Circulation, Vol 82, 359-368, Copyright © 1990 by American Heart Association
JA Goldstein, B Barzilai, TL Rosamond, PR Eisenberg and AS Jaffe
To elucidate determinants of hemodynamic compromise in patients with acute
right ventricular (RV) infarction, we studied 16 patients with
hemodynamically severe RV infarction by right heart catheterization and
two-dimensional ultrasound. Severe RV systolic dysfunction, evident by
ultrasound in all patients as RV dilatation and depressed RV free wall
motion, was associated with a broad sluggish RV waveform, diminished peak
RV systolic pressure (27.6 +/- 4.5 mm Hg), and depressed RV stroke work
(4.6 +/- 2.4 g.m/m2). Paradoxical septal motion was consistently noted. In
some cases, the septum bulged into the right ventricle in a pistonlike
fashion and appeared to mediate systolic ventricular interaction through
which left ventricular septal contraction contributed to RV pressure
generation. RV diastolic dysfunction was indicated by elevated RV
end-diastolic pressures (13.7 +/- 2.7 mm Hg), RV "dip and plateau,"
equalization of diastolic filling pressures, and reversal of diastolic
septal curvature toward the volume-deprived left ventricle. A prominent
right atrial (RA) X and blunted Y descent, indicative of impairment of RV
filling throughout diastole, were confirmed in all patients by their
relation to RV systolic events. Patients manifested one of two distinct RA
waveform morphologies differentiated by A wave amplitude and associated
with disparate clinical courses. In eight patients, an RA W pattern was
evident, characterized by augmented A waves; eight others manifested an M
pattern constituted by depressed A waves. Compared with those with an M
pattern, patients with a W pattern had higher peak RV pressures (29.6 +/-
3.8 versus 25.5 +/- 4.3 mm Hg, p less than 0.05), better cardiac output
(3.4 +/- 0.3 versus 2.9 +/- 0.7 l/min, p less than 0.05), more favorable
response to volume and inotropes, and less frequently required emergency
revascularization for refractory shock (none versus five for those with an
M pattern). Patients with a W pattern were more severely compromised if
atrioventricular dyssynchrony developed and were more dramatically improved
by restoration of physiological rhythm. Angiography in patients with
depressed A waves demonstrated more proximal coronary obstruction leading
to ischemic compromise of RA function, whereas in those with augmented A
waves, the culprit lesion was proximal to the RV but distal to the RA
branches. These results indicate that hemodynamic compromise in patients
with RV infarction is exacerbated by decreased preload reserve that is
dependent on atrial systole. The amplitude of the RA A wave, an indication
of the status of RA function, is an important determinant of RV performance
and hemodynamic compromise.
ARTICLES
Determinants of hemodynamic compromise with severe right ventricular infarction
Cardiovascular Division, Washington University School of Medicine, St. Louis, MO 63110.
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