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Gas Exchange Consequences of Left Heart Failure

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Abstract

This review explores the pathophysiology of gas exchange abnormalities arising consequent to either acute or chronic elevation of pulmonary venous pressures. The initial experimental studies of acute pulmonary edema outlined the sequence of events from lymphatic congestion with edema fluid to frank alveolar flooding and its resultant hypoxemia. Clinical studies of acute heart failure (HF) suggested that hypoxemia was associated only with the final stage of alveolar flooding. However, in patients with chronic heart failure and normal oxygenation, hypoxemia could be produced by the administration of potent pulmonary vasodilators, suggesting that hypoxic pulmonary vasoconstriction is an important reflex for these patients. Patients with chronic left HF commonly manifest a reduced diffusing capacity, an abnormality that appears to be a consequence of chronic elevation of left atrial pressure. That reduction in diffusing capacity does not appear to be primarily attributable to increases in lung water but is improved by any sustained treatment that improves overall cardiac function. Patients with heart failure may also manifest an abnormally elevated during exercise, and that exercise ventilation abnormality arises as a consequence of both alveolar hyperventilation and elevated physiologic dead space. That elevated exercise in an HF patient has proven to be a powerful predictor of an adverse outcome and hence it has received sustained attention in the HF literature. At least three of the classes of drugs used to treat HF will normalize the exercise , suggesting that the excessive ventilation response may be linked to elevated sympathetic activity. © 2011 American Physiological Society. Compr Physiol 1:621‐634, 2011.

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Figure 1. Figure 1.

Microscopic progression of cardiogenic edema (Figs. 1A through 1D) due to fluid accumulation in the lung. Modified from Staub et al. .

Figure 2. Figure 2.

Changes in arterial oxygenation and accumulation of extravascular lung water (EVLW) after the elevation of pulmonary capillary pressure (PCP) above the critical edema point (steps 4‐8) and return of PCP to control (steps 9‐11). Asterisks describe significant difference from step 1. Figure from Scillia et al. .

Figure 3. Figure 3.

Rate of fluid accumulation (Kf,c) in isolated lungs from normal dogs (open triangles) and dogs with heart failure (filled triangles) in response to elevations of pulmonary venous pressure (Pv). From Townsley et al. .

Figure 4. Figure 4.

Model data demonstrating how the solubility of a gas eliminated from blood in a model lung influences the physiologic (dashed lines) calculated for that gas with 20% anatomic dead space and three different degrees (j, k, and l) of heterogeneity. From Hlastala and Robertson .

Figure 5. Figure 5.

Response of (A) renal sympathetic nerve activity (RSNA) and (B) minute ventilation () in response to hypoxia in normal control rabbits (filled symbols) and rabbits with chronic heart failure (CHF) (open circles). Asterisks denote statistically significant increases. From Sun et al. .



Figure 1.

Microscopic progression of cardiogenic edema (Figs. 1A through 1D) due to fluid accumulation in the lung. Modified from Staub et al. .



Figure 2.

Changes in arterial oxygenation and accumulation of extravascular lung water (EVLW) after the elevation of pulmonary capillary pressure (PCP) above the critical edema point (steps 4‐8) and return of PCP to control (steps 9‐11). Asterisks describe significant difference from step 1. Figure from Scillia et al. .



Figure 3.

Rate of fluid accumulation (Kf,c) in isolated lungs from normal dogs (open triangles) and dogs with heart failure (filled triangles) in response to elevations of pulmonary venous pressure (Pv). From Townsley et al. .



Figure 4.

Model data demonstrating how the solubility of a gas eliminated from blood in a model lung influences the physiologic (dashed lines) calculated for that gas with 20% anatomic dead space and three different degrees (j, k, and l) of heterogeneity. From Hlastala and Robertson .



Figure 5.

Response of (A) renal sympathetic nerve activity (RSNA) and (B) minute ventilation () in response to hypoxia in normal control rabbits (filled symbols) and rabbits with chronic heart failure (CHF) (open circles). Asterisks denote statistically significant increases. From Sun et al. .

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H. Thomas Robertson. Gas Exchange Consequences of Left Heart Failure. Compr Physiol 2011, 1: 621-634. doi: 10.1002/cphy.c100010