HYPOVOLEMIC SHOCK AND CARDIAC CONTRACTILITY - ASSESSMENT BY END-SYSTOLIC PRESSURE-VOLUME RELATIONS

The end-systolic pressure-volume relation (ESPVR) is accepted as a loa d-independent measure of cardiac contractility. Potential curvilineari ty of the ESPVR, dependency on coronary perfusion pressure (CPP) and s ensitivity to the type of loading intervention might limit its use in hemorrhagic shock. This study compared ESPVRs obtained by caval and ao rtic occlusion under physiological loading conditions at baseline with those obtained during hemorrhagic shock (mean arterial pressure 45 mm Hg). The left ventricular (LV) pressure (tip manometer) and volume (co nductance catheter) were measured in ten anesthetized pigs. ESPVRs wer e fitted to linear and quadratic models. Within end-systolic pressure (Pes) ranges obtained under baseline conditions, ESPVR displayed only minimal curvilinearity (second-order coefficient a < 0.007) and could be accurately described by a linear model. However, nonlinearity of ES PVRs obtained over wider load ranges is suggested by negative volume a xis intercepts of the linear model. Steeper ESPVR with aortic than wit h caval occlusion (2.28 +/- 0.22 vs 3.41 +/- 0.51 mmHg/ml, ns) could n ot be proven owing to the large interindividual variance of ESPVR slop es with both loading interventions. During shock the Pes range obtaine d by caval occlusion decreased to very low levels (from 49 +/- 2 to 34 +/- 1 mmHg), ESPVR did not adequately fit either of the two models (m ean R < 0.66), and critical reduction of CPP induced negative ESPVR sl ope in four of ten experiments. In contrast, aortic occlusion at shock resulted in linear ESPVR (R = 0.927 +/- 0.029), Pes ranges (92 +/- 3 to 58 +/- 4 mmHg) comparable to the ones obtained by caval occlusion a t control (113 +/- 5 to 73 +/- 6 mmHg), and steeper ESPVR than at cont rol (3.41 +/- 0.51 to 7.38 +/- 1.0 mmHg/ml, P < 0.05). Interpretation of the increased ESPVR slope obtained with aortic occlusion as due to increased contractility in shock is, however, complicated by different Pes ranges. It is concluded that within Pes ranges obtained with cava l or aortic occlusion in situ the ESPVR can be adequately fitted to a linear model. For assessment of the inotropic response to shock the ES PVR is of limited value because (1) caval occlusion is not suitable to generate ESPVR during shock, and (2) Pes ranges obtained with identic al loading interventions differ greatly between baseline and shock and , therefore, apparent ESPVR changes are influenced by the potential no nlinearity of the ESPVR. Combining caval occlusion at baseline with ao rtic occlusion at shock would result in comparable Pes ranges. Interpr etation of results is, however, complicated by diverging effects of th e different loading interventions on the shape and slope of the ESPVR.