Why the study?
Does thoracic epidural anaesthesia improve central haemodynamics compared to metoprolol in conscious rats with acute myocardial infarction?
Does thoracic epidural anaesthesia improve central haemodynamics compared to metoprolol in conscious rats with acute myocardial infarction?
In a rat model of acute myocardial infarction, thoracic epidural anesthesia decreased indices of left ventricular wall tension and outflow impedance, showing potentially more favorable hemodynamic effects than metoprolol.
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Should not yet change practice in acute MI; hypothesis-generating for human trials of TEA versus beta-blockade.
The study aimed to compare the effects of thoracic epidural anaesthesia (TEA) with those of the beta‐adrenoceptor blocker, metoprolol, on central haemodynamics in conscious rats with acute myocardial infarction. During methohexital anaesthesia, appropriate vascular catheters were inserted, a thoracic epidural catheter was implanted and the left coronary artery was ligated. A recovery period of 1–2 h elapsed after termination of surgery and anaesthesia. Experiments were performed on four separate groups of animals (A‐D). In Group A (n= 10) mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) were measured, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated before and 10–15 min after the induction of TEA (bupivacaine 5 mg · ml‐1). In Group B (n=6) left ventricular end‐diastolic pressure (LVEDP) and maximal dP/dt were recorded as in Group A. In Group C (n = 10) central haemodynamics were measured 10 min after i.v. metoprolol (0.5 mg · kg‐1) and again 10–15 min after the addition of TEA. In Group D (n=6) LVEDP and max dP/dt were measured as in Group C. The reduction in CO, SV, HR and max dP/dt was of the same magnitude with TEA and metoprolol. TEA lowered MAP by 17%, while metoprolol did not change MAP. Metoprolol caused an increase in LVEDP from 20.8 ± 1.8 to 27.5 ± 2.7 mmHg (2.8 ± 0.2 to 3.7 ± 0.4 kPa) (P < 0.01), while TEA induced a decrease in LVEDP from 24.2 ± 1.4 to 17.8 ± 1.6 mmHg (3.2 ± 0.2 to 2.4 ± 0.2 kPa) (P < 0.05). SVR increased 27% with metoprolol but was not affected by TEA. Induction of TEA during maximal beta blockade did not cause any further changes in CO, HR, max dP/dt or SV. In this situation, however, MAP and SVR decreased significantly by 23% and 19%, respectively, and LVEDP decreased from 27.5 ± 2.7 to 20.2 ± 2.3 mmHg (3.7 ± 0.4 to 2.7 ± 0.3 kPa) (P < 0.01). Compared to metoprolol, TEA may have more favourable effects on central haemodynamics during acute myocardial infarction, as, in striking contrast to metoprolol, TEA decreased indices of wall tension and outflow impedance of the left ventricle.
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Blomberg et al. (1990) studied this question.
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