Abstract
Positive-pressure ventilation may improve gas exchange, decrease the work-cost of breathing, and rest respiratory muscles, but it also will alter cardiac output and may modify blood flow distribution. Ventilation may induce these hemodynamic changes by altering systemic venous return to the RV (RV preload), pulmonary arterial pressure (RV afterload), ventricular interdependence (LV preload), or transmural LV ejection pressure (LV afterload). These interactions are magnified when the changes in lung volume and intrathoracic pressure are increased or under conditions associated with a reduced effective circulating blood volume or cardiac contractility. An understanding of these interactions is central to the effective management of the ventilator-dependent patient.
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