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CHAPTER 1 HEART BLOCK AND THE HEART TICKLER Modern cardiac pacemakers and other implantable devices that manage disorders of heart rhythm are a result of decades of scientific research about the workings of the normal heartbeat. But there was never a simple and certain route ‘‘from bench to bedside.’’ Even in a science-based field like cardiology, important laboratory research may not, for decades, lead to improved treatments. Sometimes, too, the process works the other way: new treatments can come first and inspire new scienti fic research. The inventors of the first heart-pacing devices in the 1920s probably knew of the latest experimental findings about the heartbeat and its disorders , but this new knowledge apparently did not contribute to the design of their pacemakers or inspire new ideas about the clinical uses for the inventions . A generation later, when Paul Zoll invented a practical cardiac pacemaker in the early 1950s, he undoubtedly drew on an accumulation of laboratory research with which he was thoroughly familiar and to which he had made contributions of his own—but his attempt to treat a serious rhythm disorder by firing electrical pulses into the heart got underway because of his experiences as a clinical cardiologist (a cardiologist who treats patients) during and after World War II.1 SLOW PULSE WITH FAINTING FITS In February 1846, William Stokes (1804–78), of Dublin, a leading physician of his day and a recognized expert on diseases of the chest and use of the stethoscope, visited the Meath Hospital to see a patient named Edmund Butler. Butler was 68 years old and reported that he had been healthy until about three years earlier, ‘‘at which time he was suddenly seized with a fainting fit. . . . This occurred several times during the day, and always left him without any unpleasant effects. Since that time he has never been free from these attacks for any considerable length of time.’’ Based on Butler’s own account, Stokes gives a vivid description of the attacks: HEART BLOCK AND THE HEART TICKLER 15 There is little warning given of the approaching attack. He feels, he says, a lump first in the stomach, which passes up through the right side of the neck into the head, where it seems to explode and pass away with a loud noise resembling thunder, by which he is stupefied. This is often accompanied by a fluttering sensation about the heart. He never was convulsed or frothed at the mouth during the fit, but has occasionally injured his tongue. The duration of the attack is seldom more than four or five minutes, but sometimes less; but during that time [he] is perfectly insensible.2 To Stokes, Butler ‘‘seemed the wreck of what was once a fine, robust man. He lay generally in a half drowsy state, but when spoken to was perfectly lively and intelligent.’’ Stokes timed his patient’s pulse rate at 28 to 30 per minute. Butler’s heartbeat had ‘‘a dull, prolonged, heaving character ’’; the arteries ‘‘pulsate visibly all over the body.’’ Stokes also noticed a lack of connection between Butler’s pulse rate and the rate at which he could hear the heart beating: over the course of one minute, he detected 36 pulses at the wrist but could hear only 28 definite heartbeats. Stokes inferred that occasional inaudible ‘‘semi-beats’’ must be occurring between the regular contractions of the ventricles. ‘‘On listening attentively,’’ he could hear ‘‘occasional abortive attempts at a contraction.’’ When he reexamined Butler three months later, Stokes found that the patient’s right external jugular vein was visibly throbbing at more than twice the rate of the ventricular contractions. In the century or so before Stokes, a few medical men had noted similar collections of symptoms centering on ‘‘slow pulse with fainting fits.’’ Stokes’s observations of the mysterious condition were more detailed than any earlier physician’s, but he conceded that he could not explain everything he had observed. On one point, though, Stokes was firm: the episodes of unconsciousness were unrelated to epilepsy, injury to the spinal cord, or some other neurological source. He ascribed the attacks to ‘‘circumstance tending to impede or oppress the heart’s action.’’ Stokes followed his countryman Robert Adams (1791–1875) in attributing the condition to ‘‘fatty degeneration of the heart.’’ This implied that weakness of the heart muscle caused the slow and ‘‘heaving’’ heartbeat in the same way that weak arm and shoulder muscles might force a person doing push...

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