A patient on a ventilator develops frequent premature ventricular complexes (PVCs) after starting high levels of positive end-expiratory pressure (PEEP). Which likely mechanism is reducing the patient's Cardiac Output (CO)?

High levels of positive end-expiratory pressure (PEEP) applied during mechanical ventilation increase mean intrathoracic pressure. This elevated intrathoracic pressure compresses the great veins and right atrium, impeding venous return from the systemic circulation to the heart. Because cardiac output depends on adequate preload — the volume of blood returning to the right side of the heart — reduced venous return directly decreases preload, which in turn reduces stroke volume and cardiac output by the Frank-Starling mechanism. The resulting decrease in cardiac output can lead to myocardial irritability and ventricular ectopy such as premature ventricular complexes (PVCs). Increased venous return is the opposite of what occurs with high intrathoracic pressure; venous drainage is impeded, not enhanced. Decreased afterload from reduced transmural pressure is not the primary hemodynamic consequence of high PEEP in this context; while transmural pressures are affected, the dominant effect impairing cardiac output is the preload reduction. Increased contractility from baroreflex activation would be a compensatory response to low blood pressure, not the mechanism causing reduced cardiac output in the first place. The correct mechanism is therefore decreased preload due to impaired venous return caused by the elevated intrathoracic pressure from high PEEP.