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
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.