Abstract

Dyspnea is the major symptom experienced by patients with heart failure (HF) and points to the important role of the lungs in this syndrome. Article see p 693 Normal left ventricular diastolic function keeps the left atrial and pulmonary venous pressures low (<12 mm Hg), both at rest and during submaximal exercise.1 With this normal low pulmonary venous pressure, only a small amount of fluid and protein are filtered through gaps in the pulmonary capillary endothelial cells and into the alveolar interstitial space because the hydrostatic pressure is mostly offset by the protein osmotic pressure.2 Thus, normally the small amount of fluid and protein entering the interstitial space is cleared by lymphatic drainage into the venous circulation. An elevation of left ventricular diastolic and pulmonary venous pressures is a characteristic of HF, regardless of the ejection fraction.3 Mild elevations of pulmonary venous pressure (18–25 mm Hg) increase the flow into the interstitial space.2 When this flow exceeds the clearance ability of the lymphatics, edema accumulates in the lung interstitial space. This can be seen on a chest x-ray as Kerley B lines. The accumulation of interstitial fluid enhances the stiffness of the lungs, leading to an increase in work required to breathe, and produces the perception of dyspnea. With higher pulmonary venous pressures (>25 mm Hg), the accumulating fluid enters the alveolar space, producing pulmonary edema. This interferes with gas exchange and results in intrapulmonary shunting, leading to hypoxia. In this way, acute pulmonary edema can produce …

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