Joao Lima

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Incomplete filling and incoordinate contraction as mechanisms of hypotension during ventricular tachycardia in man.

J A Lima; J L Weiss; P A Guzman; M L Weisfeldt; P R Reid; T A Traill (Profiled Authors: Joao Lima; James Weiss; Myron Weisfeldt; Thomas Traill)

Circulation 1983;68(5):928-38.

We sought to determine mechanisms for decrease of cardiac output and for hypotension during ventricular tachycardia (VT) in man. Two-dimensional and M mode echocardiograms and left ventricular pressure from micromanometer-tipped catheters were obtained in 20 patients before, during, and at the end of induced hypotensive VT. Patients were divided into two groups according to left ventricular function in sinus rhythm as assessed by angiographic ejection fraction (EF) before electrophysiologic study. Group 1 (n = 8) had angiographic EF greater than or equal to 50% in normal sinus rhythm, and group 2 (n = 12) had EF less than or equal to 40%. During VT, left ventricular cavity volume (as indexed by short- and long-axis two-dimensional end-diastolic cavity areas) was markedly reduced in group 1, from 19.7 +/- 2 to 8.6 +/- 2 cm2 (p less than .001) and from 32.0 +/- 8 to 22.5 +/- 7 cm2 (p less than .001), respectively, but was only slightly reduced in group 2, from 34.1 +/- 6 to 31.5 +/- 7 cm2 (p = .044) and from 45.0 +/- 8 to 49.4 +/- 7 cm2 (p = NS), respectively. Conversely, left ventricular systolic function during VT (as indexed by fractional reduction in two-dimensional short- and long-axis areas) was markedly depressed in group 2, from 25.6 +/- 6% to 4.2 +/- 4% (p = .005) and from 13.7 +/- 3% to 1.8 +/- 0.8% (p less than .001), respectively, but remained at control levels in group 1. Left ventricular end-diastolic pressures increased in group 1, from 11.8 +/- 2 to 27.7 +/- 8 mm Hg (p = .005) and did not change in group 2 during VT. Pressure-dimension loops from left ventricular pressure and M mode echocardiographically determined cavity dimensions generated from the end of the VT episodes showed that diastolic pressure-dimension relationships returned to control levels with the first prolonged diastolic interval in group 1 patients, indicating that incomplete relaxation was the mechanism responsible for reduction of cardiac output during VT in these patients. Coordination of contraction and relaxation (indicated by the percent ratio of the pressure-dimension loop area to the area of the rectangle just enclosing the loop) decreased from 37 +/- 11% to 16 +/- 13% in group 2 patients during VT (p = .013) but remained at control levels in group 1 patients. Thus, during VT patients with impaired left ventricular function in sinus rhythm (group 2) developed severe discoordination, and patients with normal or near-normal function (group 1) developed incomplete relaxation to account for stroke volume deterioration and hypotension.

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