Key result
Endotoxin infusion impairs RV mechanical efficiency by ~29%, triggering right ventricular-vascular uncoupling.
Why the study?
Does endotoxin infusion alter right ventricular systolic function and mechanical efficiency in a porcine model?
Does endotoxin infusion alter right ventricular systolic function and mechanical efficiency in a porcine model?
p-value: p=<0.05
Endotoxic shock induces a biphasic right ventricular response, with initial homeometric adaptation followed by uncoupling and decreased mechanical efficiency.
May signal RV uncoupling risk in human septic shock; leaves open whether efficiency metrics translate to clinical trials.
OBJECTIVE: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. METHODS: Six 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. RESULTS: RV 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). CONCLUSIONS: In 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.
No takes yet. Share an insight, caveat, or question.
Lambermont et al. (2003) studied Endotoxic shock model (n=12). Endotoxin (lipopolysaccharide from Escherichia coli serotype 0127:B8) vs. Placebo was evaluated on Right ventricular mechanical efficiency (p=<0.05). In a porcine model of endotoxic shock, endotoxin infusion decreased right ventricular mechanical efficiency from 63% at baseline to 45% at 270 minutes (P<0.05), indicating right ventricular-vascular uncoupling.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: