- - - - - - - This final stoppage caused so-called "ischemia" (pronounced iskeemeeya), or blood lack, thereby acutely starving a large-enough piece of heart muscle, or myocardium, to disrupt its normal rhythm into the chaotic squirming of ventricular fibrillation.

- - - - - - -Like so many other medical terms, ischemia is a word with an interesting history and colorful associations. It will recur again and again in the telling of the stories in this long narrative of death, because it is so ubiquitous—and so insidious—a driving force toward the quenching of life's energies. Though starvation of the heart may offer the most dramatic example of its lurking dangers, the process of choking off oxygen and nutrition is the common denominator in a wide variety of mortal illnesses.

- - - - - Among Rudolf Virchow's many research interests was his fascination with the ways in which disease affects arteries, veins, and their contained blood constituents. He elucidated the principles of embolism, thrombosis, and leukemia and invented the words to describe them. Seeking a term to designate the mechanism by which cells and tissues are deprived of their blood supply. Virchow seized (this word is chosen advisedly) upon the Greek ischano—" I hold in check," or "I quench"—derived from the IndoEuropean root segh, which refers to "seizing" or "holding" or "causing to pause." By combining it with aima, or "blood," the Greeks had created the word ischaimos, to signify a holding in check of the flow of blood. Ischemia was chosen by Virchow to designate the consequences of diminishing or totally stopping blood How to some structure of the body, whether as small as a cell or as large as a leg or a section of heart muscle.

Diminishing is a relative term, however. When an organ's activity increases, its oxygen requirements go up, and so does its need for blood. If narrowed arteries cannot widen to accommodate this need, or if for some reason they go into tight spasm that further restricts flow, the organ's demands are not met, and it rapidly becomes ischemic. In pain and anger, the heart screams out a warning, and continues to do so until its shrieking exhortations for more blood are met, usually by the natural stratagem of the victim, who—alarmed by the distress within his chest— slows or stops the activity that is tormenting his cardiac muscle.

A ready example of this process is the suddenly overworked calf muscle of a weekend athlete who returns to jogging each year when the weather warms up in April. The discrepancy between the amount of blood required by his out-of-condition muscle and the amount that is able to force its way through his out-of-condition arteries may result in ischemia. The calf does not get enough oxygen and it cries out in an agonizing seizure, to warn the athlete manque to stop his exertions before a clump of muscle cells are starved to death, the process known as infarction. The shriek of pain in the overtaxed calf is called a cramp or a charley horse.

• Angina pectoris is nothing else than a charley horse of the heart. If it lasts long enough, its victim sustains a myocardial infarction.

Angina pectoris is a Latin phrase which translates literally as "a choking" or "throttling" (angina) "of the chest" (pectoris, the genitive case of pecttis, "chest"). It is to another medical philologist, the remarkable eighteenth-century English physician William Heberden (1710-1801), that we owe not only the term but also one of the finest descriptions of the symptoms associated with it. In a 1768 discussion of the various forms of chest pain, he wrote:

But there is a disorder of the breast marked with strong and peculiar symptoms, considerable for the kind of danger belonging to it, and not extremely rare, which deserves to be mentioned more at length. The seat of it, and sense of strangling and anxiety with which it is attended, may make it not improperly be called angina pectoris.

They who are afflicted with it, are seized while they are walking, (more especially if it be up hill, and soon after eating) with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life, if it were to increase or to continue; but the moment they stand still, all this uneasiness vanishes.

Irv Lipsiner describing what it felt like to drop dead on a tennis court:

The only thing I can recall is just—not hurting, but just collapsing. And then the lights went out, as if you're in a little room and you flip the switch. The only thing different from that was / that it was in slow motion. In other words, it didn't go out like that [here he snapped his fingers]. It went out like this [he made a lazy downward circle with his hand, like an airplane turning gently in descent toward a landing], gradually and almost in a spiral, 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.

- - - - - - 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 killer, as it is in every industrialized country of the world.

- - - - - 20 to 25 percent of Americans die suddenly, defined as unexpected death within a few hours of onset of symptoms in persons neither hospitalized nor homebound. And of these deaths, 80 to 90 percent are cardiac in origin, the remaining segment being due to diseases of the lungs, central nervous system, or the vessel into which the left ventricle pumps its blood, the aorta. When the death is not only sudden but instantaneous, there are only a few that are not the result of ischemic heart disease.

- - - - - The same Edward Jenner who introduced smallpox vaccination in 1798 was an inveterate student of disease who made a custom of following to the autopsy table as many of his deceased patients as possible. In those days. doctors performed their own postmortem examinations. As a result of his dissections, Jenner began to suspect that the narrowing he discovered in the death-room coronary arteries was directly related to the anginal symptoms he had elicited from patients during life. In a letter to a colleague, he wrote of a recent experience dissecting a heart during such an autopsy:

My knife struck something so hard and gritty as to notch it. well remember looking up at the ceiling, which was old and crumbling, conceiving that some plaster had fallen down. But on further scrutiny the real cause appeared: the coronaries were become bony canals.

When a coronary artery suddenly completes the processes of occlusion, a period of acute oxygen deprivation ensues. If the oxygen lack is of such duration and severity that the stunned and instantly bloodless muscle cells cannot recover, the pain of angina is succeeded by infarction: The affected muscle tissue of the heart goes from the extreme pallor of ischemia to frank death. If the area of death is small enough and has not killed the patient by causing ventricular fibrillation or some equally serious abnormality of rhythm, the involved muscle, now puffy and swollen, will be able to maintain a tenuous hold on existence until, with the process of gradual healing, it is replaced by scar tissue. The area of such tissue is incapable of participating in the forceful thrusting of the rest of the myocardium.

- - - - - - The result of this congestion is to drive some of the blood's fluid component through the leaking walls of the smallest vessels, resulting in swelling, or edema, of tissue. Structures like the kidney and liver are thus prevented from performing efficiently, a state of affairs made even worse by the fact that the left ventricle's weakened pump drives less of the newly oxygenated blood it receives, decreasing even the nourishment of the already-swollen organs. In this way, the general slowing down of the circulation is accompanied by a decrease in the flow of blood in and out of tissues.

- - - - - The afflicted patient becomes increasingly short of breath with even minimal exertion, since neither the heart nor the lungs can respond to the increase in the work demanded of them. Some sufferers have difficulty lying down for more than a short period of time, because they need the upright position and gravity's help to drain excess fluid from their lungs. I have known many patients for whom sleep became impossible unless their head and shoulders were elevated on several pillows, and even then they were subject to paroxysms of frightening breathlessness during the night.

- - - - - Delay it though we may, then, the victims of coronary arteriosclerosis will almost certainly die of their affliction—perhaps unexpectedly during a time when they seem to be responding well to treatment, perhaps of the gradual effects of congestive heart failure. Although its more flagrant symptoms are less commonly seen than they were in the days before the advent of effective ways to fend them off, chronic congestive failure remains a significant force in the demise of many people with ischemic heart disease. Once the heart has become so weakened that congestive failure occurs, the outlook is poor. Approximately half its victims will die within five years. As we noted earlier, along with the sharp drop in actual heart attacks in recent years has come a dramatic rise in the incidence of failure, a rise that will probably continue.

- - - -By this point, IVs will have been inserted for the infusion of cardiac drugs, and wider plastic tubes called central lines are being expeditiously inserted into major veins. The various drugs injected into the IV tubing have assorted purposes: They help to control rhythm, decrease the irritability of the myocardium strengthen the force of its contraction, and drive excess fluid 01 of the lungs, to be excreted by the kidney. Every resuscitation different. Though the general pattern is similar, every sequence every response to massage and drugs, every heart's willingness to come back—all are different. The only certainty, whether spoke or not, is that the doctors, nurses, and technicians are fighting not only death but their own uncertainties as well. In most resuscitations, those uncertainties can be narrowed down to two main questions: Are we doing the right things? and. Should we be doing anything at all?

- - - fewer than one-third of the {stroke} episodes occur in a hospital. Often there is no warning of the imminence of that final exit. No matter how much ischemia a heart has endured in the past, its defection may be sudden.

Stroke is such a ubiquitous term that there is sometimes a little fuzziness about the way it is used. To a physician, a stroke is a deficit in neurologic function resulting from a decrease in blood flow through some specific artery supplying the brain. Further, the deficit must last longer than twenty-four hours for the episode to be called a stroke. Anything else is classified as a transient ischemic attack, or TIA.

If all or this has a familiar ring, there is good reason. It is basically the same mechanism by which the heart's deficit is produced when one of its arteries fails to deliver the required volume of blood. It is that universal mechanism of ischemia, the quenching of blood flow and the parching of tissues, that is so common a denominator in the killing off of cells in so many parts of the body.

Many strokes are so small that there are few or no immediate significant symptoms to indicate what has taken place. But with time, such little strokes accumulate, and the evidence of gradual deterioration becomes clear to even the most casual observer. Walter Alvarez, the great Chicago clinician of a generation ago, once quoted "a wise old lady" who said to him, "Death keeps taking little bits of me." As his clinical description so clearly states:

She saw that with each attack of dizziness or fainting or confusion she became a little older, a little weaker, and a little more tired; her step became more hesitant, her memory less trustworthy, her handwriting less legible, and her interest in life less keen. She knew that for 10 years or more, she had been moving step by step towards the grave.

Of those so betrayed by their cerebral circulation, William Osier is reported to have said, "These people take as long to die as they did to grow up."

Almost 10 percent of elderly people diagnosed with dementia owe their situation to a series of such small strokes, a concept popularized by Alvarez in 1946, after observing it in his own father. Now called multi-infarct dementia, the process is characterized by an irregular series of abrupt little worsenings. Interestingly, this form of cerebral arteriosclerosis was first described by Alois Alzheimer in 1899, eight years before he introduced the quite different type of intellectual decline that we now call by his name.