Significance of hypotension preceding fatal ventricular tachyarrhythmias in post-coronary obstruction sudden death.

While sudden death after acute myocardial infarction or ischemia most commonly occurs in the first few minutes, usually from tachyarrhythmias, little is known of associated hemodynamics. We monitored hemodynamics for 15 minutes following coronary embolization with mercury in 31 awake dogs. In 17 nonsurvivors, mean arterial pressure (MAP) fell 7 mm Hg at 15 seconds, 15 mm Hg by 45 seconds, 27 mm Hg at 120 seconds, and continued falling until ventricular fibrillation (VF) occurred. In contrast, in 14 survivors, MAP was unchanged at 15 seconds, fell 8 mm Hg at 45 seconds, 15 mm Hg at 120 seconds, and than returned toward control. The decline in MAP was significantly greater and earlier in nonsurvivors. Heart rate increased at 15 seconds in nonsurvivors (21 bpm) but not until 75 seconds in survivors (33 bpm). Cardiac output fell significantly only in nonsurvivors. Ventricular ectopics (greater than 5 beats/15 sec) first appeared after hemodynamic changes in both groups; at 68 seconds in survivors and at 45 seconds in non survivors. While such ectopy persisted at the same frequency thereafter in both groups, VF occurred only in the more hypotensive dogs at 177 seconds. In a second series of 26 dogs, hypotension was randomly treated by intra-aortic balloon. All nine nonhypotensive dogs survived, whereas five of six untreated hypotensive dogs died compared to 2 of 11 treated ones (p less than 0.02). We conclude that significant hemodynamic changes precede ectopy, and VF and sudden coronary death occurs usually after persistence of hypotension.