Heart–Lung Interactions

Abstract The pulmonary and cardiovascular systems have profound effects on each other. Overall cardiac function is determined by heart rate, preload, contractility, and afterload. Changes in lung volume, intrathoracic pressure (ITP), and hypoxemia can simultaneously change all of these four hemodynamic determinants for both ventricles and can even lead to cardiovascular collapse. Intubation using sedation depresses vasomotor tone. Also, the interdependence between right and left ventricles can be affected by lung volume-induced changes in pulmonary vascular resistance and the rise in ITP. An increase in venous return due to negative ITP during spontaneous inspiration can shift the septum to the left and cause a decrease in left ventricle compliance. During positive pressure ventilation, the increase in ITP causes a decrease in venous return (preload), minimizing ventricular interdependence and will decrease left ventricle afterload augmenting cardiac output. Thus, positive pressure ventilation is beneficial in acute heart failure patients and detrimental in hypovolemic patients where it can cause a significant decrease in venous return and cardiac output. Recently, this phenomenon has been used to assess patient's volume responsiveness to fluid by measuring pulse pressure variation and stroke volume variation. Heart–lung interaction is very dynamic and changes in lung volume, ITP, and oxygen level can have various effects on the cardiovascular system depending on preexisting cardiovascular function and volume status. Heart failure and either hypo or hypervolemia predispose to greater effects of ventilation of cardiovascular function and gas exchange. This review is an overview of the basics of heart–lung interaction.