35 CASE 35
A 68-year-old man comes to the clinic complaining of difficulty in breathing.
The patient suffered a myocardial infarction involving the anterior wall of the left ventricle 6 months earlier. Myocardial injury reduced the ventricular ejection fraction to 40%. During the past month, the patient has gained 8 pounds. He indicates that he has difficulty sleeping when lying down, which has been getting worse over the past month.
PATHOPHYSIOLOGY OF KEY SYMPTOMS
Pulmonary edema occurs when the net volume of plasma filtered through the pulmonary capillaries exceeds the ability of the pulmonary lymphatic vessels to transport the fluid back to the vascular system. Accumulation of fluid in the pulmonary interstitium increases the distance between the alveoli and the pulmonary capillaries and, consequently, impairs gas diffusion.
Fluid exchange across the pulmonary capillaries is governed by the same balance of hydrostatic pressures and protein-mediated oncotic pressure as occurs in other capillary beds. The relatively low pulmonary capillary pressure (normally 10 to 15 mm Hg) results in the net balance for fluid exchange across the pulmonary capillaries favoring reabsorption. Consequently, there is normally very little free fluid in the pulmonary interstitial space (Fig. 35-1).
FIGURE 35–1 Hydrostatic and osmotic forces at the capillary (left) and alveolar membrane (right) of the lungs. Also shown is the tip end of a lymphatic vessel (center) that pumps fluid from the pulmonary interstitial spaces.
(Modified from Guyton AC, Taylor AE, Granger HJ: Circulatory Physiology II: Dynamics and Control of the Body Fluids. Philadelphia, WB Saunders, 1975.)
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