Circulation, Vol 68, 928-938, Copyright © 1983 by American Heart Association
JA Lima, JL Weiss, PA Guzman, ML Weisfeldt, PR Reid and TA Traill
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.
ARTICLES
Incomplete filling and incoordinate contraction as mechanisms of hypotension during ventricular tachycardia in man
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