Patient will present as → a 65-year-old man comes to the office due to 3 days of progressive dyspnea and purulent sputum production. The patient takes albuterol and tiotropium bromide for moderate chronic obstructive pulmonary disease. His medical history is relevant for a 40-pack-year smoking history, type II diabetes mellitus, hyperlipidemia, and coronary artery stenting 2 years ago. Physical exam shows a barrel-shaped chest, inspiratory crackles, hepatojugular reflux, pulsus paradoxus, and ventricular gallop. His temperature is 38.1°C (100.5°F), the pulse is 130/min, respirations are 28/min, blood pressure is 130/84 mmHg, and pulse oximetry on room air shows an oxygen saturation of 86%.
Cor pulmonale is right ventricular enlargement and eventually failure secondary to a lung disorder that causes pulmonary artery hypertension
- Lung disorders such as PE, vasculitis, ARDS, COPD (most common), asthma, and ILD cause pulmonary artery hypertension
- Pulmonary artery hypertension then leads to right ventricular failure
- Findings include peripheral edema, neck vein distention, hepatomegaly, and a parasternal lift
Pathophysiology of Cor Pulmonale
The diagnosis of cor pulmonale is usually made with an echocardiogram → increased pressure in the pulmonary arteries and right ventricle
- Spirometry can be done to look for chronic lung disease
- The gold standard diagnostic test to directly measure pulmonary pressures and assess for response to vasodilating medications is a right heart catheterization
Treatment of chronic cor pulmonale generally focuses on the underlying pulmonary disease
- Early identification and treatment of the cause are important before cardiac structural changes become irreversible
- Correct hypoxemia with long-term oxygen when resting SpO2 is ≤88% (or PaO2 ≤55 mmHg) — this reduces hypoxic pulmonary vasoconstriction and improves survival in COPD
- Diuretics are used for fluid overload and peripheral edema, but cautiously — over-diuresis lowers right ventricular preload and can drop cardiac output
- Pulmonary arterial hypertension drugs (e.g., sildenafil, bosentan) are generally not recommended for pulmonary hypertension caused by lung disease
- Right ventricular ischemia or pulmonary artery stretching can cause anginal chest pain in cor pulmonale that does not respond to nitrates
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Question 1 |
A 66-year-old man with a 50-pack-year smoking history has worsening exertional dyspnea and leg swelling. Examination shows jugular venous distension, a loud P2, and bilateral pitting edema. Echocardiography shows right ventricular hypertrophy and dilation with normal left ventricular function and normal valves. Which of the following is the most likely underlying cause of his right heart failure?
Chronic obstructive pulmonary disease | |
Constrictive pericarditis Hint: Constrictive pericarditis causes right-sided congestion with a pericardial knock and Kussmaul sign, but not right ventricular hypertrophy from pulmonary hypertension. | |
Left ventricular systolic dysfunction Hint: Left ventricular function is normal here; right heart failure from left heart disease is not considered cor pulmonale. | |
Mitral stenosis Hint: The valves are normal on echocardiography; mitral stenosis causes pulmonary hypertension from left heart disease, not lung disease. | |
Pulmonary valve stenosis Hint: Pulmonary valve stenosis is a structural valve problem and would be seen on echocardiography. |
Question 1 Explanation:
Cor pulmonale is right ventricular enlargement and failure caused by pulmonary hypertension from lung disease. Chronic obstructive pulmonary disease is the most common cause: chronic hypoxemia triggers pulmonary vasoconstriction and vascular remodeling, which raises pulmonary pressures and overloads the right ventricle. Other causes include interstitial lung disease, obstructive sleep apnea or obesity hypoventilation, and chronic pulmonary emboli. Right heart failure from left heart or valvular disease is not cor pulmonale.
Question 2 |
A 62-year-old woman with pulmonary hypertension called 911 complaining of sweating and difficulty in breathing. Upon arrival to her home the paramedics found her to have pallor, diaphoresis, tachypnea, hypotension, and tachycardia. Her pulse oximetry was 89%, so they gave her oxygen via nonrebreather mask and transported her to the emergency department (ED). She was not complaining of angina. The ED physician assistant noted her to be in acute distress with elevated jugular venous pressure, a medial heave, a tender palpable liver, a systolic murmur of tricuspid regurgitation, and an S4 gallop. ECG demonstrated right axis deviation and right ventricular hypertrophy with no ST-T changes. Her arterial blood gas (ABG) demonstrated a low PaO2 and a low PaCO2. What is her likely diagnosis?
acute coronary syndrome Hint: Marked hypotension in acute coronary syndrome occurs when the right coronary artery is affected. Acute coronary syndromes do not usually present with systolic murmurs, but patients will complain of angina and the ECG changes will include ST-segment changes. | |
cor pulmonale | |
heart failure Hint: Patients who have severe heart failure will have similar symptoms but also have pulsus alternans and pulmonary rales. | |
pulmonary embolus Hint: patients with pulmonary embolus may have hemodynamic changes but usually have a low PaO2 and a normal PaCO2. ECG may show right-axis deviation in a pulmonary embolus as well. |
Question 2 Explanation:
This patient with known pulmonary hypertension now has signs of right heart failure: elevated jugular venous pressure, a right ventricular (medial) heave, a tender enlarged liver, a tricuspid regurgitation murmur, and right ventricular hypertrophy with right axis deviation on ECG. That picture is decompensated cor pulmonale. Acute coronary syndrome usually causes angina and ST-T changes, and right ventricular infarction causes hypotension with clear lungs. Left-sided heart failure causes pulmonary rales and orthopnea rather than isolated right-sided findings. Pulmonary embolism also causes sudden dyspnea, hypoxemia, and a low PaCO2 from tachypnea and can precipitate right heart failure, so it must be excluded (CT pulmonary angiography), but the chronic right ventricular hypertrophy on ECG points to long-standing pressure overload from pulmonary hypertension.
Question 3 |
A 68-year-old man with severe chronic obstructive pulmonary disease comes to the clinic for follow-up. He reports progressive ankle swelling and exertional dyspnea. He quit smoking 1 year ago and uses a long-acting bronchodilator inhaler daily. Temperature is 37.0°C (98.6°F), pulse is 92/min, respirations are 20/min, and blood pressure is 128/76 mmHg. Resting pulse oximetry on room air is 86%. Examination shows jugular venous distension, a left parasternal heave, a loud P2, and bilateral pitting edema to the mid-shins. Echocardiography shows right ventricular dilation, an estimated pulmonary artery systolic pressure of 55 mmHg, and normal left ventricular function. Which of the following is the most appropriate intervention to improve this patient's survival?
Bosentan Hint: Endothelin receptor antagonists treat group 1 pulmonary arterial hypertension; they are not recommended for pulmonary hypertension due to lung disease and can worsen ventilation-perfusion mismatch. | |
Digoxin Hint: Digoxin may help select patients with right heart failure and atrial arrhythmias but does not improve survival in cor pulmonale. | |
Furosemide Hint: Diuretics relieve edema but must be used cautiously because over-diuresis lowers right ventricular preload; they do not improve survival. | |
Long-term supplemental oxygen | |
Sildenafil Hint: Phosphodiesterase-5 inhibitors treat pulmonary arterial hypertension; they are not recommended for pulmonary hypertension due to COPD and can worsen hypoxemia. |
Question 3 Explanation:
Long-term oxygen therapy (at least 15 hours a day) is indicated for chronic resting hypoxemia (SpO2 ≤88% or PaO2 ≤55 mmHg) and, along with smoking cessation, is the only intervention shown to improve survival in COPD. It also reduces hypoxic pulmonary vasoconstriction, the main driver of cor pulmonale. Treatment of cor pulmonale focuses on the underlying lung disease and correcting hypoxemia; diuretics are used cautiously for edema, and pulmonary arterial hypertension drugs are not recommended for pulmonary hypertension caused by lung disease.
There are 3 questions to complete.
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References: Merck Manual · UpToDate