Heart-lung interactions and pulmonary buffering: Lessons from a computational modeling study

Our objective was to separate mechanical effects on the circulation that are due to increases in pleural pressure (Ppl) from those due to increases in transpulmonary pressure (Ptp). We used a computational model of the circulation (Magder et al., 2009) which includes four static elastic compartments (systemic and pulmonary arteries and veins) and two time-varying elastances to represent the ventricles. Changes in Ppl were modeled by increasing pressure in all thoracic compartments and changes in Ptp by increasing the pressure around the pulmonary venous compliant region. When Ptp was >pulmonary venous pressure (Pvp) a switch function created the equivalent of West zone II in pulmonary vessels. Cyclic increases in Ppl or Ptp produced systolic arterial pressure variations (SPV). However, with Ppl systolic pressure fell during expiration and average pulmonary venous pressure (Pvp) decreased, whereas with cyclic Ptp systolic pressure fell during inspiration and average Pvp increased. Increases in pulmonary vascular volume reduced SPV due to cyclic Ppl, which we call pulmonary buffering, but not in those due to cyclic changes in Ptp. In conclusion, cyclic increases in Ptp produce volume sensitive SPV whereas cyclic changes in Ptp produce non-volume responsive SPV. Cyclic Ppl decrease whereas cyclic Ptp increase pulmonary vascular volume.

► Lung inflation alters blood flow by changes in pleural pressure and changes in trans-pulmonary pressure. ► Increases in pleural pressure decrease cardiac output and decrease pulmonary vascular volume. ► The blood volume in pulmonary vasculature smoothes out the effects of intermittent changes in pleural pressure on cardiac output and arterial pressure; we call this “pulmonary buffering”. ► Increased trans-pulmonary pressure decreases cardiac output when it creates zone 2 conditions in the lung and increases pulmonary vascular volume.