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 1980s. 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. When he actually entered the house, I was sitting quietly in a chair, listening to the family’s conversation but not partaking in it. 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.
I knew of Giddens’s history of angina, and I also knew that he had already sustained several full-blown myocardial infarctions. Watching the small shoulder-heaving struggle of each paroxysmal breath, I tried to imagine the condition of his heart and also attempted to put together in my mind’s eye the various elements of the way it had failed him. 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. I do it always, almost without thinking. I’m sure many of my colleagues do the same.
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. Every few beats, there was an irregular spasmodic contraction that originated from one or another rebellious focus on the left ventricle, intruding on the muscle’s ineffectual attempt to maintain its steady rhythm. 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. I knew the process well: The severity of the ischemia had cut off the regular messages that Giddens’s SA node was trying to transmit to his ventricles. 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. Any small increase in stress or decrease in oxygenation leads to a state of what the French so aptly call “ventricular anarchy,” as disordered, ineffective contractions spread every which way through the heart muscle, giving way to the totally uncoordinated rapidity known as ventricular tachycardia and then fibrillation. As I watched Giddens’s uncertain movements, I could easily tell how close he was to this series of terminal events.
The vena cavae and the pulmonary veins were distended and tense with the pressure of the blood backed up into them because of the heart’s weakness. 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.
As I watched his nostrils flare with each difficult breath, I could not help but notice that the very tip of Giddens’s nose was just a bit blue, and so were his lips—the wetness in his lungs was preventing proper oxygenation. 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. Every organ in the man’s waterlogged body had some element of edema in it.
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. The
Schaufenster schauen
strategy was being used by Giddens to give him just enough respite to avoid serious trouble as he slowly made his way up to bed.
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. She didn’t move. 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.
I felt impelled to rush to Giddens’s assistance, but something held me rooted to my chair. I didn’t do a thing, and neither did anyone else. 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. I was watching the tragedy of Horace Giddens while comfortably seated in the seventh row of a theater, at a revival of Lillian Hellman’s remarkable play
The Little Foxes
. Her clinically meticulous account of a fictional character dying of ischemic heart disease in 1900 could not have been more accurate had it been written by a cardiologist. Whole sentences of my description above are simply extracts from Miss Hellman’s stage directions. The authoritative doctor who saw Giddens at Johns Hopkins was almost certainly the same William Osler whose words were quoted some pages ago.
Hellman’s writing accurately portrays the very way in which so many of the victims of coronary ischemia still die today. For, in spite of all the delaying and comfort-enhancing tactics that modern medicine has produced in its battle against cardiac disease, the final scene in the struggle of a sick heart, now near the dawn of the twenty-first century, is often exactly like that in which Horace Giddens was the leading protagonist one hundred years 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. In Giddens’s time, careful living consisted of exactly what the term implies, a life free of physical or mental stress. Nitroglycerin was prescribed to abort angina, and a mild sedative given to allay anxiety. A certain therapeutic nihilism in vogue at the time among the university-based doctors may have been the reason they did not recommend the use of digitalis to increase the strength of the ventricle’s contraction. 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. Specifically, the cardiologist begins by evaluating not only the current condition of the patient’s heart and its coronary arteries but also the probability that worsening is so imminent that active steps must be taken to prevent it. 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. The cardiologist must have a clear sense of the types of stresses existing in a patient’s life and the likelihood that they can be changed.
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. It is the cardiologist’s skill as a physician that enables him to befriend his patient and to know him—it is inherent in the art of medicine to appreciate that the testing and medications are of limited usefulness without the talking.