A 65-year-old woman with chronic obstructive pulmonary disease comes to the office for a follow-up appointment. The patient reports increasing shortness of breath that is not relieved by her inhalers. Her other medical conditions include osteoarthritis. She is a former smoker with a 45-pack-year history. Blood pressure is 120/70 mm Hg, pulse is 75/min, and respirations are 22/min. Oxygen saturation on room air is 91% at rest. On physical examination, jugular venous pressure is elevated. There is increased intensity of the pulmonic component of S2. Breath sounds are decreased bilaterally with scattered wheezes but no crackles. There is 2+ lower extremity edema. Which of the following hemodynamic parameters is most likely to be increased in this patient?

Question

A 65-year-old woman with chronic obstructive pulmonary disease comes to the office for a follow-up appointment.  The patient reports increasing shortness of breath that is not relieved by her inhalers.  Her other medical conditions include osteoarthritis.  She is a former smoker with a 45-pack-year history.  Blood pressure is 120/70 mm Hg, pulse is 75/min, and respirations are 22/min.  Oxygen saturation on room air is 91% at rest.  On physical examination, jugular venous pressure is elevated.  There is increased intensity of the pulmonic component of S2.  Breath sounds are decreased bilaterally with scattered wheezes but no crackles.  There is 2+ lower extremity edema.  Which of the following hemodynamic parameters is most likely to be increased in this patient?

Quizplus · Accepted Answer

This patient with chronic obstructive pulmonary disease (COPD) has evidence of pulmonary hypertension complicated by right-sided heart failure. Hypoxic vasoconstriction is a physiologic mechanism unique to lung tissue that helps minimize ventilation-perfusion mismatch and increase overall gas exchange efficiency. However, chronic and diffuse pulmonary vasoconstriction, which occurs with advanced hypoxic lung disease (eg, COPD, interstitial lung disease, obesity hypoventilation syndrome), and can lead to pulmonary hypertension (ie, increased right ventricular afterload). Pulmonary hypertension typically presents with dyspnea and/or fatigue, and some patients may develop exertional angina or syncope due to reduced cardiac output. Physical examination can reveal left parasternal lift (due to right ventricular hypertrophy) and a loud pulmonic component of S2 due to high pulmonary artery pressure. Over time, the right ventricle may be unable to pump against the increased afterload and right-sided heart failure can develop, evidenced by jugular venous distension and prominent lower extremity edema. (Choices A, B, and D) The hemodynamic parameters in pulmonary hypertension secondary to hypoxic lung disease are similar to those in pulmonary arterial hypertension. Left ventricular preload and stroke volume (cardiac output) are decreased due to impaired pumping of blood through the lungs to the left atrium. Pulmonary capillary wedge pressure, an estimate of left atrial pressure and a representation of left-sided preload, is also decreased. (Choice C) Pulmonary arterial compliance decreases with pulmonary hypertension due to vascular remodeling and stiffening of the pulmonary arterial wall. Educational objective: Advanced hypoxic lung disease (eg, chronic obstructive pulmonary disease, interstitial lung disease, obesity hypoventilation syndrome) is a common cause of pulmonary hypertension (ie, increased right ventricular afterload). The increase in pulmonary arterial pressure mainly results from chronic and diffuse hypoxic vasoconstriction, with a lesser degree of vascular remodeling than in (primary) pulmonary arterial hypertension.

A 65-Year-Old Woman with Chronic Obstructive Pulmonary Disease Comes to the Office