The manifestations of heart failure depend on which ventricle is primarily affected ( Table49-2). Left ventricular failure can result from either diastolic or systolic dysfunction and can lead to increased pulmonary venous pressures, interstitial lung fluid, and pulmonary edema. Right ventricular failure leads to jugular venous distention, peripheral edema, hepatic congestion, and ascites.
The most common symptom of left-sided heart failure is breathlessness, or dyspnea, particularly with exertion.17 When pulmonary venous pressure reaches a critical level (20 mmHg), there is movement of fluid into the pulmonary interstitium, compressing airways and alveoli.1 The increased resistance to airflow intensifies the work of breathing. In addition, stimulation of the juxtacapillary receptors (J receptors) causes rapid shallow breathing. Other manifestations of pulmonary congestion include orthopnea and paroxysmal nocturnal dyspnea (PND). 18,9,,i and U Orthopnea is the sensation of breathlessness while lying flat and is relieved by sitting upright. Orthopnea results from the redistribution of intravascular blood from the gravity-dependent portions of the body to the lungs. The degree of orthopnea is usually assessed by the number of pillows a patient uses at night to avoid breathlessness. PND is severe breathlessness that awakens a patient from sleep 2 to 3 h after lying down. PND is due to the gradual reabsorption of interstitial lower extremity edema after lying down, with subsequent greater venous return to the heart and lungs.1
Clinical manifestations of left-sided heart failure due to alterations in blood flow include fatigue, altered mental status, and reduced urine output (especially during the day). At night, urine output may increase due to increases in venous return. The increased urinary frequency at night is termed nocturia. 1
Right-sided heart failure causes increased systemic venous pressures and peripheral edema. 18 Additional edema of the gastrointestinal tract causes anorexia and nausea, and right upper quadrant abdominal pain occurs as the liver becomes engorged.
Physical findings of left-sided heart failure include dusky or pale skin, diaphoresis, and cool extremities due to poor perfusion and peripheral arterial vasoconstriction.18 Pulmonary congestion commonly results in tachypnea and bilateral inspiratory crackles on auscultation. Additional auscultatory findings include rhonchi and wheezing ("cardiac asthma") due to airway edema. Pleural effusions may develop, detected by dullness to percussion at the lung bases. In advanced heart failure, Cheyne-Stokes respiration can occur and is a respiratory pattern characterized by periods of hyperventilation separated by periods of apnea. 1
Frequently, sinus tachycardia secondary to sympathetic nervous system activity is present in heart failure patients. 18 Cardiac auscultation may reveal a third heart sound (S3), an early diastolic sound resulting from abnormal filling into the dilated ventricle. Also present may be a fourth heart sound (S 4), which results from forceful atrial contraction into a stiffened ventricle. Finally, pulsus alternans (alternating strong and weak contractions detected in the peripheral pulse) may occur in advanced heart failure.1
Right-sided heart failure may result in additional physical findings due to elevated systemic venous pressures. Jugular venous distention (JVD) is common. 1,8 Engorgement of the liver results in hepatomegaly, right upper quadrant tenderness, and the presence of the hepatojugular reflux (JVD with liver palpation). Peripheral edema accumulates in the dependent areas of the body, including the ankles and legs of ambulatory patients and the presacral region of bedridden patients. 18
Radiographic manifestations of left-sided CHF generally relate to the increases in pulmonary venous pressures. 1 When the pulmonary pressures exceed 15 mmHg, hydrostatic pressure increases in the gravity-dependent edematous lower zones of the lung. Because of the higher resistance to flow in the lower regions, blood flow is selectively shunted to the upper regions, and the chest radiograph shows upper-zone vascular redistribution. As pulmonary pressures exceed 20 mmHg, interstitial edema occurs with loss of distinct vascular margins on chest x-ray. Interlobular edema results in Kerley B lines, which are short linear markings at the periphery of the lower lung fields on the chest x-ray.1 When pulmonary pressures reach 25 mmHg, alveolar pulmonary edema develops with opacification of the airspaces on x-ray. However, in patients with long-standing CHF, enhanced lymphatic drainage may minimize these radiographic findings. 1
Depending on the cause of the CHF, additional radiographic findings include cardiomegaly and pleural effusions. 1 Cardiomegaly is defined as a cardiothoracic ratio greater than 0.5 on a posteroanterior film.1 Pleural effusions may occur in either left-sided or right-sided failure but are usually the result of bilateral heart failure. High right atrial pressure may cause azygos vein enlargement on chest x-ray.
The electrocardiogram (ECG) may reveal evidence of acute myocardial infarction or ischemia as a cause of acute decompensation of CHF. In chronic CHF, the ECG usually reveals evidence of ventricular hypertrophy, atrial enlargement, or conduction abnormalities. 1
In patients with dyspnea or evidence of pulmonary edema, arterial blood gases will help define the acid-base status and are necessary to quantitate the level of respiratory effort. Hypoxia is a frequent finding with pulmonary edema and, when associated with hypercarbia and acidosis, can portend impending respiratory failure.1,8
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