphate (cAMP).

Potent pulmonary vasodilatation that benefits pts with pulmonary
hypertension.

Unlike dobutamine: milrinone is beneficial to decompensated
heart failure patients on beta-blocker therapy.

Long term milrinone infusions are arrhythmogenic, and increase
mortality.
VII. Devices for Heart Failure
5. Cardiac Resynchronization Therapy


Indicated for symptomatic patients with NYHA III-IV heart
failure AND wide QRS (>120ms).
70% of patients receiving synchronous ventricular contraction
report symptomatic improvement.
VII. Devices for Heart Failure
6. Defibrillator Therapy
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50% of heart failure patients die of sudden cardiac death.
Indicated for pts with previous MI and LVEF <30% , sustained
ventricular tachycardia, inducible ventricular tachycardia.
Morbidity/mortality benefit of ICD placement vs. antiarrhythmic drug therapy.
VII. Devices for Heart Failure
7. Left Ventricular Assist Devices (LVAD)
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Temporary device to bridge end stage pts to cardiac
transplantation.
Current research in implementing permanent LVADs is
underway.
VII. Transplant for Heart Failure
8. Transplant
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For pts with end-stage congestive heart failure
despite all interventions.
80 % 1 year survival and 60% 5yr survival.
Lifelong immunosuppression to prevent rejection, increased risk
for opportunistic infections and malignancies.
VIII.
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Management of Heart Failure
Initial Workup
Identify etiology of heart failure.
Assessment of volume status.
Complete blood count, urinalysis, serum electrolytes, renal
function, blood glucose, liver function tests, and thyroidstimulating hormone.
12-lead electrocardiogram and chest radiograph.
TTE echocardiography with Doppler.
Cardiac catheterization for patients with angina.
IX. Management of Heart Failure
ACC/AHA recommends managing heart failure according
to Stage classification.
Management of Stage A
1. Coronary disease and Cardiomyopathy risk factor management.
Patient and Family education.
2. Aggressive treatment of Diabetes, Hypertension, hyperlipidemia,
alcohol abuse, cigarette smoking, and hyperthyroidism.
3. Angiotensin-converting enzyme inhibitors are recommended.

No evidence to support life-style modifications; exercise, salt restriction, or
routine use of nutritional supplements.
Management of Stage B
ACE-I and B-blocker therapy is designed to minimize the rate of
worsening left ventricular dysfunction.
Risk factor modifications are also recommended for stage B patients.

ACE-I and B-Blockers
In any pt with history of myocardial infarction regardless of ejection
fraction.
In any pt with a reduced ejection fraction.

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Valve replacement/repair for patients with hemodynamically
significant valvular disease.

No evidence to support use of exercise and other life-style, dietary
modifications for this population.
Management of Stage C
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Continuum of care as under Stage A and B management.
ACE inhibitors and B-blockers for all stage C patients.
Digitalis for symptomatic patients.
Spironolactone in patients with NYHA IV symptoms.
Diuretics in patients with evidence of fluid overload.
Sodium restriction, dietary discretion and exercise are encouraged.
Management of Stage D

Continued management as listed for patients in stages A, B, and C.
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Low threshold for specialized treatments of mechanical circulatory support,
continuous intravenous inotropic therapy.
Referral to a heart failure program and cardiac transplantation in eligible
patients.
When to Transplant?
ACC/AHA Guidelines: Indications for Cardiac Transplantation.

Any hemodynamic compromise due to heart failure.
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Requiring IV inotropic support to maintain adequate organ perfusion.
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Peak Vo2 < 10 ml/kg/min.
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NYHA Class IV symptoms not amenable to any other intervention.

Recurrence of symptomatic ventricular arrhythmias refractory to all
therapeutic intervention.