Positive pressure ventilation (PPV) has long been thought to reduce venous return by raising PRA and therefore decreasing the pressure gradient (Pms − PRA).

But elegant physiological studies have shown that this explanation is incomplete.

Key Evidence

Fessler et al. (AJRCCM 1991): Effects of PEEP on Venous Return

Objective:

To determine whether the reduction in cardiac output seen with positive end-expiratory pressure (PEEP) is due to a decreased pressure gradient for venous return (Pms − PRA) or to other mechanisms.

Methods:

• Model: Intact canine preparation.
• Intervention: Applied 15 cmH₂O PEEP and measured cardiac output, right atrial pressure (PRA), and mean systemic filling pressure (Pms).
• Additional manipulations:
  • Carotid sinus + vagal denervation (CSV): To eliminate baroreflexes and vagal reflex control of sympathetic tone
  • Total spinal anesthesia with arterial pressure restored (SAE): To produce complete sympathetic blockade, then restore arterial pressure with epinephrine infusion
  • Abdominal binding or opening/exteriorization: To test whether increased abdominal pressure (from diaphragm displacement during PEEP) contributes to Pms rise or gradient changes.

Key Results:

Under normal conditions, PEEP raised both Pms and PRA by about the same amount, which meant that the driving pressure for venous return (Pms − PRA) stayed essentially the same. Yet, cardiac output still fell, showing that the drop in CO couldn’t be explained simply by a reduced gradient. When baroreflexes were blocked with CSV or SAE, the rise in Pms was blunted (confirming that part of the Pms increase is reflex-mediated) but opening or binding the abdomen had little effect on how much Pms rose. It was only when abdominal binding raised PRA disproportionately or when SAE prevented the normal reflex rise in Pms that the gradient actually fell and further reduced venous return.

Conclusion:

• PEEP raises both PRA and Pms in parallel via mechanical and reflex mechanisms.
• Reduced cardiac output during PEEP cannot be explained solely by a lower pressure gradient for venous return—other mechanisms (e.g., ↑ venous resistance) must be involved.

Vieillard-Baron et al., Anesthesiology 2001 – SVC Collapsibility and Preload Dependence

Objective:

To determine whether dynamic inspiratory collapse of the superior vena cava (SVC) (a “zone 2” condition) limits right ventricular (RV) filling and output in mechanically ventilated patients, and whether this effect can be reversed by volume expansion.