Authors: Sherwin B Nuland
How We Die (6 page)
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 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. 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.
In spite of Jenner’s observations and a gradual increase in understanding the way in which coronary obstruction injures the heart, it took until 1878 before a physician was able to diagnose a myocardial infarction correctly. Dr. Adam Hammer of St. Louis, a German refugee from the repression following the unsuccessful revolutions of 1848, sent off to a medical journal in Vienna his case report, entitled “
Ein Fall von thrombotischem Verschlusse einer der Kranzarterien des Herzens
,” “A Case of Thrombotic Occlusion of One of the Coronary Arteries of the Heart.” (Here an interesting twist of language presents itself: The German term for coronary artery is
Kranzarterie
, a
Kranz
being a wreath or a crown of flowers, which thus bestows an entirely new and quite poetic significance on the valentine image.) 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. As he put it so frankly in his journal article: “In the face of this universal remedy, even the most subtle misgivings, including the religious ones, eventually yield.” Hammer’s persistence was rewarded by finding a pale yellow-brown myocardium (its color signifying infarction) and a completely occluded coronary artery, confirming his insight.
Ein Fall von thrombotischem Verschlusse einer der Kranzarterien des Herzens
,” “A Case of Thrombotic Occlusion of One of the Coronary Arteries of the Heart.” (Here an interesting twist of language presents itself: The German term for coronary artery is
Kranzarterie
, a
Kranz
being a wreath or a crown of flowers, which thus bestows an entirely new and quite poetic significance on the valentine image.) 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. As he put it so frankly in his journal article: “In the face of this universal remedy, even the most subtle misgivings, including the religious ones, eventually yield.” Hammer’s persistence was rewarded by finding a pale yellow-brown myocardium (its color signifying infarction) and a completely occluded coronary artery, confirming his insight.
During the following decades, the principles of ischemic heart disease and infarction became gradually established. With the invention of the electrocardiogram in 1903, physicians were able to trace the messages carried by the heart’s conduction system of fibers, and they soon learned to interpret the tracings made by electrical changes taking place when the heart muscle is endangered by a decreased blood supply. 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.
The left ventricle, the most powerful part of the cardiac pump and the Source of the muscular strength that nourishes every organ and tissue of the body, is injured in virtually every heart attack—each cigarette, each pat of butter, each slice of meat, and each increment of hypertension make the coronary arteries stiffen their resistance to the flow of blood.
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.
Chronic congestive failure is the direct result of the scarred and weakened myocardium’s inability to contract with enough force to push out the necessary volume of blood with each stroke. 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. 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 backpressure of inadequately ejected blood causes the heart’s chambers to balloon out and remain dilated. 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. As a cardiologist colleague has put it, “Heart failure begets heart failure.” The proprietor of that heart is beginning to die.
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. 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.
The elevated pressure that is transmitted from the venae cavae back into the body’s veins causes the feet and ankles to swell, but when patients are bedridden, gravity forces the fluid to collect in the tissues of the lower back and thighs. 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. A professor of cardiology recently wrote me: “There are many patients with terminal, intractable congestive heart failure whose final hours—or days—of life are made uncomfortable and even miserable by their drowning, while physicians can only watch helplessly, and use morphine for sedation. It isn’t a pleasant exit.” Not only the heart itself but the long-range damage inflicted by soggy, anemic tissues has plenty of other ways to kill. 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 result is to increase the body’s total fluid volume instead of decreasing it, thereby adding to the problems of the already-overworked heart. 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.
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