PROTAMINE-INDUCED HYPOTENSION IN HEART OPERATIONS - APPLICATION OF THE CONCEPT OF VENTRICULAR-ARTERIAL COUPLING

Citation
M. Oe et al., PROTAMINE-INDUCED HYPOTENSION IN HEART OPERATIONS - APPLICATION OF THE CONCEPT OF VENTRICULAR-ARTERIAL COUPLING, Journal of thoracic and cardiovascular surgery, 112(2), 1996, pp. 462-471
Citations number
33
Categorie Soggetti
Respiratory System","Cardiac & Cardiovascular System",Surgery
ISSN journal
00225223
Volume
112
Issue
2
Year of publication
1996
Pages
462 - 471
Database
ISI
SICI code
0022-5223(1996)112:2<462:PHIHO->2.0.ZU;2-G
Abstract
Protamine sulfate often causes hypotension during heparin neutralizati on. The concept of ventricular-arterial coupling was applied to determ ine whether a negative inotropic effect or a vasodilating effect of pr otamine was the major contributing factor to this hypotension. Thirty- five patients who underwent cardiac operations were studied during ope ration by measuring instantaneous left ventricular pressure and aortic how to examine the end-systolic pressure-volume relationship. We obta ined end-systolic elastance and effective arterial elastance values in a beat-to-beat fashion with a single-beat estimation method. In 28 of the 35 patients (80%), mean arterial pressure decreased more than 10 mm Hg with protamine infusion, Parameters were compared at the followi ng three points: before a decrease in mean arterial pressure (control) , at maximally decreased mean arterial pressure (maximum), and at a mi ddle point between control and maximum values (midpoint). At both midp oint and maximum, mean arterial pressure decreased significantly (cont rol 79.6 +/- 12.6 mm Hg, midpoint 66.5 +/- 10.8 mm Hg, maximum 52.7 +/ - 9.9 mm Hg; p < 0.01). Similar changes were observed in effective art erial elastance (control 2.00 +/- 0.75 mm Hg/ml, midpoint 1.60 +/- 0.5 3 mm Hg/ml, maximum 1.31 +/- 0.46 mm Hg/ml; p < 0.01). Although the de crease in end-systolic elastance at midpoint (control 3.08 +/- 1.61 mm Hg/ml, midpoint 2.92 +/- 1.68 mm Hg/ml) did not reach statistical sig nificance, end-systolic elastance significantly decreased at maximum ( 2.63 +/- 1.46 mm Hg/ml; p < 0.01). Continuous measurements showed that the decreases in mean arterial pressure and effective arterial elasta nce always preceded the depression of end-systolic elastance and that afterload reduction by vasodilating effect of protamine was the mechan ism most likely to have initiated the hypotension. Delayed decrease in contractility may be ascribed to reduced coronary perfusion pressure caused by vasodilation or to a direct effect of protamine.