Terminal echocardiographic findings during death process in man and dogs.

Serial echocardiographic imaging was performed to assess terminal mechanical changes of cardiac chambers and valves, as well as sequential echocardiographic features of blood stasis, inside the heart after mechanical asystole in 7 hospitalized adults who died without apparent cardiac disease and in 7 experimental dogs sacrificed by a means of asphyxia. Marked reduction of wall motion became manifest shortly after the electrocardiograms had generated into a slow junctional rhythm with intraventricular conduction defect, an idioventricular rhythm, or an extreme sinus bradycardia. Total cessation of cardiac wall and valve motion followed; the aortic valve remained closed, with mitral and tricuspid valves semiopen after total cardiac asystole. Liquid whole blood inside the heart became echogenic shortly before mechanical asystole had approached, and homogenous echogenicity usually first appeared on the right side of the heart. As the death process progressed and total asystole persisted, the acoustic intensity of the intracavitary echoes increased, tending to form amorphous masses, with some showing rather well-defined borders. Such echocardiographic features were noted to indicate red thrombi in experimental dogs. The cardiac dimensions (left ventricle and aorta) decreased after total cardiac asystole.

Terminal cardiac electrical activity in adults who die without apparent cardiac disease.

Prolonged electrocardiographic (Holter) recording was performed to analyze terminal electrical events in 23 hospitalized adults who died without apparent cardiac disease. Most patients showed a gradual slowing of heart rate with shifting of cardiac pacemaker downward from the sinus node or atria to the atrioventricular junction and ventricles, resulting in cardiac asystole. Dominant bradyarrhythmia was more common than ventricular tachyarrhythmia (83 vs 17%). Agonal ST-segment elevation was not uncommon (26%). These terminal electrical events became manifest from 1 to 450 minutes (mean 62) before cessation of cardiac electrical activity. Forty-eight percent of the patients continued to show deteriorating sinus or atrial activity up to the last moment. The mechanism of bradycardiac asystole in patients with no apparent cardiac disease may be attributed to generalized anoxic and toxic depression of the sinus node and subsidiary pacemakers, together with neurogenic suppression of these structures.