Phase-related changes in right ventricular cardiac output under volume-controlled mechanical ventilation with positive end-expiratory pressure

Abstract

Increases in PEEP during volume-controlled mechanical ventilation leads to respiration-phase-specific reduction of right ventricular cardiac output, with a significantly pronounced decrease during the inspiration phase. This decrease in cardiac output should be taken into particular consideration for patients with already critically reduced cardiac output.

Hyperventilation-Induced Hypotension During Cardiopulmonary Resuscitation

“…3 Conversely, the physiological consequences of hyperventilation and of prolonged ventilation intervals result in a persistently positive intrathoracic pressure during the decompression phase of CPR, thereby decreasing cardiac preload 6 and cardiac output 7 and impeding right ventricular function. 8 Increased tidal volume is also known to adversely affect cardiac output. 9 In the present study, the mean intrathoracic pressure was significantly elevated in animals treated with higher ventilation rates.…”

Acute Renal Failure and Mechanical Ventilation: Reality or Myth?

“…29 This change increases right ventricular afterload, leading to a decrease in emptying and ultimately a decrease in left ventricular preload. [29][30][31][32] Left ventricular distensibility also decreases, with an associated decrease in left ventricular function, especially with PEEP greater than 15 cm H 2 O. The decrease in left ventricular function causes a decrease in venous return to the right side of the heart and an increase in pulmonary artery pressures.…”

“…The decrease in left ventricular function causes a decrease in venous return to the right side of the heart and an increase in pulmonary artery pressures. [30][31][32] In studies in animals, the effects of PEEP on hemodynamic parameters have varied. In one study, PEEP up to 14 cm H 2 O did not adversely affect ejection fraction or left ventricular end-diastolic volume but at levels greater than 21 cm H 2 O had marked effects on these 2 parameters.…”

Mechanisms of orthostatic intolerance following very prolonged exercise

“…An important, novel finding from the present study was the relation between the degree of hyperventilatory-induced hypocapnia with both hypotension and reduced MCAv. In animal studies, the related physiological consequences of hyperventilation result in a persistently positive intrathoracic pressure, thereby decreasing cardiac preload (10) and Q (6) and impeding right ventricular function (54). Increased tidal volume is also known to adversely affect Q (22).…”