Congestive heart failure

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Heart failure
ICD-10 I50.0
ICD-9 428.0
DiseasesDB 16209
MedlinePlus 000158
eMedicine med/3552 
MeSH D006333

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Synonyms and Related Key Words: CHF, pump failure, left heart failure, right heart failure, chronic heart failure, acute heart failure, flash pulmonary edema, congestion, systolic dysfunction, LV dysfunction, LV failure, impaired filling, reduced cardiac output, pulmonary edema

Overview

  • 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.
  • There are two broad categories of heart failure:
  1. Systolic Heart Failure and
  2. Diastolic Heart Failure.

Differential Diagnosis of Causes of Heart Failure

A. Left Ventricular Failure

Most Common Causes:

Expanded List of Causes:

B. Right Ventricular Failure

Most Common Causes:

Other Causes:

C. Others


Pathophysiology & Etiology

Epidemiology of Heart Failure

Prevalance

  • Estimated 2005 prevalence in adults age 20 and older: 5,300,000 (about 2,650,000 males, and 2,650,000 females).

Incidence [1]

  • Data from the NHLBI’s Framingham Heart Study indicate that;[2]
  1. Heart failure (HF) incidence approaches 10 per 1,000 population after age 65.
  2. 75% of heart failure cases have antecedent hypertension. About 22% of male and 46% of female myocardial infarction (MI) victims will be disabled with heart failure within following 6 years.
    • At age 40, the lifetime risk of developing heart failure for both men and women is 1 in 5.
    • At age 40, the lifetime risk of heart failure occurring without antecedent myocardial infarction is 1 in 9 for men and 1 in 6 for women.
    • The lifetime risk doubles for people with blood pressure >160/90 mm Hg compared to those with blood pressure <140/90 mm Hg.
  • A study conducted in Olmsted County, Minnesota, showed that the incidence of heart failure (ICD9/428) has not declined during two decades, but survival after onset has increased overall, with less improvement among women and elderly persons. [3]

Classification Schemes of Heart Failure

Framingham Criteria

Major Criteria

Minor Criteria

Boston Criteria of Congestive Heart Failure

  • Category I: History
  • Category II: Physical Examination
  • Category III: Chest Radiography

No more than 4 points are allowed from each of three categories; hence the composite score (the sum of the subtotal from each category) has a possible maximum of 12 points.

The diagnosis of heart failure is classified as "definite" at a score of 8 to 12 points, "possible" at a score of 5 to 7 points, and "unlikely" at a score of 4 points or less.

New York Heart Association Criteria (NYHA)

  • 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.

Stage 1

Patients “at Risk”

Stage 2

Patients with structural heart disease, but no history of signs or symptoms 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 heart failure.

Stage 4

Despite of maximal medical therapy, symptoms of heart failure at rest and advanced structural heart disease.

  • Awaiting for heart transplantation
  • Requiring continuous inotropic or mechanical support
  • Hospital management of heart failure

Risk Factors for the Development of Heart Failure

  1. Demographic factors
    • Age
    • Gender
    • Low socioeconomic status
  2. Lifestyle-related factors
    • Tobacco and coffee consumption
    • Alcohol consumption
    • Dietary sodium intake
    • Recreational drug use: Cocaine, methamphetamines.
  3. Comorbidities
  4. Echocardiographic factors
    • Ventricular dimension
    • Ventricular mass
    • Diastolic filling impairment
  5. Pharmacological factors
  6. Biochemical
  7. Genetic risk factors

Risk Factors Associated with Heart Failure Progression and Outcomes

  1. Clinical
  2. Echocardiographic
    • Ejection fraction
    • Exercise ejection fraction
    • Ventricular dimensions
    • Sphericity index
    • Prolonged isovolumic relaxation
    • Restrictive mitral filling
    • Changes in E/A ratio
    • Mitral regurgitation
    • Contractile reserve
    • Left ventricular mass
  3. Exercise Tolerance
    • Exercise duration
    • Peak O2 consumption
    • VE/VCO2
    • Anaerobic threshold 6-minute walk test
  4. Hemodynamics
  5. Electrophysiological
    • Conduction delay
    • Atrial arrhythmia
    • Family history of sudden death
    • Presence of late potentials
    • QT dispersion
    • T wave alternans
  6. Neurohormonal
  7. Natriuretic factors
  8. Cytokines and others

Differential Diagnosis of Heart Failure

Heart Failure Secondary to Coronary Artery Disease

A. Underlying Mechanisms

  1. Ischemic Preconditioning
    • Reductions in ischemia-related apoptosis
    • Increases in endogenous adenosine
    • Activation of potassium-adenosine triphosphate (K+-ATP) channels
  2. Electrical Dysfunction
    • QT prolongation
    • Increased susceptibility to arrhythmia
    • QT dispersion
  3. Mechanical Dysfunction
    • Systolic dysfunction
    • Diastolic dysfunction
  4. Biochemical Dysfunction
    • Increases in beta-adrenergic receptor density
    • Changes in structural and regulatory proteins
    • Shift to FFA as a proffered metabolic substrate
    • Lactate production
    • Elevated BNP concentration

B. Utilisation of Clinical Data

Management of heart failure due to coronary artery disease are primarily influenced by following parameters:

  1. An estimate of the relative proportions of:
    • Viable but ischemic myocardium
    • Nonviable myocardium
    • Viable non-ischemic myocardium
  2. The technical feasibility of successful mechanical revascularization
  3. The extent and severity of comorbidities in the individual patient

Cardiomyopathies and Inflammatory Diseases

Restrictive Cardiomyopathies
Dilated Cardiomyopathies
Inflammations

Congestive Heart Failure as a Consequence of Valvular Heart Disease

Congestive Hert Failure Secondary to Congenital Heart Disease

A. Causes of Congestive Heart Failure in Adults with Unoperated Congenital Heart Diseases

B. Causes of Congestive Heart Failure in Adults with Operated Congenital Heart Diseases

Right Ventricular Failure

Factors affected right ventricle and to be eliminated during management of congestive heart failure. A. Right ventricular myocardial dysfunction

  1. Right ventricular myocardial infarction
  2. Dilated cardiomyopathy
  3. Right ventricular dysplasia

B. Primary right ventricular pressure overload

  1. Left ventricular failure
  2. Mitral valve disease
  3. Atrial myxoma
  4. Pulmonary veno-occlusive disease
  5. Cor pulmonale
  6. Pulmonic stenosis
  7. Ventricular septal defect
  8. Aortopulmonary communication

C. Primary right ventricular volume overload

  1. Pulmonic regurgitation
  2. Tricuspid regurgitation
  3. Atrial septal defect
  4. Partial anomalous pulmonary venous return

D. Impediment to right ventricular inflow

  1. Tricuspid stenosis
  2. Cardiac tamponade
  3. Constrictive pericarditis
  4. Restrictive cardiomyopathy

Heart Failure in Cardiac Tamponade, Constrictive Pericarditis, and Restrictive Cardiomyopathy

Electrocardiography

Chest X-ray

Echocardiography

  • Evaluation of left ventricular function and ejection fraction
  • Wall motion abnormalities
  • Detection of mitral regurgitation
  • Detection of aortic stenosis
  • Measurement of pulmonary artery pressure
  • Detection and evaluation of aneurysms

Exercise Stress Tests

Exercise Stress Tests is useful in measuring the "functional capacity" of patients. It is also helpful in follow up period for evaluation of congestive heart failure treatment.

Myocardial Viability Studies

  • Dobutamine echocardiography
  • Nuclear tests (SPECT or PET)
  • Cardiac MRI

Cardiac Catheterization

Coronary angiography for evaluation of coronary arteries and right heart catheterization for assessment of pulmonary artery resistance.

Management of Heart Failure

Pharmacotherapy

A. Acute Pharmacotherapy

  1. Diuretics
  2. Nitroprusside
  3. Nesiritide
  4. Milrinone
  5. Dobutamine
  6. Dopamine
  7. Nitroglycerine

B. Chronic Pharmacotherapy

Antiarrhythmic Drugs

Antiarrhythmic therapy should be considered as a therapy to prevent sudden death. There are multiple causes of the for sudden death including ventricular tachycardia, ventricular fibrillation as low as pulmonary emboli, hyperkalemia, and primary bradyarrhythmias.

Over 50% of patients will have asymptomatic non-sustained ventricular tachycardia and there is no general indication for treatment of this arrhythmia.

Metabolisms of following anti-arrhythmic drugs are significantly affected in patients with congestive heart failure;

  1. Quinidine
  2. Procainamide
  3. Disopyramide: Contraindicated in patients with heart failure.
  4. Moricizine
  5. Lidocaine
  6. Mexiletine
  7. Tocainide
  8. Flecainide
  9. Propafenone
  10. Amiodarone

Renin-Angiotensin-Aldosteron System Related Drugs

  1. ACE Inhibitors
    • ACE Inhibitors (ACEI) should be considered as first-line therapy for the treatment of patients with clinical heart failure due to reduced LVSD, patients with asymptomatic LV dysfunction, and for patients who are at high risk for the development of heart failure due to the presence of coronary, cerebrovascular, or peripheral vascular disease.
    • Treatment should not be deferred in patients with few or no symptoms because of the significant mortality benefit derived from ACEI therapy.
    • Initial therapy usually consist of 12.5 mg tid of captopril, 2.5 mg bid of enalapril, or 2.5 mg daily lisinopril. The optimal dose is usually established by change 4 to 6 weeks. ACE inhibitors are rarely adequate for the treatment of congestion without the use of diuretics.
    • 5-10 % patients cannot tolerate ACE inhibitors because of cough. Cough can be a sign of elevated left-sided filling pressures. Sometimes cough will diminish with the treatment of heart failure. Angiotensin 2 receptor blockers are now being studied as a substitute for ACE inhibitors. Renal artery stenosis should be considered if there's a decline in renal function with the initiation of ACE inhibitors.
  2. Angiotensin receptor blockers (ARB)
  3. Aldosterone Antagonists

Anticoagulants

The annual incidence of systemic and pulmonary embolism in patients with heart failure is 2-5%. This is not that is similar from the risk of severe bleeding among patients to its anticoagulants which is 0.8-2.5% per year.

As a result anticoagulation is not routinely recommended in the current guidelines for the treatment of heart failure. However among those patients with a atrial fibrillation, a history of emboli, or multiple intracardiac thrombi, or akinesis or dyskinesis detected on echo should be anticoagulated.

Beta Blockers

  • 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.
  1. Bisoprolol
  2. Bucindolol
  3. Carvedilol
  4. Metoprolol
  5. Nevibolol

Ca Channel Blockers

Although calcium channel blockers cause vasodilation their overall benefit is minimized by the fact that they have a negative inotropic effect and by the reflex activation of the sympathetic nervous system.

These agents are not recommended as vasodilators in patients with congestive heart failure, however they may be useful as antihypertensive agents in patients with diastolic dysfunction.

Diuretics

  • 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.
  • Although thiazide diuretics are effective in mild heart failure they are usually inadequate for the treatment of severe heart failure.
  • Thiazide diuretics have also been associative with hyponatremia.
  • Fluid retention usually responds best to furosemide (Lasix) and at doses of 10 to 20 mg per day. The patient should be told to return to their position in the next three to seven days for further assessment including assessment of their potassium concentration. Weight loss should not exceed 1 to 2 pounds/day.
  • If there is no response to the initial dose then it can be increased by at least 50%. The maintenance dose of the diuretics lower than that required to initiate diuresis.
  • If the patient gains more than two pounds and they are instructed to double the dose of their loop diuretic.
  • Once the baseline weight has been re-established than they can resume their previous status.
  • Intermittent use of metolazone into dose of 2.5 or 5 mg can be given if the patient is refractory to furosemide Lasix. Metolazone should be given in the inpatient setting.
  • The role of potassium sparing diuretics such as spironolactone (Aldactone), amiloride, or triamterene remains the subject of controversy.
  • Extreme caution is necessary when adding a potassium sparing agent to the regiment that includes ACE inhibitors particularly when diabetes or renal disease is present because the patient can become hyperkalemic.
  • Electrolyte replacement:

ACE inhibitors reduce potassium excretion, but most patients with good renal function require potassium supplementation during daily therapy with the diuretics such as furosemide (Lasix) despite of ACE inhibitors therapy.

  • Dietary supplementation is rarely adequate.
  • Hypokalemia can aggravate arrhythmia is precipitate muscle cramps.
  • Potassium levels >6 (particularly when occurs rapidly) can be associated with reduction in myocardial contractility.
  • Patients are actually at higher risk of hyperkalemia and hypokalemia. The goal is to maintain a potassium between 3.8 and 4.5 mEq.
  • Unless the hypokalemia is very severe and at life-threatening level, potassium should be replaced by oral administration.
  • For IV route, It should not be administered more than 10 mEq per hour.
  • Patients who use diuretics usually require approximately 20-60 mEq/day of oral potassium.
  • Extra potassium should be given after the patient has noted diuresis or weight change. If patient lost more than two pounds, the electrolyte's level should be checked every three days.
Loop Diuretics
  • 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.
Thiazide Diuretics
  • Inhibit the Na+/Cl- co transporter in the distal convoluted tube.
  • Recommended for management of chronic heart failure.
Potassium Sparing Diuretics

Nitrates

  • Nitrates can be added to ACE inhibitors to relieve symptoms of congestion.
  • The addition of a nitrate and ACE inhibitor may improve exercised tolerance.
  • The combination of hydralazine and nitrates is useful when ACE inhibitors are not well tolerated.
  • Hydralazine by itself is only an arterial vasodilator and does not reduced ventricular filling pressures to the same extent that nitrates and ACE inhibitors do. In fact when used alone it can stimulate sympathetic tone reflexively. The combination of hydralazine and nitrates has been shown to decrease mortality as well as improve the left ventricular ejection fraction and exercise capacity in patients with heart failure. However the combination of hydralazine and nitrates has been found to be less effective than ACE inhibitors.
  • The major uses this combination is in those patients who are intolerant of ACE inhibitors.

Positive Inotropics

  1. Agents that increase intracellular cAMP
  2. Agents that affect sarcolemmal ion pumps/channels
  3. Agents that modulate intracellular calcium mechanisms by either:
  4. Drugs having multiple mechanisms of action
    • Pimobendan
    • Vesnarinone
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.
  • Commonly used in patients with heart failure and atrial fibrillation to reduce the ventricular response rate.
  • Mortality has not been shown to be improved with use of digoxin, but the use of digoxin has been associated with a reduction in hospitalization.
  • There is no need to load a patient with digoxin for most patients with normal renal function 0.25 mg of digoxin daily is usually adequate. In the only patient or in those patients with renal impairment a dose of 0.125 mg per day may be adequate.
  • Drugs increase the same concentration of digoxin include antibiotics and anticholinergic agents as well as amiodarone, quinidine and verapamil.
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.

Biventricular Pacing

Biventricular pacing or cardiac resynchronization therapy is;

  • Indicated for symptomatic patients with NYHA III-IV heart failure and wide QRS complex (>120ms).
  • 70% of patients receiving synchronous ventricular contraction report significant symptomatic improvements.

Implantation of Intracardiac Defibrillator

  • 50% of heart failure patients die of sudden cardiac death.
  • ICDs are indicated for patients with previous myocardial infarction and LVEF <30%, sustained ventricular tachycardia, inducible ventricular tachycardia.
  • Morbidity/mortality benefit of ICD placement vs. anti-arrhythmic drug therapy is controversial.

Ultrafiltration

The process of ultrafiltration consists of the production of plasma water from whole blood across a semipermeable membrane (hemofilter) in response to a transmembrane pressure gradient. Possible benefits of ultrafiltration as follow;

  1. Provides fluid regulation
    • Relieve pulmonary edema
    • Reduce ascites and/or peripheral edema
    • Hemodynamic stabilization
    • Improve oxygenation
    • Facilitate blood product replacement without excess volume
    • Enable parenteral nutritional support without excess volume
  2. Improves solute regulation
    • Correct acid-base balance
    • Correct serum sodium content
    • Eliminate myocardial depressant factors or known toxins
    • Correct uremia
    • Correct hyperkalemia
    • Correct other electrolyte disturbances
  3. Helps to establish homeostasis
    • Reset water omostat
    • Restore diuretic responsiveness
    • Reduce neurohormonal activation

Cardiac Surgery

  • Resection of non-viable myocardium
  • Revascularization without resection of non-viable myocardium
  • Dor procedure: Surgical resection of infarcted myocardium and left ventricular reconstruction.
  • Placement of a passive containment device to prevent progressive cardiac dilation (Under investigation)

Left Ventricular Assist Devices

  • LVADs are temporary devices to bridge end stage patients to cardiac transplantation.
  • Current clinical research in implementing permanent portable LVADs is underway, and first studies have promising results.

Cardiac Transplantation

  • For patients with end-stage congestive heart failure despite all interventions.
  • 80% 1 year survival and 60% 5 year survival.
  • Lifelong immunosuppressive therapy to prevent (or postpone) rejection, increased risk for opportunistic infections and malignancies.

AHA/ACC Guidelines: Indications for heart 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.

Exercise and Daily Activities

  • Patient should have uninterrupted exercise at least four days a week including a walking program.
  • Rowing machines usually are too vigorous of exercise.
  • Patients with heart failure should avoid weightlifting.
  • The patient should not routinely lift more than 20 pounds.
  • Patients can continue their sexual activity. Some patients take 2.5 or 5.0 mg of sublingual nitroglycerin before sexual activity.

Prognosis

Mortality Associated with Heart Failure

Based on the 44-year follow-up of the NHLBI’s Framingham Heart Study:

Hospital Discharges

  • Hospital discharges for heart failure rose from 400,000 in 1979 to 1,084,000 in 2005, an increase of 171%. (NHDS / NHLBI and AHA calculations).

Cost

• The estimated direct and indirect cost of heart failure in the United States for 2008 is $34.8 billion.

Pathological Findings

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change

  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change

  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change


  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change

  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change

  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change


  • Lung, congestion, heart failure cells (hemosiderin laden macrophages)

    Lung, congestion, heart failure cells (hemosiderin laden macrophages)

  • Lung, Congestive Heart Failure, bone marrow embolus

    Lung, Congestive Heart Failure, bone marrow embolus

  • Lung, pulmonary edema in patient with congestive heart failure due to heart transplant rejection

    Lung, pulmonary edema in patient with congestive heart failure due to heart transplant rejection


  • HEART: Congestive heart failure, hydropic change

    HEART: Congestive heart failure, hydropic change

  • HEART Congestive heart failure, hydropic change

    HEART Congestive heart failure, hydropic change

  • Spleen, congestion, congestive heart failure

    Spleen, congestion, congestive heart failure

References

  1. ↑ Disease and Stroke Statistics - 2008 Update, American Heart Association. Accessed on 09 March 2008
  2. ↑ Lloyd-Jones DM, Larson MG, Leip EP, Beiser A, D'Agostino RB, Kannel WB, Murabito JM, Vasan RS, Benjamin EJ, Levy D; Lifetime Risk for Developing Congestive Heart Failure. Framingham Heart Study. Circulation. 2002; 106: 3068–72 PMID 12473553
  3. ↑ Véronique L. Roger, Susan A. Weston, Margaret M. Redfield, Jens P. Hellermann-Homan, Jill Killian, Barbara P. Yawn, Steven J. Jacobsen Trends in Heart Failure Incidence and Survival in a Community-Based Population JAMA. 2004; 292: 344-50 PMID 15265849

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