Respiratory Physiology & Neurobiology 182 (2012) 60–70 Contents lists available at SciVerse ScienceDirect Respiratory Physiology & Neurobiology j o ur nal homep age : www.elsevier.com/locate/resphysiol Heart–lung interactions and pulmonary buffering: Lessons from a computational modeling study Sheldon Magder ∗ , Brent Guerard McGill University Health Centre, Division of Critical Care, Canada a r t i c l e i n f o Article history: Accepted 8 May 2012 Keywords: Pulmonary buffering Computational modeling study West zone a b s t r a c t 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. © 2012 Elsevier B.V. All rights reserved. 1. Introduction Because lungs are strategically placed between the right and left ventricles, changes in lung inflation and thoracic pressure impact the circulation. These interactions are especially important when ventilation is provided by a mechanical ventilator and positive inspiratory pressures, for the settings on the device can profoundly affect blood flow (Magder, 2009). Two major forces dominate the process of lung inflation. First, the magnitude of lung inflation is determined by the pressure across the lungs, which is called transpulmonary pressure (Ptp), and which is determined by the dif- ference between alveolar and pleural pressure, and the compliance of the lung tissue. Second, when the chest is intact, the inspira- tory pressure also must overcome the compliance of the chest wall and thereby increases Ppl. Although changes in Ppl are related to changes in Ptp, changes in Ppl and Ptp can have different effects on the pulmonary circulation and their relative contributions can be altered by disease or ventilator settings. The heart is surrounded by Ppl and thus changes in Ppl alter the relationship of the inflow to the right heart and the outflow from the left heart relative to ∗ Corresponding author at: Royal Victoria Hospital, 687 Pine Av W, Montreal, Quebec, Canada H3A 1A1. E-mail address: Sheldon.magder@muhc.mcgill.ca (S. Magder). the rest of the body (Butler, 1983). On the other hand, alveolae sur- round small collapsible vessels in the pulmonary circulation so that increases in Ptp increase the pressure around these vessels relative to the heart. Increasing Ptp thus can potentially increase the load on the right heart and also empty volume from pulmonary vessels during lung inflation. There is still controversy as to whether the dominant effect of lung inflation is due to reduction of inflow to the right heart due to the increase in Ppl (Scharf et al., 1977; Magder, 2004) or due to the increases load on the right heart due to the increase in Ptp with lung inflation (Jardin et al., 1981; Vieillard- Baron et al., 1999). Thus our first objective was to assess the relative importance of these two components of lung inflation. To isolate the effect of just a change in Ppl from changes in Ptp requires that there be a change in Ppl without a change in Ptp. This can be done experimentally in animals by casting the chest to prevent lung expansion (Passerini et al., 1988) or, as performed by Scharf et al. (1977), by connecting the airway to the pleural space so that changes in airway pressure and changes in Ppl are equal. Iso- lation of the effects of changes in Ptp from changes in Ppl requires completely removing the lungs from the restraining effect of the chest wall. Both these experimental needs produce very unphysi- ological conditions and are associated with fluid losses, changes in blood gases, reflex adjustments and compromise of right ventricu- lar function. Changes in the volume and pressure of the right heart also can result in direct inter-ventricular interactions, which make 1569-9048/$ – see front matter © 2012 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.resp.2012.05.011