The hemodynamic effects of ventilation can be grouped into three concepts: 1) Spontaneous ventilation is exercise; 2) changes in lung volume alter autonomic tone and pulmonary vascular resistance and can compress the heart in the cardiac fossa; and 3) spontaneous inspiratory efforts decrease intrathoracic pressure, increasing venous return and impeding left ventricular ejection, whereas positive-pressure ventilation decreases venous return and unloads left ventricular ejection. Spontaneous inspiratory efforts may induce acute left ventricular failure and cardiogenic pulmonary edema. Reversing the associated negative intrathoracic pressure swings by using noninvasive continuous positive airway pressure rapidly reverses acute cardiogenic pulmonary edema and improves survival. Additionally, in congestive heart failure, states increasing intrathoracic pressure may augment left ventricular ejection and improve cardiac output. Using the obligatory changes in venous return induced by positive pressure breathing, one can quantify the magnitude of associated decreases in venous flow and left ventricular ejection using various parameters, including vena caval diameter changes, left ventricular stroke volume variation, and arterial pulse pressure variation. These parameters vary in proportion to the level of cardiac preload reserve present, thus accurately predicting which critically ill patients will increase their cardiac output in response to fluid infusions and which will not. Common parameters include arterial pulse pressure variation and left ventricular stroke volume variation. This functional hemodynamic monitoring approach reflects a practical clinical application of heart-lung interactions.
Keywords: functional hemodynamic monitoring; heart–lung interactions; left ventricular afterload; mechanical ventilation; spontaneous ventilation.