How We Die Read Online Free PDF Page B

like—[he hesitated briefly in thought, then pursed his lips and blew his breath out in a slow diminuendo]—this. The change from light to dark was very evident, but the speed with which it happened was—well, gradual.
    I was aware that I’d collapsed. I felt like somebody took the life out of me. It felt like—I’m thinking of a scene—I had a dog that was hit by a car, and when I looked at that dog on the ground—he was dead already—he just looked like the same dog, only shrunk. You know, shrunk—uniformly. That’s how I felt. I felt like—[he made a sound like air going out of a balloon] “Pffft.”
    Lipsiner’s light went out precisely the way it did because the circulation to his brain had been suddenly shut off. As the oxygen in the organ’s now-stagnant blood was steadily used up, the brain began to fail—sight and consciousness were turned down as though by the gradual twist of a dial rather than the suddenness of a switch. That was Irv Lipsiner’s slow-motion spiral into oblivion, and almost death. The mouth-to-mouth breathing and chest massage of the cardiopulmonary resuscitation forced air into his lungs and drove blood to his vital organs until his heart decided, for reasons of its own, to resume its responsibilities. Like most sudden cardiac deaths in nonhospitalized people, Irv Lipsiner’s episode was caused by ventricular fibrillation.
    Lipsiner felt no ischemic pain. The probable cause of his fibrillation was some transient chemical stimulation of a supersensitive area left on his heart muscle by the attack of 1974. As to why the fibrillation occurred when it did, there is no way to be certain; but a quite plausible guess is that it was related to the stress of too much tennis on that Saturday afternoon, which could have caused the release into his circulation of extra adrenaline, and this in turn may have made a coronary artery go into spasm and set off the irregular rhythm. Such are the occasional vagaries of ischemic heart disease that Lipsiner was left with no new damage to his heart, although he never again played more than two consecutive hours of tennis.
    The fact that Lipsiner experienced no cardiac charley horse before he began fibrillating makes this particular case of heart seizure somewhat unusual—the majority of people who drop dead probably do feel ischemic pain of the characteristic sort. Like its equivalent in the calf, the onset of ischemic cardiac pain is sudden and severe. It has been most commonly described by its sufferers as constricting, or viselike. Sometimes it manifests itself as a crushing pressure, like an intolerable blunt weight forcing itself against the front of the chest and radiating down the left arm or up into the neck and jaw. The sensation is frightening even to those who have experienced it often, because each time it recurs it is accompanied by awareness of the possibility (and quite a realistic awareness it is) of impending death. The sufferer is likely to break out into a cold sweat, feel nauseated, or even vomit. There is often shortness of breath. If the ischemia does not let up within approximately ten minutes, the oxygen deficiency may become irreversible, and some of the deprived cardiac muscle will go on to die, the process called myocardial infarction. If that happens, or if the oxygen lack is sufficient to scramble the heart’s conduction system, some 20 percent of the afflicted will perish in the throes of such an episode before reaching an emergency room. That figure drops by at least half if transportation to a hospital is possible within the period cardiologists call “the golden hour.”
    Eventually, about 50 to 60 percent of people with ischemic heart disease will die within an hour of one of their attacks, whether the first or a later one. Since 1.5 million Americans suffer a myocardial infarction each year (70 percent of which occur in the home), it is not difficult to understand why coronary heart disease is America’s biggest