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  • Title: Thoracic epidural anaesthesia disrupts the protective mechanism of homeometric autoregulation during right ventricular pressure overload by cardiac sympathetic blockade: a randomised controlled animal study.
    Author: Missant C, Rex S, Claus P, Derde S, Wouters PF.
    Journal: Eur J Anaesthesiol; 2011 Jul; 28(7):535-43. PubMed ID: 21505344.
    Abstract:
    CONTEXT: Thoracic epidural anaesthesia (TEA) is increasingly used in high-risk surgical patients. We recently demonstrated that TEA-mediated cardiac sympathicolysis prevents the native right ventricular positive inotropic response to the induction of acute pulmonary hypertension. OBJECTIVES: In this subsequent study, we induced a selective TEA after acute pulmonary hypertension had been established. We hypothesised that TEA in these circumstances would also exert negative inotropic effects on the right ventricle, not being mediated by possible effects on vasotonus, right ventricular coronary flow dynamics or right ventricular oxygen balance. DESIGN: Randomised placebo-controlled animal study. SETTING: University hospital animal laboratory. INTERVENTIONS: Eighteen pigs were instrumented with an epidural catheter at the thoracic or lumbar level, a right ventricular pressure-volume catheter, transonic flow probes around the pulmonary artery and the right coronary artery, a pressure catheter in the pulmonary artery and a 22-G catheter within a right ventricular free wall coronary vein. Right ventricular pressure overload was induced by constricting the pulmonary artery. After haemodynamic stabilisation, animals were then assigned to receive TEA (n = 6, 1 ml bupivacaine 0.5%), lumbar epidural anaesthesia (LEA) (n = 6, 4 ml bupivacaine 0.5%) or control (n = 6, isotonic saline). The extent of the sympathetic block was assessed by thermography. Final measurements were performed 30 min after the induction of epidural anaesthesia. RESULTS: Pulmonary artery constriction increased pulmonary artery effective elastance and right ventricular contractility in all groups. TEA caused a sympathetic block ranging from C6 to T6, whereas LEA caused a block from T13 to L5. TEA decreased right ventricular contractility (1.5 ± 0.6 vs. 3.2 ± 0.9 mW s ml(-1)) and cardiac output (1.8 ± 0.3 vs. 2.4 ± 0.3 l min(-1)), although systemic vascular resistance was unaffected. In the LEA group, systemic vascular resistance decreased, but right ventricular contractility remained unchanged. Right ventricular coronary flow, oxygen delivery and consumption were comparable between the groups. CONCLUSION: During acute pulmonary hypertension, selective blockade of cardiac sympathetic nerves by TEA acutely abolished the protective adaptation of right ventricular contractility to right ventricular pressure overload and deteriorated systemic haemodynamics. This effect was attributable solely to the depression of right ventricular contractility and was neither the result of impaired right ventricular coronary flow dynamics nor of systemic vasodilation.
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