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A Journal on Anesthesiology, Resuscitation, Analgesia and Intensive Care
ORIGINAL ARTICLES ANESTESIOLOGY
Minerva Anestesiologica 2001 March;67(3):133-47
Alterations in left ventricular-arterial coupling and mechanical efficiency produced by remifentanil during cardiac anesthesia
Pittarello D., Bonato R., Armellin G., Sorbara C.
Università degi Studi - Padova Dipartimento di Farmacologia ed Anestesiologia Sezione di Anestesiologia
Background. The performance of the cardiovascular system depends on the interaction of the left ventricle and arterial system. An appropriate coupling of these two components is important to quantify the efficiency of myocardium, determined by Ea/Ees. The end-systolic elastance of the left ventricle (Ees) is an index of contractility which is independent of loading conditions, while the arterial end-systolic elastance (Ea) represents the properties of the arterial system. The aim of our study is to investigate the effects of a bolus of remifentanil (R) on myocardial efficiency.
Methods. In a period of 3 months we examined prospectively the effects of R in a group of 12 patients, ASA IV, 49-75 years old, submitted intraoperatively to cardiac anesthesia for revascularization of myocardium. After induction of anesthesia and before the beginning of surgery, a bolus of R (1 µg/kg/min) was administered and with the use of trans-esophageal echocardiography we determined both the left ventricle end-systolic volume and end-diastolic volume to assess, with different end-systolic arterial pressures, the ventricle elastance (Ees) and arterial elastance (Ea) before and after administration of R.
Results. The present findings indicate that R decreases the ventricular elastance from 6.07 mmHg/ml/m2 to 4.8, with a less decrease of arterial elastance from 3.69 mmHg/ml/m2 to 3.07.
Conclusions. The results suggest that R preserves a good left ventricular-arterial coupling and mechanical efficiency, despite a little increase of coupling, probably because ventricular and arterial properties are so matched as to minimize the systolic work of the left ventricle.