Author + information
- Received July 30, 1991
- Revision received November 12, 1992
- Accepted November 17, 1992
- Published online June 1, 1993.
- William J. Dreyer, MD, FACC∗,
- Stephen M. Paridon, MD, FACC,
- David J. Fisher, MD, FACC and
- Arthur Garson Jr., MD, MPH, FACC
- ↵∗Address for correspondence: William J. Dreyer, MD, Pediatric Cardiology, Texas Children's Hospital, 6621 Fannin, Houston, Texas 77030.
Objectives. We explored the hypothesis that residual outflow tract obstruction and ventricular hypertrophy associated with rapid ventricular rhythm contribute to sudden death, in part because they result in humoral or hemodynamic changes that predlspose to ventricular fibrillation, such as increased catecholamine release or decreased coronary flow, or both.
Background. Ventricular arrhythmia after surgical repair of tetralogy of Fallot has been associated with sudden death, particularly in patients with residual right ventricular hypertension. However, the mechanisms by which sudden death occurs remain unclear.
Methods. Seven awake, unanesthetized mature beagles with chronically elevated right ventricular pressure (high pressure group: right ventricular/left ventricular systolic pressure ratio >0.5) were compared with six beagles with low right ventricular pressure at rest and at the end of 5 min of ventricular pacing at 240 beats/min (low pressure group).
Results. In the high pressure group, cardiac output decreased during ventricular pacing (compared with sinus rhythm) from 304 ± 21 to 218 ± 21 ml/min per kg (p < 0.01) and plasma norepinephrine increased substantially fron 673 ± 64 to 1,847 ± 92 pg/ml (p < 0.01). Comparable changes were not observed in the low pressure group. Plasma epinephrine levels were similar in both groups at rest and did not change with pacing. Postpacing norepinephrine levels from both groups correlated positively with both right ventricular systolic and diestolic pressure at rest and correlated negatively with the change in cardiac output from rest to pacing. Regional right ventricular myocardial blood flow increased with pacing in the low pressure group, whereas in the high pressure group it was increased at rest and did not increase further with pacing.
Conclusion. During ventricular pacing, dogs with right ventricular outflow tract obstruction and high right ventricular pressure had a decrease in cardiac output and an increase in plasma norepinephrine, coupled with a loss of right ventricular myocardial blood flow reserve. Similar changes may occur in postoperative patients with similar hemodynamics and tachyarrhythmia and could contribute to the occurrence of ventricular fibrillation and sudden death.
☆ This study was supported in part by Grant HL-24916 from the National Institutes of Health, Bethesda. Maryland and by a grant from the J.S. Abercrombie Foundation, Houston, Texas.
- Received July 30, 1991.
- Revision received November 12, 1992.
- Accepted November 17, 1992.