Bernard Lambermont

Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency

OBJECTIVEnTo investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency.nnnMETHODSnSix anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers.nnnRESULTSnRV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05).nnnCONCLUSIONSnIn the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency.

Comparison between single-beat and multiple-beat methods for estimation of right ventricular contractility

Objective:It was investigated whether pharmacologically induced changes in right ventricular contractility can be detected by a so-called “single-beat” method that does not require preload reduction. Design:Prospective animal research. Setting:Laboratory at a large university medical center. Subjects:Eight anesthetized pigs. Interventions:End-systolic elastance values obtained by a recently proposed single-beat method (Eessb) were compared with those obtained using the reference multiple-beat method (Eesmb). Measurements and Main Results:Administration of dobutamine increased Eesmb from 1.6 ± 0.3 to 3.8 ± 0.5 mm Hg/mL (p = .001), whereas there was only a trend toward an increase in Eessb from 1.5 ± 0.2 to 1.7 ± 0.4 mm Hg/mL. Esmolol decreased Eesmb from 1.7 ± 0.3 to 1.1 ± 0.2 mm Hg/mL (p = .006), whereas there was only a trend for a decrease in Eessb from 1.5 ± 0.2 to 1.3 ± 0.1. Conclusions:The present method using single-beat estimation to assess right ventricular contractility does not work as expected, since it failed to detect either increases or decreases in right ventricular contractility induced by pharmacologic interventions.

Cardiovascular haemodynamics and ventriculo-arterial coupling in an acute pig model of coronary ischaemia-reperfusion

Although reperfusion after coronary occlusion is mandatory for myocardial salvage, reperfusion may trigger a cascade of harmful events (reperfusion injury) adding to myocardial injury. We investigated effects of reperfusion on left ventricular (LV) haemodynamics and ventriculo‐arterial (VA) coupling in pigs following acute myocardial ischaemia induced by coronary artery occlusion. Experiments were performed in six animals, with measurements of cardiac and arterial function at baseline, after 60 min of ischaemia (T60) and after 2 (T180) and 4 h of reperfusion (T300). Ventriculo‐arterial coupling was assessed using the ventriculo‐arterial elastance ratio of paper, as well as using a ‘stiffness coupling’ and ‘temporal coupling’ index. Reperfusion following ischaemia (T180 versus T60) induced a progressive decline in cardiovascular function, evidenced by a decrease in mean arterial blood pressure, cardiac output and ejection fraction which was not restored at T300. Although reperfusion also induced an increase in slope of the end‐systolic pressure–volume relationship (ESPVR), the ESPVR curve shifted to the right, associated with a depression of contractile function. Histology demonstrated irreversible myocardial damage at T300. The ventriculo‐arterial elastance ratio and the ‘stiffness coupling’ index were unaffected throughout the protocol, but the ‘temporal coupling’ parameter indicated a relative shift between heart period and the time constant of the arterial system. It is unlikely that these alterations are attributable to ischaemic injury alone. The combination of both the stiffness and temporal coupling index may provide more information when studying ventriculo‐arterial coupling than the more commonly used ventricular end‐systolic stiffness/effection arterial elastance (Ees/Ea) ratio.

Effects of reperfusion on left ventricular hemodynamics and ventriculo-arterial coupling in acutely ischemic pigs

Rapid restoration of coronary blood flow following a period of myocardial ischemia (due to coronary occlusion) is mandatory to preserve the cardiac muscle. Reperfusion, however, not necessarily restores cardiac function, and cellular damage of the cardiac muscle cells following reperfusion (reperfusion injury) is well documented. The aim of this study was to investigate the effects of reperfusion on left ventricular (LV) hemodynamics and on left ventriculo-arterial (VA) coupling in acutely ischemic pigs.