Although it is tempting to conclude that changes in SAP during positive-pressure ventilation reflect perturbations in LV preload and afterload, the relation between changes in SAP and ventricular volumes during ventilation is unknown. Furthermore, the mechanism by which SAP varies during ventilation could involve processes independent of changes in the LV preload or afterload. SAP could vary during positive-pressure ventilation because of a direct transmission of the increased ITP to the aorta in a fashion analogous to phases 1 and 2 of a Valsalva maneuver. Inspiration would increase SAP similarly to the way it increases in the initial phase of a Valsalva maneuver. If this were the case, stroke volume would eventually decrease because of the associated decrease in venous return, although SAP would remain elevated as long as ITP remained elevated. Most importantly, however, is that the increase in SAP would be in phase with inspiration, whereas any decrease in SAP would not. Furthermore, SAP could decrease during positive-pressure expiration because of the withdrawal of ITP-sup-ported arterial pressure in the setting of a decreased aortic blood volume and in a fashion analogous to the release phase (phase 3) of a Valsalva maneuver. Here the decrease in SAP would invariably follow inspiration but need not reflect a decrease in stroke volume. Furthermore, these ventilation-associated changes in SAP need not be related to changes in LV volume, nor do they need to be influenced to a relative degree by the level of LV contractility, but they would reflect only the changes in ITP. zyrtec tablets
To separate these mechanisms, we studied the effect of positive-pressure ventilation on SAP and the LV midaxis cross-sectional area in patients undergoing coronary artery bypass surgery. We tested the hypothesis that changes in SAP during a positive-pressure breath are induced solely by in-phase changes in ITP and need not reflect changes in stroke volume, end-diastolic volume, or end-systolic volume. We reasoned that if the inspiration-associated increases in the pulmonary blood flow increased the LV preload, thus increasing SAP, then the increase in SAP would be similar whether the chest was open or closed, because changes in ITP would not primarily alter this interaction. However, if changes in ITP or ventricular interdependence were the primary factors altering LV SAP or preload, respectively, then closing the chest would accentuate the effect by inducing greater amounts of increased ITP and reduced systemic venous return. Finally, since Perel et al initially described this phenomena in patients following a cardiopulmonary bypass, we strove to assess the above interaction both before and after a bypass to ascertain whether the hemodynamic alterations known to occur following a bypass altered the subjects’ response.