Congestive heart failure (CHF) is a symptom complex characterized by pulmonary congestion, peripheral edema, jugular venous distention, hepatojugular reflux and an S3 gallop on physical exam. The complex usually manifests as shortness of breath, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, weakness or fatigue. Not all symptoms or manifestations are always present, and there may even be a paucity of findings in persons with mild heart failure. The Studies of Left Ventricular Dysfunction (SOLVD) Prevention Trial showed that asymptomatic left ventricular dysfunction with an impairment of the ejection fraction to 0.35 or less was associated with progression to symptomatic heart failure over the ensuing three years. The diagnosis is usually made when signs of fluid overload, an S3 gallop, characteristic radiographic abnormalities (cardiomegaly, pulmonary edema, congestion, Kerley B lines), jugular venous distention and hepatojugular reflux are present with a typical history as stated above. Compensation for decreased cardiac output is driven by an exagerated response of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS).

Heart failure occurs when the ability of the heart to pump blood is impaired resulting in a decrease in the ejection fraction. The impairment may occur during either the systolic (impaired contractility) or diastolic (impaired relaxation of the ventricle resulting in incomplete filling) phase of the cardiac cycle, and may occur in either the right or left ventricles. The end result is a decrease in the delivery of oxygenated blood to vital organs. CHF is not a final diagnosis but is the result of some underlying etiology (coronary artery disease, post myocardial infarction, hypertension, valvular abnormalities, cardiomyopathy, myocarditis, infiltrative diseases, etc).

The degree of impairment caused by heart failure is rated by a scale called the New York Heart Association Classification. This scale is ideal as it allows physicians to grade the patients condition on initial presentation and provides a means to assess response to therapy. The classification is as follows:

CLASS I - no limitation of physical activity

CLASS II- slight limitation of physical activity during strenuous exertion

CLASS III- marked limitation of physical activity but patient comfortable at rest

CLASS IV - severly limited physical activity and patient symptomatic at rest

Lab abnormalities commonly seen in CHF include hyponatremia secondary to activation of the renin-angiotensin-aldosterone system. An acute exacerbation of the impaired cardiac output may result in renal hypoperfusion, which may manifest as an increase in BUN and creatinine. Acute renal failure may be further exacerbated by overly aggressive administration of diuretics in an effort to reverse volume overload. B-type natriuretic peptide (BNP) is elevated greater than 100 pg/mL, and is a good initial screening test when patients present with pulmonary symptoms or edema.

Treatment of CHF depends on the nature of the disorder (systolic vs. diastolic). An echocardiogram is a good initial test to make this distinction and guide the initial choice of medications used. Calculation or measurement of the ejection fraction from an echocardiogram or MUGA scan, respectively, allows an assessment of the severity of impairment and the prognosis. Other techniques available to determine the ejection fraction include contrast angiography, electron beam computed tomography and magnetic resonance imaging. The most appropriate treatment is correction of the underlying etiology (coronary artery disease, valvular dysfunction, arrhythmias, infiltrative diseases, etc.). Standard outpatient treatment of systolic heart failure consists of an ACE inhibitor or ARB and a  beta blocker (coreg or metopropol succinate) with or without digoxin and loop diuretics added for symptom control. Once ACEI/ARB and beta blockers are started, their doses should be increased to the maximally tolerated dosages for appropriate RAAS and SNS inhibiton, respectively.  In patients with a poor response to high dose loop diuretic therapy, metolazone (Zaroxolyn) 2.5 to 5 mg given orally one hour before the loop diuretic dose may increase diuresis. In patients in whom ACE inhibitors are contraindicated, hydralazine plus a long acting nitroglycerine preparation are indicated or they may be added to the above combination therapy (ACEI/ARB + beta blocker) when there is an inadequate response such as is seen in persons of African heritage. Spironolactone should be added to patients with NYHA stage III or IV disease.  Cardiac resynchronization (biventricular pacing) with an implantable cardiac defibrillator are additional measeures to improve symptoms and survival, respectively. In severe cases of systolic heart failure requiring intensive care, dobutamine (2. 5 - 10 mcg/kg/min) is a potential therepeutic choice as it has both a positive ionotropic effect on the heart and it decreases afterload. Alternatively, intravenous sodium nitroprusside is an effective vasodilator for symptomatic relief, and nesiritide may alleviate symptoms.  Vasopressin receptor antagonists may be used to treat the associated hyponatremia if other therapies fail or if symptoms dictate intervention.

Diastolic heart failure, like systolic dysfunction, is treated by correcting the underlying etiology. Symptomatic therapy consists of diuretics, beta blockers or the calcium channel blockers, verapamil or diltiazem. The calcium channel blocker nifedipine should not be used as it may increase the heart rate and aggrevate cardiac ischemia. Patients with diastolic heart failure are very dependent on the effects of the atrial component of the left ventricular filling phase. Therefore, it is imperative to make every effort to maintain sinus rhythm in these patients. All patients with CHF should be started on a low sodium diet to help prevent or treat fluid retention.