Congestive Heart Failure Disease

BASICS

DESCRIPTION

Congestive heart failure (CHF) is the principal complication of heart disease. It is a pathophysiologic state produced by an abnormality in cardiac pump function (either transient or prolonged). The heart is unable to transport blood in a sufficient flow to meet metabolic needs. CHF occurs at some time in most cases of severe heart disease.

This produces a variety of clinical circumstances from acute left ventricular dysfunction (due to tachyarrhythmia, bradyarrhythmia, and acute myocardial infarction) to chronic left ventricular dysfunction (due to chronic volume/pressure overload as seen in valvular heart disease)
Two physiologic components explain most of the clinical findings of CHF - most patients have findings consistent with both mechanisms:
- an inotropic abnormality resulting in diminished systolic emptying (systolic failure)
- a compliance abnormality in which the ability of the ventricles to accept blood is impaired (diastolic failure).
System(s) affected: Cardiovascular, Pulmonary
Genetics: N/A
Incidence/Prevalence in USA:
- Most common inpatient diagnosis for patients over 65
Predominant age: Varies by etiology of heart disease
Predominant sex:
- Male > Female - ages 40-75
- Male = Female - ages 75 and over

SIGNS AND SYMPTOMS

Early and mild impairment:
- Basilar rales
- Positive hepatojugular reflux
- Faint S3 gallop
- Nocturia
- Dyspnea on exertion-cardinal sign of left heart failure
- Deteriorating exercise capacity
- Fatigue
- Difficulty breathing
- Weakness
- Tachypnea with mild exertion
Moderate impairment:
- Nocturnal nonproductive cough
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Wheezing, especially nocturnal in absence of history of asthma or infection (cardiac asthma)
- Anorexia
- Fullness to dull pain in RUQ
- Tachypnea at rest
- Anxiety
- Hepatomegaly with tenderness to palpation
- Cool extremities due to peripheral vasoconstriction
- Prominent rales over bases
- Right pleural effusion
- Edema
- Gallop rhythm
- Diastolic hypertension
- Elevated jugular venous pressure
- Cardiomegaly
Severe impairment:
- Cerebral dysfunction
- Abdominal bloating (ascites)
- Cyanosis
- Hypotension
- Pulsus alternans
- Anasarca
- Frothy and/or pink sputum
- Increased P2
- Cardiac cachexia
- Cheyne-Stokes respirations

CAUSES

Myocardial infarction
Cardiomyopathy
- Alcoholic
- Viral
- Long-standing hypertension
- Drugs (e.g., cyclosporine)
Valvular abnormalities
- Aortic stenosis or regurgitation
- Rheumatic heart disease (mitral and aortic valvular disease)
Volume overload
Cardiac depressants; negative inotropes (e.g., beta blockers)
Arrhythmias, eg, atrial fibrillation
High output states
- Hyperthyroidism
- Beriberi heart disease

RISK FACTORS

Iatrogenic inappropriate reduction of intensity of therapy
Inappropriate Na+ and/or fluid excess
Patient non-compliance
Intercurrent arrhythmia, eg, atrial fibrillation
Administration of drug with negative inotropic effects
Inappropriate physical, emotional, or environmental stress
Thyrotoxicosis, pregnancy, or any condition associated with increased metabolic demand

DIAGNOSIS

LABORATORY

Lab findings - early and mild to moderate in severity
- Respiratory alkalosis
- Mild azotemia
- Decreased erythrocyte sedimentation rate
- Proteinuria (usually less than 1 gm/24 h that clears with treatment)
Lab findings - severe
- Increased creatinine
- Hyperbilirubinemia in severe cases
- Dilutional hyponatremia with treatment in severe cases

Drugs that may alter lab results: N/A
Disorders that may alter lab results: N/A

PATHOLOGICAL FINDINGS

Early and acute
- Firm lungs with microscopic revealing engorged capillaries with thickening of the alveolar septa with extravasation of red cells and edema fluid
- Liver is engorged, firm, and fluid-filled. Microscopic - reveals dilated central hepatic veins and sinusoids.
Late and chronic
- Hemosiderin deposits in lungs
- "Nutmeg" liver with centrilobular necrosis
- Occasionally hemorrhagic nonbacterial enterocolitis with hemorrhagic necrosis secondary to mesenteric vasoconstriction

SPECIAL TESTS

N/A

IMAGING

X-ray - mild changes: pulmonary artery wedge pressure = 18-23 mm Hg (2.4-3.1 kPa)
- Increased heart size
- Increased blood flow to the upper lobes
- Equalization of flow between the upper and lower lobes
X-ray - moderate severe pulmonary artery wedge pressure = 20-25 mm Hg (2.7-3.3 kPa)
- Interstitial edema
- Kerley's B lines
- Perivascular edema
- Subpleural effusions
X-ray - severe changes: pulmonary artery wedge pressure > 25 mm Hg (> 3.3 kPa)
- Alveolar edema
- Butterfly pattern of pulmonary edema

DIAGNOSTIC PROCEDURES

Echocardiographic studies
Cardiac catheterization, both right and left, for full diagnosis and prognosis

TREATMENT

APPROPRIATE HEALTH CARE

Inpatient when severe

GENERAL MEASURES

Immediate treatment of the heart failure
Search for underlying correctable conditions
Eliminate contributing factors when possible
Supplemental oxygen
Antiembolism stockings
Fluid and sodium restriction. Education about this is imperative for long term control. Daily weights guide overall therapy.
Identify and control underlying correctable conditions (e.g., acute MI, valvular disease, hyperthyroidism, but most commonly inadvertent salt and/or fluid overload)

SURGICAL MEASURES

Heart valve surgery - possibly, if defective heart valve is responsible; mitral valve repair especially helpful if mitral regurgitation is aggravating CHF
Cardiac transplantation - to be considered in patients (age < 55) without other disqualifying medical problems, who are developing CHF unresponsive to other therapeutic maneuvers, and who are felt to have a life expectancy of less than a year

ACTIVITY

During severe stage, bed rest with elevation of head of bed and anti-embolism stockings to help control leg edema
Gradual increase in activity with walking will help increase strength

DIET

Sodium restriction (initially 4 gm sodium qd)
Weight reduction diet if appropriate
Low fat diet to retard coronary artery disease
Appropriate fluid restriction

PATIENT EDUCATION

Printed patient information available from:
- American Heart Association, 7320 Greenville Avenue, Dallas, TX 75231, (214)373-6300
- American College of Cardiology, 911 Old Georgetown Road, Bethesda, MD 20814, (301) 897-5400

FOLLOW UP

PREVENTION/AVOIDANCE

Treatment of underlying disorders when possible

POSSIBLE COMPLICATIONS

Electrolyte disturbance
Atrial and ventricular arrhythmias
Mesenteric insufficiency
Protein enteropathy
Digitalis intoxication

EXPECTED COURSE AND PROGNOSIS

Result of initial treatment is usually good, whatever the cause
Long-term prognosis variable. Mortality rates range from 10% with mild symptoms to 50% with advanced, progressive symptoms.

MISCELLANEOUS

ASSOCIATED CONDITIONS

See Causes

AGE-RELATED FACTORS

Pediatric: Usually associated with congenital heart disease
Geriatric: Medications may need dosage adjustment
Others: N/A

PREGNANCY

If occurs, will require special care

OTHER NOTES

N/A

ABBREVIATIONS

CCF = congestive cardiac failure

Clinical Investigations

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