How we die sherwin nuland pdf download.How We Die Pdf Free Download
Sherwin B. Enhance your purchase. New Edition: With a new chapter addressing contemporary issues in end-of-life careA runaway bestseller and National Book Award winner, Sherwin Nuland’s How We Die has become the definitive text on perhaps the single most universal human concern: death.
This new edition includes an all-embracing and incisive afterword that examines the current state of health care and our relationship with life as it approaches its terminus. It also discusses how we can take control of our own final days and those of our loved ones. Shewin Nuland’s masterful How We Die is even more relevant than when it was first published.
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Page 1 of 1 Start over Page 1 of 1. How We Die. Sherwin B Nuland. Atul Gawande. Hermann Hesse. When Breath Becomes Air. Paul Kalanithi. Board book. How We Live. Special offers and product promotions 7. Please check ‘EMI options’ above for more details. About the Author Sherwin B.
Nuland, MD, was Clinical Professor of Surgery at Yale University until his retirement in , though he continues to teach Biomedical Ethics and Medical History to Yale undergraduates, and serve the university in various capacities. In hardcover and paperback, How We Die was on the New York Times bestseller list for a total of thirty-four weeks, and has been translated into twenty-nine languages. Nuland and his family live in Connecticut. About the author Follow authors to get new release updates, plus improved recommendations.
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Want more? Advanced embedding details, examples, and help! Knopf : Distributed by Random House, Inc. Includes index The strangled heart — A valentine–and how it fails — Three score and ten — Doors to death of the aged — Alzheimer’s disease — Murder and serenity — Accidents, suicide, and euthanasia — A story of AIDS — The life of a virus and the death of a man — The malevolence of cancer — Hope and the cancer patient — The lessons learned “There is a vast literature on death and dying, but there are few reliable accounts of the ways in which we die.
The intimate account of how various diseases take away life, offered in How We Die, is not meant to prompt horror or terror but to demythologize the process of dying to help us rid ourselves of that fear of the terra incognita. Each one of death’s diverse appearances is as distinctive as that singular face we each show during our lives.
Behind each death is a story. Nuland, a surgeon and teacher of medicine, tells some stories of dying that reveal not only why someone dies but how.
He offers a portrait of the experience of dying that makes clear the choices that can be made to allow each of us his or her own death. There are no reviews yet. 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 shriek of pain in the overtaxed calf is called a cramp or a charley horse. When it originates in the heart muscle, we use the much more elegant term angina pectoris. Angina pectoris is nothing else than a charley horse of the heart.
If it lasts long enough, its victim sustains a myocardial infarction. It is to another medical philologist, the remarkable eighteenth-century English physician William Heberden — , that we owe not only the term but also one of the finest descriptions of the symptoms associated with it.
In a 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.
Males are most liable to this disease, especially such as have past their fiftieth year. After it has continued a year or more, it will not cease so instantaneously upon standing still; and it will come on not only when the persons are walking, but when they are lying down, especially if they lie on the left side, and oblige them to rise up out of their beds. In some inveterate cases it has been brought on by the motion of a horse, or a carriage, and even by swallowing, coughing, going to stool, or speaking, or by any disturbance of mind.
His brain died because the fibrillating and finally stilled heart could no longer pump blood to it. A few years ago, I met a man who was miraculously resuscitated from such an apparent sudden cardiac death. Irv Lipsiner is a tall, broad-shouldered stockbroker who has been an avid athlete all his life. Although he requires insulin for long-standing diabetes, the disease has had no physical effects on his vigorous good health, or so it would appear at first glance. But he did have a small heart attack when he was forty-seven years old, which is exactly the age at which his father died from the same cause.
That episode left his heart muscle with only minimal damage, and he continued his active life without restriction.
Late on a Saturday afternoon in , when he was fifty-eight years old, Lipsiner was beginning his third hour of tennis at the Yale indoor courts when two of his partners left, necessitating a switch from doubles to singles.
The practice rally was just beginning when, without warning or premonitory pain, he slumped to the floor unconscious. Two physicians, by luck playing on an adjacent court, rushed to his aid and found him glassy-eyed, unresponsive, and not breathing.
There was no heartbeat. Assuming correctly that he was in ventricular fibrillation, they immediately began cardiopulmonary resuscitation, continuing it for what seemed to them an interminable time, until the ambulance arrived. By then, Lipsiner had begun to respond, even resuming a spontaneous regular heartbeat as his airway was intubated and he was placed in the ambulance. I met him some years later, on the horse farm where he lives.
Every day, he takes time out from work to go riding or play tennis, usually singles. Here is 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. The only thing different from that was that it was in slow motion. 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 felt like somebody took the life out of me. You know, shrunk —uniformly. 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.
Lipsiner felt no ischemic pain. 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.
Since 1. When all natural causes are taken into account, approximately 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 victims of ischemic heart disease are betrayed by their eating and their smoking and their inattention to such simple housekeeping chores as exercise and the maintenance of normal blood pressure. There is little randomness in the choices made by cardiac ischemia.
Long before we knew about the lurking perils of cholesterol, cigarettes, diabetes, and hypertension, the medical world was beginning to recognize specific characteristics in those persons who seemed destined for cardiac death. Like lucky Lipsiner, most of them do not actually suffer death of cardiac muscle but are victimized by a rhythm suddenly made disorderly by the effect of ischemia or sometimes local chemical changes on an electrical conduction system already sensitized by a previous injury, whether it was recognized or not.
But the usual way in which people succumb to ischemic heart disease these days is not the way of Lipsiner or McCarty. Decline is most often gradual, with plenty of warnings and much successful treatment before the final summons. The killing off of increments of heart muscle takes place over a period of months or years, until that besieged and enervated pump simply fails. It then gives up, for lack of strength or because the command system that controls its electrical coordination can no longer recover from yet another breach of its authority.
Those laboratory doctors who are convinced that medicine is a science have accomplished so much that those bedside doctors who know it is an art can often, by careful timing and skillful choice of what is now available to them, provide victims of heart disease with long periods of improvement and stable health.
The fact remains, however, that each day fifteen hundred Americans will die of cardiac ischemia, whether its course has been sudden or gradual. Although preventive measures and modern methods of treatment have been reducing the figure steadily since the mids, it is virtually impossible for any slope of decline to change the picture for the vast majority of those who carry the diagnosis today or in whom it will be made in the next decade.
This will be the subject of the first pages of the chapter that follows. It is made almost entirely of muscle, called myocardium, wrapped around a large central space that is subdivided into four chambers: A vertical front-to-back wall of tissue, called the septum, separates the large space into right and left portions, and a transverse sheet at right angles to the septum divides each of those portions into upper and lower parts, making four in all.
Because they have a certain degree of independence from one another, the portions on either side of the vertical septum are often called the right and left heart. On each side, the transverse sheet separating top from bottom is perforated by a central opening fitted with a one-way valve that allows blood to pass easily from the upper chamber called the atrium down into the lower chamber the ventricle.
In a healthy heart, the valves close tightly when the ventricle is filled, to prevent blood from regurgitating back up into the atrium. The atria are primarily receiving chambers, and the ventricles are pumping chambers. Consequently, the portion of the cardiac muscle around the upper part of the heart does not have to be as thick as that of the more powerful ventricles below them. In a sense then, we have not one heart but two, attached side by side to each other by the septum; each has an upper chamber to receive and a lower one to pump.
In recognition of this division of labor, physicians for centuries have differentiated between the two routes of blood by calling them the lesser and greater circulations. The mechanism of a living heart is a masterpiece of nature. This complicated series of events requires intricate coordination, which is accomplished by messages sent out along microscopic fibers that originate from a tiny ellipse-shaped clump of tissue near the top of the right atrium, in its back wall very close to the entrance of the superior vena cava.
It is at this very spot, where the cava empties into the atrium, that the blood starts out on its circuitous journey through the heart and lungs, and there could be no more appropriate point to position the source of the stimulus that makes it all happen.
This little bit of tissue, called the sinoatrial or SA node, is a pacemaker that drives the coordinated beating of the heart. Awestruck anew each time they viewed the proud independence of an exposed animal heart, wise men of ancient civilizations proclaimed that this supernal mechanism of boldly autonomous flesh must be the dwelling place of the soul.
For the sustenance required for its forceful labors, the heart muscle, or myocardium, is supplied by a group of separate and distinct vessels, which, because they originate in encircling arteries that wind around the heart like a crown, are called coronary.
In health, these coronary arteries are the friends of the heart; when they are diseased, they betray it at its most needful moments. So commonly do the coronary arteries betray the heart whose muscle they are meant to sustain, that their treachery is the cause of at least half of all deaths in the United States. The average age of the first infarction of women is in the mid-sixties, but men are more likely to have that terrifying experience ten years earlier.
Although the coronary arteries have by that age reached the critical degree of narrowing necessary to threaten the viability of heart muscle, the process begins when its victims are much younger. An oft-quoted study of soldiers killed in the Korean War revealed that some three-quarters of these young men already had some arteriosclerosis in their coronary vessels.
Varying degrees of it can be found in virtually every American adult, having begun with adolescence and increasing with age. The obstructing material takes the form of yellowish white clumps called plaques, which are densely adherent to the inner lining of the artery and protrude into its central channel.
The process of atheroma formation being by far the most common cause of arteriosclerosis, it is usually referred to as atherosclerosis, hardening by atheroma. As an atheroma progresses, it becomes larger and tends to coalesce With neighboring plaques at the same time that it is absorbing calcium from the bloodstream.
The result is the gradual accumulation of an extensive mass of crusted atheroma that lines a vessel for a considerable distance, making it increasingly gritty, hard, and narrowed.
An atherosclerotic artery has been compared to an old length of much-used, poorly maintained pipe whose inner diameter is lined with thick, irregular deposits of rust and embedded sediment. Even before the cause of angina pectoris and infarction was understood to be a narrowing of the coronary arteries, a few physicians were beginning to make observations about the hearts of those people who died of the process.
The same Edward Jenner who introduced smallpox vaccination in 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. 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.
I 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. Adam Hammer of St. Hammer had been called in consultation to see a suddenly stricken thirty-four- year-old man who was in such a rapidly worsening state of collapse that death was imminent.
Although physicians knew the mechanism of myocardial ischemia, the diagnosis of infarction caused by it had never been made, or even thought of. As he watched helplessly while his patient died, Hammer suggested to his colleague that a completely occluded coronary artery had caused death of heart muscle, and he decided that an autopsy was mandatory to prove his novel theory.
It was no easy matter to obtain permission from the grief-stricken family, but the experienced Hammer overcame their objections by the timely application of that perennial solvent of reluctance, a handful of dollars. During the following decades, the principles of ischemic heart disease and infarction became gradually established. Other diagnostic techniques were discovered apace, including the fact that injured myocardium releases certain chemicals or enzymes whose identifiable presence in the blood aids in detecting infarction.
An individual infarction involves that part of the muscle wall supplied by the particular coronary artery that is occluded, a part that most commonly measures two or three square inches in surface area. The specific culprit almost half the time is the left anterior descending coronary artery, a vessel that passes down the front surface of the left heart toward its tip, tapering as it gives off subdivisions that enter the myocardium.
The frequent involvement of this artery means that approximately half of infarctions involve the front wall of the left ventricle. Its back wall is supplied by the right coronary artery, which accounts for 30 to 40 percent of occlusions; the lateral wall is supplied by the left circumflex coronary artery, which contributes 15 to 20 percent. When a coronary artery suddenly completes the process 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. Each time a person recovers from a heart attack of any size, he has lost a little more muscle to the increasing area of scar tissue, and the power of his ventricle becomes just a bit less. As atherosclerosis progresses, the ventricle may gradually weaken even when there is no frank heart attack.
Coronary occlusions in smaller branches of the main vessels may give no signals to announce themselves, but they continue nevertheless to diminish the force of cardiac contraction.
Eventually, the heart begins to fail. It is the chronic disease of heart failure, and not the sudden end of the James McCartys, that carries off approximately 40 percent of the victims of coronary artery disease. Differing combinations of instigating circumstances and tissue damage determine the type and degree of danger in which each individual heart finds itself at any particular stage of its decline.
One or another factor may predominate at a given point: Sometimes it is the susceptibility to spasm or thrombosis of the partially occluded coronary arteries; sometimes it is the sick cardiac muscle whose damaged communication system is so confused and hyper-excitable that it fibrillates with minimal stimulus; sometimes it is the communication system itself, which becomes sluggishly loath to transmit signals, so that it falters, slows, or even allows the heart to stop altogether; sometimes it is a ventricle too scarred and weakened to eject a sufficient fraction of the blood that has poured into it from its atrium.
When the 20 percent of cardiac patients who die in a McCarty-like first attack are added to those who expire suddenly after weeks or years of worsening disease, the total figure for sudden deaths amounts to some 50 to 60 percent of people who have ischemic heart disease. The remainder die slowly and uncomfortably of one of the variations of what is called chronic congestive heart failure. Although or perhaps because the death rate from heart attacks has decreased by approximately 30 percent in the past two or three decades, mortality due to congestive heart failure has gone up by one- third.
When the blood that has already entered the heart cannot be efficiently pumped forward into the greater and lesser circulations, some of it backs up into the veins that are returning it, causing backpressure in the lungs and other organs from which it is coming. 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 ventricular muscle thickens in an attempt to compensate for its own weakness. Thus the heart becomes enlarged and appears more formidable, but it is now only a thing of blustering braggadocio.
Huffing and puffing, it speeds up the rate of its beat, trying to put out more blood. Before long, it finds itself in the ever-worsening plight of having, Alice-like, to run faster just to keep up.
The exertions of the distended, thickened heart require more oxygen than the narrowed coronary arteries can bring it, and the faltering myocardium may be damaged further, or perhaps new abnormalities of rhythm will appear. Some of these abnormalities are lethal—ventricular fibrillation and similar disturbances of rhythm kill almost half of the patients in heart failure.
So, no matter how boastful its bombast, the failing heart continues to fail, in a kind of vicious circle of trying to disguise its own inadequacies by straining to compensate for them. 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. 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.
Patients in heart failure suffer also from chronic fatigue and listlessness, owing to a combination of the added effort of breathing and the poor tissue nutrition caused by low cardiac output. Although rare today, it was not uncommon in my medical school years to come upon a patient sitting upright in bed, belly and legs swollen with fluid, throwing himself into almost convulsive heavings of shoulders and gaping mouth while struggling fiercely for each individual gasping breath as if it were his last chance to save his own life.
In the wide-open mouths of these combatants in losing campaigns against imminent mortality, one could usually detect the blueness of deoxygenated lips and tongues, parchment-dry even though the dying patients were drowning. Doctors feared to do anything that might worsen the already intolerable eye-bulging anxiety of a man being submerged in his own waterlogged tissues, hearing only the horrible wheeze and gurgling of his own death agony. In those days, we had little to offer a terminal sufferer except sedation, with the full and merciful knowledge that every bit of relief brought the end closer.
Although nowadays less common, such scenes are sometimes still enacted. Eventually, the abused organs themselves fail. When the kidneys or liver are gone, so, too, is life. Kidney failure, or uremia, is an exit for some cardiac patients and so, on occasion, is inadequacy of liver function, frequently signaled by the appearance of jaundice.
Not only does the heart fool itself into overactivity, it may also fool the organs that might be able to help it out of its troubles. The kidney should be able to filter enough extra salt and water out of the blood to decrease the load on the heart, but congestive failure causes it to do just the opposite.
Because the kidney correctly senses that it is getting less blood than normal, it compensates by producing hormones that actually cause reabsorption of the salt and water it has already filtered, so that they are returned to the circulation. The failing heart thus outsmarts the kidney and itself at the same time; the self-same organ that is trying to be its friend becomes its inadvertent enemy. Heavy, wet lungs with a sluggish circulation are an ideal breeding ground for bacteria and advancing inflammation, which is why so many cardiac patients die of pneumonia.
But the heavy, wet lungs do not need the help of bacteria to do their killing. A sudden worsening of their waterlogged state, called acute pulmonary edema, is the frequent final event for patients with long-standing heart disease. Whether due to new cardiac damage or a temporary overload resulting from unexpected exercise or emotion, or perhaps just a little too much salt in a sandwich I know of a man who died of what some might call acute pastrami-generated heart failure , the excessive fluid volume dams up and floods the lungs.
Severe air hunger rapidly supervenes, the gurgling, wheezing respirations begin, and finally the poor oxygenation of the blood causes either brain death or ventricular fibrillation and other rhythm disturbances, from which there is no return.
All over the world, at this very instant, there are people dying in this way. The final passage of some of them is epitomized in the case history of another man whose death I witnessed. In the reference frame of chronic heart disease, Horace Giddens might be called Everyman.
The details of his illness graphically depict one of the common patterns in the inexorable downhill course of cardiac ischemia. Giddens was a successful forty-five-year-old banker in a small southern town when his path crossed mine in the late s. He had just returned home from an extended stay at The Johns Hopkins Hospital in Baltimore, where his physician had sent him in desperation, hoping that the progression of his increasingly severe angina and heart failure might be slowed, or at least ameliorated; virtually every known treatment had already failed.
Trapped in a strife-ridden marriage, Giddens had made the difficult journey to Baltimore as much to separate himself from the enervating enmity of his wife, Regina, as he had to seek some relief for his heart. But it was too late—his disease was found to be so far advanced that he was beyond help from any available therapy. After all the tests and consultations, the Hopkins doctors told him, as sensitively as they could, that even they could not help him—he was no candidate for any treatment other than palliative medication.
For Horace Giddens, there would be no angioplasty, no bypass, no heart transplant. I was making a purely social visit to his home on the evening he returned from Baltimore courageously facing the certainty that he would soon be dead. Although it was understood that Giddens was on his way home, his unfeeling wife seemed not to know or even care about the exact time of his arrival.
That entrance was a difficult moment to watch. The tall, gaunt Giddens came shuffling into the living room, grimacing with breathlessness, his narrow shoulders held firmly in the supporting grip of the adoring family maid.
From a large photograph on the piano, I could tell that he had once been a robustly good- looking man, but now his grayish face was tired and drawn. He walked stiffly, as if with enormous effort, and carefully, seemingly unsure of his balance; he had to be helped into an armchair.
After nearly forty years as a doctor, this kind of conjecture is a common preoccupation of mine when I find myself socially in the presence of the sick. It is an automatic drill, a self-testing, and in its own peculiar way, a kind of empathy as well.
What I visualized behind the breastbone of Horace Giddens was an enlarged, flabby heart that was no longer able to beat with anything resembling vigorous energy. More than three inches of its muscular wall had been replaced by a large whitish scar, and there were several other smaller areas of scarring as well. It was as though various parts of the ventricles were trying to break free of the intrinsic automaticity of the process, while the SA node struggled to maintain its declining authority.
Unable to get their accustomed call, the ventricles feverishly begin to initiate beats on their own, starting each pulsation from whichever spontaneous spot on the myocardium chooses to meet the challenge. The leathery lungs resembled gray-blue water- soaked sponges, overloaded with puffy edema and barely able to rise and fall like the gentle pink bellows they once were.
The whole blood-choked image reminded me of an autopsy I once saw of a man who had hanged himself—his livid purplish face was engorged and bulging, its plethoric features almost unrecognizable as human. Giddens had lived his life well, and borne with philosophical resolve the slings and arrows fired at him by his malicious wife.
He had devoted his life to the seventeen-year-old daughter who idolized him, and to the fulfillment of the trust put in him by the people of his town, whose admiration and respect he had earned by dint of simple probity and the wisdom of sound financial management of their savings.
But now he had come home to die. The laboriously shuffling gait was the product of ankles and feet so swollen they seemed to bulge out over the tops of shoes made too small by the tightly constrained wet flesh within them. Pump failure was only part of the reason that walking was such an enormous effort for Giddens.
He must have been agonizingly aware of the effort expended in each step he took, knowing that even the smallest increase in activity might bring on the dreaded pain of angina, since the hair-thin channels of his rigid coronary arteries were incapable of delivering any added requirement of blood. Giddens sat down in the armchair and spoke briefly with his family, seemingly unaware of my presence.
Tiring in both body and spirit, he then climbed laboriously up the staircase to his bedroom, stopping several times to look down and say a few words to his wife. As I watched him do this, I was reminded of a practice commonly resorted to by so-called cardiac cripples in order to disguise the advanced state of their illness: A patient feeling the onset of an anginal attack while on his daily stroll finds it useful to stop and gaze with feigned interest into a shop window until his pain disappears.
The Berlin-born medical professor who first described the face- and sometimes life- saving procedure to me called it by its German name of Schaufenster schauen, or window-shopping. Horace Giddens died on a rainy afternoon only two weeks later. Although present, I was unable to lift a finger to help him.
I could do nothing but sit by while his wife verbally abused him, until he suddenly threw his hand up to his throat, as though gesturing toward the brutal pathway of his radiating angina.
His pallor suddenly increasing, he began to gasp, then shakily groped for the solution of nitroglycerin that lay on a coffee table in front of the wheelchair in which he sat.
He managed only to get his fingers around it, but it fell from his trembling hand to the floor and shattered, spilling the precious medicine that might have widened his coronary arteries just enough to save him. Panic-stricken and breaking out into a cold sweat, he begged Regina to find the maid, who knew where his reserve bottle was kept. Increasingly agitated, he tried to shout, but the only sound to come out of his mouth was a hoarse whisper, too small to be heard outside the room.
The look on his face was heartrending to see, as he realized the futility of his strangled efforts. He made a sudden furious spring from his wheelchair to the stairs, taking the first few steps like a desperate runner trying with his last iota of energy to reach safety. On the fourth step, he slipped, gasped hungrily for air, seized the railing, and, in one great exhausted effort of grimacing finality, reached the landing on his knees. Frozen in my place, I gazed up the stairs at him and saw his legs give way.
Everyone in that room heard the crumpling sound of his body falling forward, just out of view. Giddens was still alive, but barely. Regina, with the calm dispatch of an experienced assassin, called out to two of the servants to carry him into his room.
The family physician was summoned. Within a few minutes, and long before the doctor arrived, his stricken patient was dead. Although I have assumed that the specific mechanism that killed Horace Giddens was ventricular fibrillation, it may have been acute pulmonary edema, or the terminal condition called cardiogenic shock, in which the left ventricle is just too weak to maintain a blood pressure high enough to sustain life.
Among those of us who will succumb to ischemic heart disease, these three events will account for the vast majority of deaths. They can occur in sleep and they can happen so rapidly that only minutes pass before the moment of death. If medical help is at hand, the worst of their accompaniments can be lessened by morphine or other narcotics. The miracles of modern biomedicine can delay them for years. But every victory over ischemic heart disease is only a triumph of temporizing.
The unremitting progression of atherosclerosis will continue, and each year there will be those more than half a million Americans who will die because the natural order demands it: Though it is a seeming paradox, natural death is the only way by which our species can be perpetuated.
By now, it may have become apparent why I was unable to lift a finger to help the unfortunate man who was dying before my eyes. Her clinically meticulous account of a fictional character dying of ischemic heart disease in could not have been more accurate had it been written by a cardiologist. The authoritative doctor who saw Giddens at Johns Hopkins was almost certainly the same William Osler whose words were quoted some pages ago.
Although many victims of ischemic heart disease still die in their first episode, like James McCarty, most follow a course more like that of Horace Giddens, in which the initial infarction or the evidences of ischemia are survived, then followed by a long period of careful living.
Nitroglycerin was prescribed to abort angina, and a mild sedative given to allay anxiety. Digitalis would not have prevented the coronary spasm that probably carried Giddens off, but it would certainly have lessened the chronic congestive failure from which he suffered so badly during his last months.
Nowadays, things are different. The spectrum of options available to treat ischemic heart disease mirrors the succession of accomplishments of modern biomedical science itelf, ranging from simple changes in lifestyle to the transplantation of a heart. Ischemia does its ruinous work in a variety of ways, and the myocardium needs help against every one of them. It is the job of the cardiologist to provide that help.
In order to do that, he or she must know the nature of the enemy and the details of the strategy it is using in any given campaign. To this end, a group of tests have been developed that are now so commonly utilized, their names and acronyms have become part of the common parlance of patients and their friends: Thallium stress test, MUGA, coronary angiogram, cardiac ultrasound, and Holter monitor are just a few.
Even with the objective information provided by such tests, it is impossible to give sound advice to a patient without understanding a great deal about his or her life and personality. It is not enough to measure the fraction of contained blood ejected by the ventricle with each contraction or to know the residual caliber of the narrowed coronary arteries, the mechanics of myocardial contraction, the output of the heart, the hypersensitivity to irritable stimuli of its electrical system, or any of those other factors so assiduously and impersonally determined in laboratories and X-ray units.
Family history, dietary and smoking patterns, probability of compliance with medical advice, plans and hopes for the future, dependability of a support system of family and friends, personality type, and potential for modification if necessary—these are all factors that must be given proper weight in making decisions about treatment and long-term prognosis. 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.
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. 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.
How we die sherwin nuland pdf download.How we die : reflections on life’s final chapter
WebOct 12, · HOW WE DIE SHERWIN NULAND PDF. How We Die: Reflections on Life’s Final Chapter. Sherwin B. Nuland, Author, Nuland, Author Alfred A Knopf Inc $24 Missing: download. WebAbout the Author of Sherwin Nuland How We Die PDF Free Download Book. Editorial Reviews From Publishers Weekly The NBA nonfiction winner, Yale physician . WebJan 15, · DOWNLOAD NOW». Attempting to demythologize the process of dying, Nuland explores how we shall die, each of us in a way that will be unique. Through .
How we die sherwin nuland pdf download.How We Die: Reflections of Life’s Final Chapter, New Edition – Sherwin B. Nuland
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Knopf : Distributed by Random House, Inc. Includes index The strangled heart — A valentine–and how it fails — Three score and ten — Doors to death of the aged — Alzheimer’s disease — Murder and serenity — Accidents, suicide, and euthanasia — A story of AIDS — The life of a virus and the death of a man — The malevolence of cancer — Hope and the cancer patient — The lessons learned “There is a vast literature on death and dying, but there are few reliable accounts of the ways in which we die.
The intimate account of how various diseases take away life, offered in How We Die, is not meant to prompt horror or terror but to demythologize the process of dying to help us rid ourselves of that fear of the terra incognita. Each one of death’s diverse appearances is as distinctive as that singular face we each show during our lives. Behind each death is a story. Nuland, a surgeon and teacher of medicine, tells some stories of dying that reveal not only why someone dies but how.
He offers a portrait of the experience of dying that makes clear the choices that can be made to allow each of us his or her own death. There are no reviews yet. Be the first one to write a review. Books for People with Print Disabilities. Internet Archive Books. Scanned in China.