A 53-year-old man comes to the office with progressive exertional dyspnea. He has smoked 2 packs of cigarettes per day for the last 35 years. Physical examination shows increased anteroposterior diameter of his chest. Auscultation reveals decreased breath sounds and scattered wheezes throughout his lungs. Examination of his extremities is unremarkable. Echocardiography reveals moderate dilation of the right ventricle and increased central venous pressure. The absence of peripheral edema in this patient is best explained by which of the following compensatory mechanisms?

Question

A 53-year-old man comes to the office with progressive exertional dyspnea.  He has smoked 2 packs of cigarettes per day for the last 35 years.  Physical examination shows increased anteroposterior diameter of his chest.  Auscultation reveals decreased breath sounds and scattered wheezes throughout his lungs.  Examination of his extremities is unremarkable.  Echocardiography reveals moderate dilation of the right ventricle and increased central venous pressure.  The absence of peripheral edema in this patient is best explained by which of the following compensatory mechanisms?

Quizplus · Accepted Answer

11ec160b_3a88_120c_9249_23d56389caae_MD0001_00 This patient has dyspnea, signs of lung hyperinflation, and a heavy smoking history, suggesting chronic obstructive pulmonary disease (COPD). Chronic hypoxia in COPD can lead to pulmonary vasoconstriction, increased pulmonary artery pressure, and right heart failure (ie, cor pulmonale), which is confirmed by this patient's echocardiogram. In turn, right heart failure leads to increased central venous pressure and elevated peripheral capillary hydrostatic pressure, encouraging the development of peripheral edema. Fluid movement across the capillary wall (filtration) into the interstitium is dependent on hydrostatic pressure, oncotic pressure, and capillary permeability. It is tightly balanced by lymphatic drainage, which returns interstitial fluid to the vasculature. Peripheral edema (accumulation of excess fluid in the interstitial space) develops when transcapillary plasma filtration exceeds the resorptive capacity of the lymphatics. Factors that favor development of edema include: Elevated capillary hydrostatic pressure: Higher capillary pressures increase plasma filtration into the interstitium, particularly in dependent tissues. Causes include sodium and water retention (eg, heart failure, renal failure), arteriolar dilation (eg, dihydropyridine calcium channel blockers), and impaired venous return (eg, venous thrombosis). Decreased plasma oncotic pressure: Plasma proteins (eg, albumin) generate oncotic pressure that pulls interstitial fluid back into the capillary bed venules. Edema develops in conditions with decreased albumin levels (eg, nephrotic syndrome, cirrhosis, malnutrition). Lymphatic obstruction: Decreased lymphatic return impairs removal of excess interstitial fluid. Common causes of lymphatic obstruction include filariasis, invasive malignancies, and iatrogenic etiologies (eg, surgical lymph node dissection and radiation therapy). The peripheral lymphatics can significantly increase lymphatic drainage from baseline, allowing compensation for increased capillary fluid filtration that can temporarily delay the development of peripheral edema. However, because the peripheral lymphatics offload fluid to the central venous system (via the thoracic duct), which in heart failure is already volume overloaded, the overall ability to compensate is limited. (Choices A and D) Although increased plasma oncotic pressure and decreased capillary permeability oppose edema formation, neither is associated with COPD. Severe COPD may cause polycythemia due to hypoxemia, but erythrocyte concentration does not affect plasma oncotic pressure. (Choice B) In patients with heart failure, activation of the renin-angiotensin-aldosterone system (RAAS) leads to increased aldosterone levels that cause sodium and water retention (exacerbating edema formation). Volume expansion causes increased atrial/brain natriuretic peptide release, which can partially counteract the effects of RAAS activation; however, aldosterone levels remain elevated. (Choice C) Decreased interstitial fluid pressure favors flow into the interstitium and would contribute to the development of peripheral edema. Educational objective: Peripheral edema results from the accumulation of fluid in the interstitial spaces. Factors that promote edema include elevated capillary hydrostatic pressure, decreased plasma oncotic pressure, and impaired lymphatic drainage. In chronic heart failure, increased lymphatic drainage initially offsets factors favoring edema, temporarily delaying edema development.

A 53-Year-Old Man Comes to the Office with Progressive Exertional