- Orthopnea, paroxysmal nocturnal dyspnea, dyspnea at rest
and during exertion, fatigue.
- Jugular vein distention, peripheral pitting edema, sinus tachycardia,
basilar rales or coarse bubbling rales throughout both lung fields,
cardiomegaly, S3 gallop sound, liver enlargement.
- Left ventricular systolic or diastolic dysfunction.
Congestive heart failure (CHF) is a complex clinical syndrome characterized by dysfunction of the left, right, or both ventricles
and the resultant changes in neurohormonal regulation. This syndrome is accompanied by effort intolerance, fluid retention, and shortened survival. It is often a terminal stage of heart disease, occurring after all reserve capacity and compensatory mechanisms of the myocardium
and peripheral circulation have been exhausted. Initially, the syndrome was described as a state of fluid overload with congestion of the lungs caused by a failing heart. It is, however, now well recognized that in many patients the predominant symptom may be a reduction of functional
capacity because of poor exercise tolerance associated with limited cardiac reserve.
Heart failure results from myocardial dysfunction that impairs the heart’s ability to circulate blood at a rate sufficient
to maintain the metabolic needs of peripheral tissues and various
organs. It follows myocardial damage when the compensatory hemodynamic
and neurohormonal mechanisms are overwhelmed or exhausted and results
from the loss of a critical amount of functioning myocardium due
to acute myocardial infarction (MI), prolonged cardiovascular stress (hypertension,
valvular disease), toxins (eg, alcohol abuse), or infection; in
some cases, there is no apparent cause (idiopathic cardiomyopathy).
Heart failure is a relatively common clinical disorder, estimated to affect more than 5 million patients in the United States. Each
year, new cases of CHF develop in about 550,000 patients. Morbidity
and mortality rates are high; annually, approximately 1 million
patients require hospitalization for CHF, approximately 6.5 million
hospital-days. Each year 50,000 to 60,000 patients die of this condition.
Approximately one-third to one-half of the deaths in patients with CHF are secondary to the progression of cardiac insufficiency
and its associated conditions. The remainder of the patients with CHF
die of sudden cardiac death, presumably related to electrical instability and
ventricular arrhythmias and other cardiovascular conditions as well
as from noncardiovascular causes.
Data describing the natural history of CHF are limited because this condition has not been extensively studied in a prospective manner. The Framingham heart study showed that men in whom clinical symptoms of CHF developed had a 62% probability of dying within 5 years of the onset of symptoms. Subsequent studies in patients with dilated or congestive cardiomyopathy indicate that heart failure is a progressively deteriorating condition, with 20–40% of patients dying within 5 years after the onset of illness; other studies show that patients with advanced CHF (New York Heart Association [NYHA] class IV) have a 40–50% annual mortality rate.
When an excessive workload is imposed on the heart by increased systolic blood pressure (pressure overload), increased diastolic
volume (volume overload), or loss of myocardium, normal myocardial cells
hypertrophy in an effort to enhance contractile force of the normal
areas. The subsequent alterations in biochemistry, electrophysiology,
and contractile function lead to mechanical alterations of myocardial
function: The rate of contraction slows, the time to develop peak
tension increases, and myocardial relaxation is delayed. Peak force
development may be well preserved with enough viable myocardium
and adequate time for the development of force. Thickening of the
ventricular wall limits the rate of ventricular filling (diastolic dysfunction),
which is worsened by increased heart rate because it shortens the
duration of ventricular filling. The force of myocardial contraction
is eventually reduced as cell loss and hypertrophy continue, leading
to significant geometric ventricular alterations and increased volumes.
This process of chamber dilatation or hypertrophy is known as cardiac remodeling.
After the initial compensatory phase, the increase in intracavitary volume is usually associated with further reductions in ventricular
ejection fraction (progressive systolic dysfunction) and eventually
with abnormalities in the peripheral circulation from activation
of various neurohormonal compensatory mechanisms.
The ensuing CHF is characterized by a reduced contraction response to increase in volume (flattened Frank-Starling curve) and a reduced
left ventricular ejection fraction (LVEF). The abnormal neurohormonal
responses lead to increased systemic sympathetic tone and activation
of the renin-angiotensin system. Production of angiotensin increases,
causing peripheral vasoconstriction. The increase in peripheral
arterial resistance limits cardiac output during exercise. The increased levels
of angiotensin II also stimulate release of aldosterone by the adrenal
glands, enhancing sodium retention and thus leading to fluid retention
and peripheral edema.
Myocardial (pump) failure and CHF are not necessarily closely related in time. Patients are often initially asymptomatic, with
the signs and symptoms of CHF developing only after several months
of myocardial failure and decreased ejection fraction. Cardiac output
does not increase adequately during exercise, but it can be normal
at rest during this period. Although patients may be asymptomatic
or slightly symptomatic at rest, with the ejection fraction unchanged, alterations
in peripheral vasculature occur with slowly rising peripheral resistance
during exercise. Exercise performance slowly becomes limited because the
peripheral vasculature cannot meet the increased metabolic needs
of exercising skeletal muscles.
Although the precise mechanism by which hemodynamic responses and neurohormonal factors interact to cause progressive clinical
deterioration in CHF is unknown, the hemodynamic and neurohormonal
abnormalities that increase cardiac wall stress can lead to cell
slippage, morphologic myocardial cell changes, and structural remodeling
of the heart. The dilatation of the ventricular cavity and change
in its shape can eventually lead to mitral regurgitation. The increase
in cardiac pressures and volume may also trigger myocardial ischemia,
especially in patients with underlying coronary artery disease (CAD).
The myocardial hypertrophy can enhance cardiac metabolic demands and may increase the risk of ischemia in patients with CAD. In addition,
prolonged activation of neurohormonal axes may be deleterious to the heart in an independent manner: High concentrations of norepinephrine
and angiotensin II can exert direct ...