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sobriquet “the Pope of German Medicine.” No single individual has ever contributed more to the understanding of the ways in which disease wreaks its havoc on human organs and cells than did Rudolf Virchow (1821–1902).
    Virchow, a professor of pathology at the University of Berlin for almost fifty years, produced more than two thousand books and articles, not only on medicine but on anthropology and German politics as well. So liberal a member of the Reichstag was he that the autocratic Otto von Bismarck once challenged him to a duel. Being given the choice of weapons, Virchow ridiculed the upcoming encounter out of existence before it took place—by insisting that it be fought with scalpels.
    Among Rudolf Virchow’s many research interests was his fascination with the ways in which disease affects arteries, veins, and their contained blood constituents. He elucidated the principles of embolism, thrombosis, and leukemia and invented the words to describe them. Seeking a term to designate the mechanism by which cells and tissues are deprived of their blood supply, Virchow seized (this word is chosen advisedly) upon the Greek ischano —“I hold in check,” or “I quench”—derived from the Indo-European root segh , which refers to “seizing” or “holding” or “causing to pause.” By combining it with aima , or “blood,” the Greeks had created the word ischaimos , to signify a holding in check of the flow of blood. Ischemia was chosen by Virchow to designate the consequences of diminishing or totally stopping blood flow to some structure of the body, whether as small as a cell or as large as a leg or a section of heart muscle.
    Diminishing is a relative term, however. When an organ’s activity increases, its oxygen requirements go up, and so does its need for blood. If narrowed arteries cannot widen to accommodate this need, or if for some reason they go into tight spasm that further restricts flow, the organ’s demands are not met, and it rapidly becomes ischemic. In pain and anger, the heart screams out a warning, and continues to do so until its shrieking exhortations for more blood are met, usually by the natural stratagem of the victim, who—alarmed by the distress within his chest—slows or stops the activity that is tormenting his cardiac muscle.
    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 calf does not get enough oxygen and it cries out in an agonizing seizure, to warn the athlete manqué to stop his exertions before a clump of muscle cells are starved to death, the process known as infarction. 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.
    Angina pectoris is a Latin phrase which translates literally as “a choking” or “throttling” ( angina ) “of the chest” ( pectoris , the genitive case of pectus , “chest”). It is to another medical philologist, the remarkable eighteenth-century English physician William Heberden (1710–1801), that we owe not only the term but also one of the finest descriptions of the symptoms associated with it. In a 1768 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