Lung Biology in Health & Disease Volume 157 by Steven M. Scharf, Michael R. Pinsky, Shelly Magder
By Steven M. Scharf, Michael R. Pinsky, Shelly Magder
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It has been recognized for well over 100 years that inspiration, which decreases pleural pressure, both encourages influx of blood into the chest and hinders the egress of blood from the chest. This dual action leads to increases in venous return from the periphery into the right heart and impedance to ventricular ejection from the left side of the heart. Hence, to understand the degree to which normal and exaggerated inspiration affects cardiovascular function, one needs to understand the factors which control the return of blood from the periphery to the right heart, venous return (Chapter 5), and the factors that control the ejection of blood from the left heart (Chapter 8).
Obstructive and restrictive lung diseases lead to greatly exaggerated inspiratory and mildly exaggerated swings in expiratory intrathoracic pressures. These changes may be directly transmitted to the heart and great vessels. By altering venous return and/or left ventricular ejection, exaggerated swings in intrathoracic pressure may also influence blood oxygen delivery to the periphery beyond any alterations caused by abnormal gas exchange across diseased lungs. In addition, a number of clinical cardiovascular signs in lung disease are due to the abnormal cardiovascular-respiratory interactions seen in lung disease.
Virtually all cardiac output from the right ventricle goes through pulmonary circulation. Pulmonary vascular resistance is heavily dependent on lung volume. As lung volume increases or decreases below functional residual capacity pulmonary vascular resistance generally increases. Lung injury of various types also increases pulmonary vascular resistance. Combining several factors that increase pulmonary vascular resistance, such as applying high levels of positive end-expiratory pressure in the presence of lung injury, can lead to large increases in pulmonary vascular resistance and compromise of right ventricular function.