In cor pulmonale, pulmonary hypertension increases the heart’s workload. To compensate, the right ventricle hypertrophies to force blood through the lungs. However, the compensatory mechanism begins to fail, and larger amounts of blood remain in the right ventricle at the end of diastole. This causes ventricular dilation. In response to hypoxia, the bone marrow produces more red blood cells, resulting in polycythemia. Then the blood’s viscosity increases, further aggravating pulmonary hypertension, increasing the right ventricle’s workload, and causing heart failure.

Cor pulmonale is most commonly caused by COPD. Less frequent causes may include the following:

Cor pulmonale eventually may lead to biventricular failure. Depending on the severity of cor pulmonale, hepatomegaly, edema, ascites, and pleural effusions may develop. Because of polycythemia, the risk of thromboembolism also increases.

As long as the heart can compensate for the increased pulmonary vascular resistance, your patient will report signs and symptoms associated with the underlying disorder, occurring mostly in the respiratory system. The patient is most likely to
complain of a chronic productive cough, exertional dyspnea, wheezing respirations, fatigue, and weakness.

Cor pulmonale progresses with dyspnea (even at rest) that worsens on exertion, tachypnea, orthopnea, edema, weakness, and right upper quadrant discomfort. Chest examination typically discloses characteristics of the underlying lung disease.

On inspection, you may find such signs of cor pulmonale (and right ventricular failure) as dependent edema and distended neck veins. Drowsiness and alterations in consciousness may also occur.

Palpation may disclose tachycardia and a weak pulse (from decreased cardiac output), an enlarged and tender liver, hepatojugular reflux, and a prominent parasternal or epigastric cardiac impulse.

Chest auscultation yields various findings, depending on the cause of cor pulmonale. If the patient also has COPD, auscultation may detect crackles, rhonchi, and diminished breath sounds. With disease secondary to upper airway obstruction or damage to the respiratory control center, auscultation findings may be normal except for a right ventricular lift, a gallop rhythm, and a loud pulmonic component of S₂.

If the patient has tricuspid insufficiency, you’ll hear a pansystolic murmur at the lower left sternal border. The murmur’s intensity increases when the patient inhales, distinguishing it from a murmur caused by mitral valve disease. Also, you may hear a right ventricular early murmur that increases on inspiration and can be heard at the left sternal border or over the epigastrium. You may also auscultate a systolic pulmonary ejection sound.