HEART FAILURE: An Overview and tutorial for residents teaching medical students
From Ask Dr Wiki
Michael W.Tempelhof, M.D.
Duke University Medical Center
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.
Framingham Definition of Heart Failure
- Paroxysmal nocturnal dyspnea
- Neck vein distention
- 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
- Bilateral ankle edema
- Nocturnal cough
- Dyspnea on ordinary exertion
- Pleural effusion
- 30% decrease in baseline vital capacity
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.
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.
Patients “at Risk”:
- Diabetes mellitus
- Coronary artery disease
- Exposure history to cardiac toxins:
- History of cardiotoxic drug therapy.
- History of alcohol abuse.
- Familial history of cardiomyopathy
- 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
- 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.
- 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
Prevalence, Incidence, Demographics and Mortality.
- 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.
- 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.
Dollars and Mortality
- 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.
Inadequate cardiac output and systemic perfusion results in a dichotomous neurohormonal pathway activation.
- In an effort to increase forward output the sympathetic nervous system increases heart rate and myocardial contractility.
- Circulating catecholamines create arteriolar vasoconstriction in non-essential vascular beds.
- Catecholamines also stimulate secretion of renin from the juxtaglomerular apparatus of the kidney.
- 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.
- 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.
- 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.
Heart Failure Types
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.
- -Older pt.
- -Ischemia, valvular disease
- Physical Exam findings
- -S3 and soft heart sounds
- -Chamber Enlargement
- -Reduced Ejection Fraction
- Diastolic: heart failure abnormality in relaxation function leading to a defect in ventricular filling.
- -Younger pt.
- -Hypertension history, PND symptoms
- Physical Exam findings
- -Less evidence of fluid overload ie less edema
- -NO Cardiomeagly
- -Pulmonary congestion
- -Very prominent LVH with NORMAL Ejection Fraction
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.
Low Output vs. High 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)
- -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
Etiology of Heart Failure
- Ischemic: accounts for 60% of cases.
- high output states
- infiltrative diseases
- drug toxicity (doxorubicin and ETOH)
- inflammatory diseases
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.
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.
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.
- Assess and grade systolic vs diastolic dysfunction.
- Assess for other etiologies: valvular heart disease, cardiac tamponade, pericardial constriction, and infiltrative or restrictive cardiomyopathies.
- Hypervolemic hyponatremia: secondary to increases in extracellular fluid volume and a normal total body sodium.
- Secondary hyperaldosteronism: contributing to mild hypokalemia with mild hypernatremia.
- 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)
- Elevated urine specific gravity
- Elevated BUN, creatinine
Hepatic Function: (from congestive hepatomegaly)
- Elevated AST, ALT, LDH
- Best utilized to differentiate heart failure vs. pulmonary disease as etiology to dyspnea.
- BNP levels correlate with heart failure severity and correlate with disease progression.
Metabolic exercise testing:
- To further characterize pulmonary vs. cardiac.
- Peak oxygen consumption <14 ml/kg/min indicates cardiac etiology and predicts a poor prognosis.
Drugs/Devices for Heart Failure
- 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.
- Furosemide, bumetanide, ethacrynic acid and torsemide.
- Inhibit the Na+/K+/2Cl- symporter.
- Furosemide IV has direct vasodilatory effect.
- Providing additional blood pressure reduction.
- Relaxes pre-contracted pulmonary venules: beneficial for treatment of Pulmonary Edema.
- 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.
- 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.
- 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).
- For ACE-intolerant patients, hydralazine and nitrates in combination are effective afterload and preload reducing agents.
- ACE inhibitors do have mortality benefit over hydralazine and nitrates.
- Hydralazine and nitrates may be added to ACE inhibitors when additional vasodilation is necessary or pulmonary hypertension is present.
- 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.
- Activates beta-1 receptors resulting in enhanced cardiac contractility.
- Long-term dobutamine infusions are arrhythmogenic and increase mortality.
- 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.
- 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.
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.
- 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. anti-arrhythmic drug therapy.
Left Ventricular Assist Devices (LVAD)
- Temporary device to bridge end stage pts to cardiac transplantation.
- Current research in implementing permanent LVADs is underway.
Transplant for Heart Failure
- 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.
Management of Heart Failure
- Identify etiology of heart failure.
- Assessment of volume status.
- Complete blood count, urinalysis, serum electrolytes, renal function, blood glucose, liver function tests, and thyroid-stimulating hormone.
- 12-lead electrocardiogram and chest radiograph.
- TTE echocardiography with Doppler.
- Cardiac catheterization for patients with angina.
Management of Heart Failure
ACC/AHA recommends managing heart failure according to Stage classification.
Management of Stage A
- Coronary disease and Cardiomyopathy risk factor management. Patient and Family education.
- Aggressive treatment of Diabetes, Hypertension, hyperlipidemia, alcohol abuse, cigarette smoking, and hyperthyroidism.
- 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.
- In any pt with history of myocardial infarction regardless of ejection fraction.
- In any pt with a reduced ejection fraction.
- Risk factor modifications are also recommended for stage B patients.
- 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
- 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.
- 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.
- Requiring IV inotropic support to maintain adequate organ perfusion.
- Peak Vo2 < 10 ml/kg/min.
- NYHA Class IV symptoms not amenable to any other intervention.
- Recurrence of symptomatic ventricular arrhythmias refractory to all therapeutic intervention.