Free How We Die by Sherwin B. Nuland

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