Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations

Andre Y. Denault, John Gorcsan, Michael R. Pinsky
2001 Journal of applied physiology  
Denault, Andre Y., John Gorcsan III, and Michael R. Pinsky. Dynamic effects of positive-pressure ventilation on canine left ventricular pressure-volume relations. J Appl Physiol 91: [298][299][300][301][302][303][304][305][306][307][308] 2001.-Positive-pressure ventilation (PPV) may affect left ventricular (LV) performance by altering both LV diastolic compliance and pericardial pressure (Ppc). We measured the effect of PPV on LV intraluminal pressure, Ppc, LV volume, and LV cross-sectional
more » ... in 17 acute anesthetized dogs. To account for changes in lung volume independent of changes in Ppc and differences in contractility, measures were made during both open-and closed-chest conditions, during closed chest with and without chest wall binding, and after propranolol-induced acute ventricular failure (AVF). Apneic end-systolic pressure-volume relations (ESPVR) were generated by inferior vena caval occlusions. With the open chest, PPV had no effects. With the chest closed, PPV inspiration decreased LV end-diastolic volume (EDV) along its diastolic compliance curve and decreased end-systolic volume (ESV) such that the end-systolic pressure-volume domain was shifted to a point left of the LV ESPVR, even when referenced to Ppc. The decrease in EDV was greater in control than in AVF conditions, whereas the shift of the ESV to the left of the ESPVR was greater with AVF than in control conditions. We conclude that the hemodynamic effects of PPV inspiration are due primarily to changes in intrathoracic pressure and that the inspirationinduced decreases of LV EDV reflect direct effects of intrathoracic pressure on LV filling. The decreases in LV ESV exceed the amount explained solely by a reduction in LV ejection pressure. afterload; canine model; heart-lung interactions; mechanical ventilation; preload; ventricular function POSITIVE-PRESSURE VENTILATION can alter left ventricular (LV) function through complex and interactive mechanisms that alter both LV preload and afterload (9, 33). For a given tidal volume, ventilatory rate, and chest wall lung mechanics, the relative importance of each mechanism appears to depend on the underlying ventricular function and circulating blood volume. These complex interactions have frustrated the analysis of the determinants of LV function during positive-pressure ventilation, necessitating analysis of LV functional changes only during periods of apnea or averaged throughout the respiratory cycle. However, dynamic changes in LV function and output usually occur throughout the ventilatory cycle and, as our laboratory recently demonstrated, can result in clinically relevant insights (32). These complex changes in LV function during positive-pressure ventilation function would be more clearly understood if an evaluation of the effect on both LV pressure (Plv) and LV volume could be performed. Suga and Sagawa (48) described a method of analyzing LV ejection performance by plotting the Plv-LV volume relationship obtained during alterations in load. They observed that, in the isolated heart preparation, the end-systolic pressure (ESP)-volume relationship (ESPVR) was relatively load insensitive, and its slope was proportional to contractility (49). With the use of measures of the LV ESPVR, contractility has been characterized during apnea in animal and human studies (2, 18, 24, 27) . Thus the LV end-diastolic volume (EDV)-LV end-systolic volume (ESV) interaction should not alter the LV ESPVR, if transmural Plv is used for Plv. If intermittent positive-pressure ventilation (IPPV) only altered LV performance by decreasing EDV through a decrease in venous return, then the decrease in EDV should precede the decrease in ESV. However, if intrathoracic pressure (ITP) alters LV afterload, then the inspiratory LV ESP-ESV point should shift downward and to the left of the apneic LV ESPVR when ESP is measured as LV intraluminal pressure alone. Finally, if mechanical interactions not characterized by changes in ITP alone improved LV ejection, then the shift in the LV ESP-ESV point at end inspiration should be to a point to the left of the transmural LV ESPVR. Accordingly, even if one knew LV distending pressure or its change or LV dimensions or their change, it would still be difficult to dissect out the primary and secondary forces that define heart-lung interactions during positive-pressure ventilation, unless simultaneous measurements were made of Plv and LV volume during these maneuvers and they were compared with apneic baseline values. The above argument underscores the importance of the dynamic assessment of the Plv-LV volume relation in aiding our understanding of heart-lung interactions,
doi:10.1152/jappl.2001.91.1.298 pmid:11408444 fatcat:5vp67p3ymjewbfixdahynmwupe