Pathophysiology

HF usually originates with left-sided ventricular failure (Figure 19-2), which is systolic HF. This side is most affected by hypertension, valvular dysfunction, and coronary artery disease. When the ventricle fails to pump enough blood to meet the metabolic needs of the body, baroreceptors in the circulatory system cause reflex sympathetic nervous system activation. Veins and arteries constrict to increase critical organ, especially cardiac, perfusion. The Frank-Starling mechanism increases preload to increase myocardial contractile strength. HR increases, also to ensure perfusion. These changes reduce the blood flow to the kidneys, where receptors act to release renin, starting the angiotensin-aldosterone cascade, which leads to further vasoconstriction and sodium and water retention.

As HF progresses, the compensatory mechanisms can no longer maintain homeostasis. Rapid heart rhythm reduces the amount of blood pumped and, consequently, oxygen perfusion. Peripheral vasoconstriction forces the heart to pump harder, and the renin-angiotensin-aldosterone mechanism causes overfilling of the heart. The overall result is left-sided ventricular failure. The pulmonary system experiences increasing capillary pressure and fluid leakage into the interstitial space, resulting in pulmonary edema. As a further result, blood pools in the right ventricle, causing increased pressure in the systemic circulation (right-sided heart failure). This distends visceral veins, the liver and spleen become engorged, and jugular vein distention (JVD) and tissue edema in the extremities become evident, particularly in dependent areas such as the ankles and legs.

Diastolic HF is caused by a stiff left ventricle with decreased compliance and impaired relaxation, causing increased end-diastolic pressure. This leads to decreased ventricular filling. The causes and symptoms are similar to those of systolic failure, but the treatment may be different.

Disease Process

HF is a clinical syndrome characterized by signs and symptoms of volume overload and inadequate tissue perfusion. Common causes of HF are ischemic heart disease, systemic hypertension, valve disease, hypertrophic cardiomyopathy from end-stage hypertension, restrictive cardiomyopathy, hypothyroidism and hyperthyroidism, atrial fibrillation, and COPD.

Assessment

Perform a complete history and physical examination that includes measurement of lying, sitting, and standing BP and pulse. In general, left-sided heart failure manifests as pulmonary signs and symptoms; right-sided heart failure causes systemic signs and symptoms. Both left- and right-sided heart failure are present in most patients. The onset is often gradual and subtle. Left-sided symptoms include paroxysmal nocturnal dyspnea (PND), dyspnea on exertion (DOE), S3 (S4 may be present with hypertension) heart sounds, arrhythmias, and pulsus alternans. Right-sided symptoms include fatigue, syncope, decreased exercise tolerance, hepatomegaly, peripheral edema, JVD, ascites, decreased appetite, and early satiety.

Perform diagnostic tests (Table 19-3) to rule out other possible causes for the symptoms, to determine underlying causes of HF, and to establish a baseline from which to monitor the patient. Obtain a complete blood count because anemia can mask heart failure symptoms. Renal function studies are especially important for dosage determination. Potassium levels are crucial because of the risk for arrhythmia. Obtain blood glucose testing because the risk of heart failure was found to be 2.4- and 5-fold increased in men and women, respectively, in the Framingham study. Order thyroid function tests, especially if atrial fibrillation is detected. Brain natriuretic peptide (BNP) is an FDA-approved diagnostic tool that is a reliable measure of cardiac function in both systolic and diastolic failure. A low BNP rules out HF; BNP may have a role in monitoring of patients with HF. Classify HF according to systolic or diastolic heart failure to determine appropriate treatment.