Authors: Sherwin B Nuland
How We Die (8 page)
Having tested and talked, it is time to treat. Treatment is directed at decreasing the stress to which the heart is exposed, building up its reserve and resiliency for the long term, and correcting the specific abnormalities discovered during the process of testing. Implicit in all therapies is the necessity to do whatever is possible to slow the advance of atherosclerosis, recognizing that it can never be stopped entirely. Implicit also is the thesis that the heart is far more than just another stolidly stupid pump—it is a responsive, dynamic participant in the enterprise of life, capable of adaptation, accommodation, and, to some extent, repair.
William Heberden, without knowing it, described in 1772 what we may now recognize as a classic example of the way in which a properly designed exercise program may build up the heart’s ability to respond to those challenging moments when increased work is demanded of it. Writing of patients with angina, he reported: “I know one who set himself a task of sawing wood for half an hour every day, and was nearly cured.” Although the handsaw has nowadays been replaced by the stationary bicycle, the principle is the same.
A wide variety of cardiac medications is available to help the heart muscle and its conduction system in their resistance to the effects of ischemia, and most assuredly there will be more. There are even drugs that may be used within the first few hours of a coronary occlusion, to dissolve the brand-new clot that has caused the final bit of obstruction in the atherosclerotic vessel. There are drugs to decrease myocardial irritability, prevent spasm, dilate coronary arteries, strengthen the heartbeat, diminish accelerations of rate, drive out the excess load of water and salt in congestive failure, slow down the clotting process, decrease cholesterol levels in the blood, lower blood pressure, allay anxiety—and every one of them carries with it the possibility of undesirable or frankly dangerous side effects, for whose treatment, of course, there are still other drugs. Cardiologists of today tread a fine line between so drying out a patient that he is too weakened to live normally, and allowing him so much of a fluid load that he is in danger of lapsing into serious congestive failure.
In no area of human infirmity have the wizardries of electronics contributed so much as in the management of heart disease. Although diagnosis has been the primary beneficiary of their miracles, therapy, too, has been enhanced by the physicists and engineers who deal in such esoterica. We now have pacemakers to do the job of the SA node; they safely trigger a predictable and steady beat. There are defibrillators that not only reassert control when the heart’s mechanism becomes frivolous but even have the added virtue of being implantable directly into the patient, so that response to irregular rhythm is automatic and instantaneous.
Surgeons and cardiologists have devised operations to reroute blood around obstructions in coronary arteries and to widen narrowed vessels with balloons, techniques known respectively as the coronary artery bypass graft, or CABG (predictably pronounced
cabbage
), and angioplasty. When all else fails, an occasional patient fulfills the criteria to have his whole heart chucked out and replaced with a healthy secondhand one. All these operations, when the candidate is carefully chosen, have high rates of success. And yet, after each one, the process of atherosclerosis continues to lick at life. Widened arteries frequently plug up again, grafted vessels develop atheromata, and the symptoms of ischemia too often return to their old myocardial haunts.
cabbage
), and angioplasty. When all else fails, an occasional patient fulfills the criteria to have his whole heart chucked out and replaced with a healthy secondhand one. All these operations, when the candidate is carefully chosen, have high rates of success. And yet, after each one, the process of atherosclerosis continues to lick at life. Widened arteries frequently plug up again, grafted vessels develop atheromata, and the symptoms of ischemia too often return to their old myocardial haunts.
Delay it though we may, then, the victims of coronary atherosclerosis 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. There are now many more Horace Giddenses and many fewer James McCartys.
The reasons for this are several. The most obvious is that not only physicians but also community facilities have considerably improved their ability to cope with the urgent situations created by myocardial infarction. Speedy response by highly skilled paramedics and efficient transfer to an emergency room have meant better treatment during the first crucial hours, and the in-hospital intensive care itself has vastly improved. But another factor is at least equally important. More effective methods of medical care in general have resulted in the survival of increasing numbers of people to an older age, an age at which weakened cardiac pumping and consequent congestive failure are more commonly a problem. The incidence of heart failure in people younger than fifty-five has actually dropped—the great increase in overall numbers occurs entirely in the population older than sixty-five. More than 2 million Americans have some degree of heart failure that restricts their activities and undermines their vitality. When it becomes severe, it carries a mortality rate of 50 percent in two years. Thirty-five thousand people will die of it annually, far fewer than the 515,000 who will succumb to an actual heart attack, but a large number nevertheless.
Those whose hearts do not quit because of ventricular fibrillation and arrest will eventually die for the reasons previously enumerated: They cannot breathe well enough to oxygenate blood, their kidneys or liver can no longer cleanse their bodies of toxic substances, bacteria run rampant through their systems, or they simply cannot sustain a blood pressure high enough to maintain life and, most particularly, the function of the brain. This last-named condition is called cardiogenic shock. It and pulmonary edema are by far the most common cardiac enemies that are perpetually being fought in intensive care units and emergency rooms. The patients and their medical allies will win most of those battles, at least temporarily.
Having countless times watched those teams fighting their furious skirmishes, and having often been a participant or their leader in years past, I can testify to the paradoxical partnering of human grief and grim clinical determination to win that actuates the urgencies swarming through the mind of every impassioned combatant. The tumultuous commotion of the whole reflects more than the sum of its parts, and yet the frenzied work gets done and sometimes even succeeds.
As chaotic as they may appear, all resuscitations follow the same basic pattern. The patient, almost invariably unconscious because of inadequate blood flow to the brain, is quickly surrounded by a team whose mission is to pull him back from the edge by stopping his fibrillation or reversing his pulmonary edema, or both. A breathing tube is rapidly thrust through his mouth and down into his windpipe so that oxygen under pressure can be forced in to expand his rapidly flooding lungs. If he is in fibrillation, large metal paddles are placed on his chest and a blast of 200 joules is fired through his heart in an attempt to stop the impotent squirming, with the expectation that a regular beat will return, as it frequently does.
If no effective beat appears, a member of the team begins a rhythmic compression of the heart by forcing the heel of his hand down into the lowest part of the breastbone at a rate of about one stroke per second. By squeezing the ventricles between the flatness of the yielding breastbone in front and the spinal column in back, blood is forced out into the circulatory system to keep the brain and other vital organs alive. When this form of external cardiac massage is effective, a pulse can be felt as far away as the neck and groin. Although one might think otherwise, massage through an intact chest results in far better outcomes than does the direct manual compression that was the only known method when I had my grim encounter with the obstinacy of James McCarty’s myocardium some forty years ago.
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 out of the lungs, to be excreted by the kidney. Every resuscitation is 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 spoken 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?
Far too often, nothing helps. Even when the correct answer to both questions is an emphatic
yes
, the fibrillation may be beyond correction, the myocardium unresponsive to the drugs, the increasingly flabby heart resistant to massage, and then the bottom falls out of the rescue attempt. When the brain has been starved of oxygen for longer than the critical two to four minutes, its injury becomes irreversible.
yes
, the fibrillation may be beyond correction, the myocardium unresponsive to the drugs, the increasingly flabby heart resistant to massage, and then the bottom falls out of the rescue attempt. When the brain has been starved of oxygen for longer than the critical two to four minutes, its injury becomes irreversible.
Actually, few people survive cardiac arrest, and even fewer among those already seriously ill people who experience it in the hospital itself. Only about 15 percent of hospitalized patients below the age of seventy and almost none of those who are older can be expected to be discharged alive, even if the CPR team somehow manages to succeed in its furious efforts. When an arrest occurs elsewhere than the hospital, only 20 to 30 percent survive, and these are almost always those who respond quickly to the CPR. If there has been no response by the time of arrival in the emergency room, the likelihood of survival is virtually zero. The great majority of the responders are, like Irv Lipsiner, victims of ventricular fibrillation.
The tenacious young men and women see their patient’s pupils become unresponsive to light and then widen until they are large fixed circles of impenetrable blackness. Reluctantly the team stops its efforts, and the entire scene becomes transformed from a vital image of imminent heroic rescue to the dejected gloom of failure.
The patient dies alone among strangers: well-meaning, empathetic, determinedly committed to sustaining his life—but strangers nonetheless. There is no dignity here. By the time these medical Samaritans have ceased their strenuous struggles, the room is strewn with the debris of the lost campaign, more so even than was McCarty’s on that long-ago evening of his death. In the center of the devastation lies a corpse, and it has lost all interest for those who, moments earlier, were straining to be the deliverers of the man whose spirit occupied it.
What has happened is the culmination of a straightforward series of biological events. Whether programmed by his genes, self-imposed by the habits of his life, or, as is usually the case, a combination of both, a man’s coronary arteries have been unable to bring sufficient blood to nourish the muscle of his heart; the heartbeat became ineffective, the brain went too long without oxygen, and the man died. Approximately 350,000 Americans suffer a cardiac arrest each year, and the vast majority of them die; fewer than one-third of the 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. In some 20 percent of people, it may even happen, as it did for Lipsiner, without pain. Whatever mystery attaches to such a death is imposed on it by those who live. It is a tribute to the human spirit that the life preceding triumphs over the ugly events that most of us will experience as we die, or as we move toward our last moments.
The experience of dying does not belong to the heart alone. It is a process in which every tissue of the body partakes, each by its own means and at its own pace. The operative word here is
process
, not
act, moment
, or any other term connoting a flyspeck of time when the spirit departs. In previous generations, the end of the faltering heartbeat was taken to indicate the end of life, as though the abrupt silence beyond it intoned a soundless signal of finality. It was a specified instant, recordable in the chronicle of life and marking a full stop after its concluding word.
process
, not
act, moment
, or any other term connoting a flyspeck of time when the spirit departs. In previous generations, the end of the faltering heartbeat was taken to indicate the end of life, as though the abrupt silence beyond it intoned a soundless signal of finality. It was a specified instant, recordable in the chronicle of life and marking a full stop after its concluding word.
Today the law defines death, with appropriate blurriness, as the cessation of brain function. Though the heart may still throb and the unknowing bone marrow create new cells, no man’s history can outlive his brain. The brain dies gradually, just as Irv Lipsiner experienced it. Gradually, too, every other cell in the body dies, including those newly alive in the marrow. The sequence of events by which tissues and organs gradually yield up their vital forces in the hours before and after the officially pronounced death are the true biological mechanisms of dying. They will be discussed in a later chapter, but first it is necessary to describe the prolonged form of dying that is old age.
III
Three Score and Ten
N
O ONE DIES
of old age, or so it would be legislated if actuaries ruled the world. Every January, just when the harsh autocracy of winter has tightened its hoary hold, the U.S. government releases its yearly “Advance Report of Final Mortality Statistics.” Neither among the top fifteen causes of death nor anywhere else in that soulless summary is there to be found a listing for those among us who just fade away. In its obsessive tidiness, the Report assigns the specific clinical category of some fatal pathology to every octo- and nonagenarian in its neat columns. Neither do those few whose age is recorded in three digits escape the orderly nomenclature of the tabulators. Everybody is required to die of a named entity, by order not only of the Department of Health and Human Services but also of the global fiat of the World Health Organization. In thirty-five years as a licensed physician, I have never had the temerity to write “Old Age” on a death certificate, knowing that the form would be returned to me with a terse note from some official record-keeper informing me that I had broken the law. Everywhere in the world, it is illegal to die of old age.
O ONE DIES
of old age, or so it would be legislated if actuaries ruled the world. Every January, just when the harsh autocracy of winter has tightened its hoary hold, the U.S. government releases its yearly “Advance Report of Final Mortality Statistics.” Neither among the top fifteen causes of death nor anywhere else in that soulless summary is there to be found a listing for those among us who just fade away. In its obsessive tidiness, the Report assigns the specific clinical category of some fatal pathology to every octo- and nonagenarian in its neat columns. Neither do those few whose age is recorded in three digits escape the orderly nomenclature of the tabulators. Everybody is required to die of a named entity, by order not only of the Department of Health and Human Services but also of the global fiat of the World Health Organization. In thirty-five years as a licensed physician, I have never had the temerity to write “Old Age” on a death certificate, knowing that the form would be returned to me with a terse note from some official record-keeper informing me that I had broken the law. Everywhere in the world, it is illegal to die of old age.
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