How We Die by Sherwin B. Nuland

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.
    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