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 693Normal 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 life-threatening respiratory failure.Chronic elevation of pulmonary venous pressures, as occurs in mitral stenosis, stimulates fibrosis, which decreases fluid transudation. This impairs pulmonary function, but makes it possible for some patients to chronically tolerate high pulmonary venous pressures without developing overt pulmonary edema. 4 The elevated pulmonary venous pressure in HF also increases the pressure in the pulmonary arteries, both due to the passive effects of increased downstream pressure and due to pulmonary vasoconstriction. 5,6 In addition, the elevated pulmonary venous pressure contributes to the pulsatile load, raising systolic pulmonary artery pressure. 7 The resulting pulmonary hypertension increases the load on the right ventricle, contributes to exercise intolerance, and indicates a poor prognosis.The study by Cao et al 8 in this issue of Circulation: Cardiovascular Imaging used an innovative magnetic resonance technique to provide detailed information on the important interaction of the heart and lungs in HF. Using gadolinium first-pass perfusion imaging, the time variations in signal intensity were converted to a contrast concentration time curve. With the assumption that pulmonary perfusion is a linear system, indicator dilution theory was used to assess the pulmonary blood flow by assessing the maximum signal intensity and the time course of the signal change. The rate of blood flow (perfusion) into small regions o...