The Man Who Touched His Own Heart

by Rob Dunn

  Then there was another problem. Then another. More improvisation. Gibbon and his team were getting closer and closer to the finish line—trying his device on humans—but it was such a long race.

  What Gibbon had hoped for during the years and years he worked on his machine was medical success; he wanted to be able to treat patients. But those all around him had begun to talk about popular success, media success. Gibbon hated the idea of his work garnering publicity. He believed a doctor should heal in anonymity. Gibbon wanted to solve problems, not discuss them. But he had little choice. Even before Gibbon tried to use the machine on people, the media came to him. As Miller Wayne noted in his book King of Hearts, “Few spectacles are as beguiling as a man trying to play God with electricity and steel.” It did not help that one of Gibbon’s “team members” was Thomas J. Watson, the chairman of IBM (the same man after whom IBM would name its most impressive computer, the computer that won against a human on the game show Jeopardy!). Watson8 provided financial support and allowed his engineers to work with Gibbon to make the device more automatic (and robotlike). The collaboration with Watson had the effect of lending the endeavor an even greater science-fiction mystique than it might have had otherwise. Life magazine described the machine as a “robot, a gleaming, stainless steel cabinet as big as a piano.”

  In 1949, the team members tried the robot on bigger animals: dogs. They were able to stop the heart of each of nine dogs and then replace the function of those dogs’ hearts with the machine. In one case, this had worked for forty-six minutes. Time magazine announced this success and left little ambiguity about the next step—humans. The same year, the National Heart Institute awarded Gibbon and Jefferson Medical College $26,8279 to speed up the development of the machine. Gibbon’s colleagues and the public believed heart surgery was about to change. But Gibbon and his team were less sure. They were still unhappy with the portion of the machine that oxygenated the blood.10

  Two years later, the opportunity to use the machine on a human arose when Gibbon was operating on a fifteen-month-old girl, again at Jefferson College. Her heart was not beating properly. With her parents’ consent, Gibbon and his team opened her chest and inserted a catheter into the two largest veins entering her heart (veins with blood depleted of oxygen). The catheters were connected by plastic tubing to the giant machine, which would add oxygen to the blood in the tubes by way of two pumps, the first of which pumped the blood to the machine’s artificial lungs and the second of which pumped it through. A third pump sent the oxygenated blood back into the body through a tube connected to an artery in the girl’s groin.11 Six assistants controlled the machine itself. But something was wrong. Gibbon cut into what he was sure was the source of her problem, her right atrium, where it was expected that she had an atrial-septal defect, a hole between the two atria of the heart. But he couldn’t find the hole. He felt around to no avail, searching and searching. The baby bled to death before he could find and mend what was broken. Only later, during the autopsy, did Gibbon learn that the defect in her heart was on the outside, not the inside. He had been searching in the wrong place. He had not done an angiogram; Jefferson did not have the right equipment or team. Gibbon mourned the baby for the rest of his life. But he continued with his machine.

  Later the same year, Gibbon and Alibritten were presented with another chance. In January of 1953, an eighteen-year-old freshman at Wilkes College in Wilkes-Barre, Pennsylvania, Cecelia Bavolek, came into the hospital complaining of shortness of breath and an irregular heartbeat. She was (wrongly) diagnosed with rheumatic heart disease (secondary to a streptococcal infection) and asked to return in two months for a checkup. She reappeared in the hospital on March 29 and her symptoms were much worse—fever; chills; an enlarged, murmuring heart. Forssmann’s cardiac-catheterization approach was used to examine her heart, and she was found to have an atrial-septal defect, the same sort of heart problem that the baby had been thought to have, the same hole in the heart. Every time her heart pumped oxygenated blood from her left atrium to her left ventricle, a large volume of that blood went through a hole in the septum, the wall separating the two atria, and back into the right atrium. Gibbon scheduled her for surgery on May 6, 1953. He was surer this time of the diagnosis. He and Alibritten readied their machine for the surgery, priming it with donor blood. Anxious about the surgery, Alibritten had been unable to sleep the night prior. Then the hour came: they wheeled Cecelia next to the heart-lung machine and opened her chest. Cecelia’s veins and arteries were connected to the pipes of the machine; its oxygenator began working. Everything proceeded more or less according to plan. But the defects in her heart were more severe than Gibbon had thought they would be: the hole was the size of a half-dollar. What he’d imagined would be a six-minute surgery lasted ten minutes, and then fifteen. More time passed. Gibbon began to doubt himself, and then, what was worse, a technical problem arose. The heart-lung machine clogged. Dr. Bernie Miller, who was assisting on the procedure (and who was by then in charge of the day-to-day activities in Gibbon’s lab), had to try to get the machine going again; it had run out of blood thinner. Miller was able to keep it going, partially manually, while Gibbon continued to work. Things were desperate. At twenty minutes, they were fourteen minutes beyond the moment when death would have occurred without a heart-lung machine. His hands fumbled to sew shut the giant hole he had found. Twenty-two minutes. He looked at her face. It still seemed flush with blood. Twenty-four minutes. He stitched madly. The nurses looked on; their faces blanched. Twenty-five minutes. Twenty-five and a half minutes. Was Cecelia’s face becoming slightly paler? Twenty-six minutes. Gibbon was done. He quickly took her off the machine, and her heart… restarted! It restarted, as did her lungs. She breathed in deeply and recovered well over the next weeks before going on to a long, successful life.12 Time magazine proclaimed that Gibbon had “made the dream a reality.” James Le Fanu described the heart-lung machine as “among the boldest and most successful feats of man’s mind.”13 Cecelia would live to the age of sixty-six; the heart-lung machine would live even longer. In ever more novel forms, it would live forever.

  Model II of Jack Gibbon’s lifesaving but enormous heart-lung machine, the ancestor of the tiny heart-lung machines found in every hospital today. (Courtesy of the Thomas Jefferson University Archives and Special Collections, Scott Memorial Library, Philadelphia)

  Gibbon himself had relatively modest hopes for how the machine would be used. As he said to a Time magazine reporter after the successful surgery on Cecelia, “The machine is not a cure-all for all heart conditions. It will probably be used chiefly on patients born with a deformed heart. It can’t help coronary artery disease… But now, for the first time, it is possible to look into the heart.”14 Gibbon was humble in his hopes and humble too in his sense of what he had accomplished. When asked by reporters to pose with Cecelia and his machine, he declined. He was, he said, camera shy.

  Jack Gibbon and Cecelia Bavolek, whose life was saved thanks to the heart-lung machine, one piece of which sits before them, humbly, in the picture. (Courtesy of the Thomas Jefferson University Archives and Special Collections, Scott Memorial Library, Philadelphia)

  Gibbon would perform two more surgeries that July using his heart-lung machine. His patients, both five-year-old girls, died. In one of the two surgeries, just as in his first, the death was attributable to a misdiagnosis. He grieved for those children deeply; their deaths, he thought, represented his failures, and he never cut into another body. He hired a trained cardiologist at the hospital and built a catheterization lab—the two together might, he thought, have saved the baby and the child who had died due to incorrect diagnoses. But he personally was finished; he never operated on the heart again. According to his friend Willem Kolff, he never even wanted to see the heart-lung machine again. He did not even prominently report the successful operation, burying it instead in a relatively obscure surgical journal. Gibbon eventually came to focus on his private practice and teaching, and then
he retired altogether, to paint. Maly, for her part, decided to go back to school to obtain her master’s degree in social work (she would later become a marriage counselor). But others picked up the device as he set it down. Gibbon’s machine allowed surgeons, for the first time, to work on a heart in which the blood had been drained away and details could be seen. They could work for tens of minutes, and with those minutes, they would try everything possible, and then a few more things.

  With a few tweaks (and the benefit of other advances in heart surgery), the heart-lung machine has gone on to allow an entire range of heart surgeries. Through those surgeries, the heart-lung machine is saving lives even as you read. Heart-lung machines are much smaller and almost foolproof, and they can be used to bypass the entire heart (as Gibbon’s did) or just the right or the left side. Since the 1960s, most major hospitals have employed perfusionists whose job it is to operate the heart-lung machines. Compared to an actual heart, these machines remain crude, and yet they are profoundly important, a symbol of the power of technology but also of the limits thereof. The device’s abilities, after all, are fleeting. The machine is useful for minutes or hours, not days or years. When a patient is on a heart-lung machine, the lungs do not receive blood, and even if the brain survives, the lungs would ultimately die, flutter and fail.15 Then, of course, when the electricity goes out, the heart-lung machine stops. Even when the electricity stays on, the heart-lung machine can break. Each machine needs tending to, constant repair. A human heart, a real heart, might last a hundred years without maintenance. Yet Gibbon and his team had replicated, however temporarily, two features of the workings of the heart, oxygenation and movement of the blood. With this, he and his team set the stage for many new surgeries that had previously been impossible. But he had also made another step, one toward the replacement, piece by piece, of the functions of the heart.16

  Gibbon’s machine was a temporary electromechanical replacement for one of the cardiovascular system’s functions, respiration. But from very early on in the story of the heart, it seemed as though a more permanent electromechanical fix might be possible; it seemed that one might be able to, at the very least, replace faulty wiring in the heart. The heart can short out in many different ways. It is not the only electrical part of the body. Every cell in the body runs on electricity, but the electricity of the heart is special. It is more intense, measurable, and consequential. It is this measurable electricity on which an electrocardiogram (or EKG) relies. Electro-derives from the Greek for “amber,” which, like electricity, was perceived to have the power to attract. Gram is from the Greek word meaning “drawing” or “writing”; think of the word telegram. An electrocardiogram represents the telegrams being sent electrically by the heart and measurable anywhere in the body. The first EKGs were performed in primitive form on dogs; the dogs were made to stand in salt water that would conduct (and, ultimately, help record) the electricity of the beating heart. With time, better conductors were developed. Now, a very simple machine can be hooked up to your skin (one electrode on each arm, one on each leg) to record your electrical rhythm. EKG monitors can even be worn on the body, a form of electric fashion. EKGs record the initiation of the contraction of the atria and then the contraction of the ventricles, a predictable hill, then a mountain (with a few small subsequent hills), then a hill again when the ventricles finish contracting. If everything goes right, this topography of the body’s electricity repeats for an entire life, billions of rises, billions of falls.17

  The electricity in the heart triggers the heart to pump in two steps. In the first step, a signal from the sinoatrial node (which sounds complicated but is just a cluster of cells on the top of the right atrium) spreads and simultaneously causes the atria to contract and signals a second node, the atrioventricular, to do the same (which causes the ventricles to contract). The resulting contraction of the heart is like the contraction of a snake swallowing its prey: the muscle fibers encircling each chamber of the heart shorten during contraction and squeeze the blood. The sinoatrial node discharges its signal one hundred times per minute, and so, in order to maintain the slower resting heartbeat characteristic of most human hearts, the nervous system must constantly send signals to slow the heart. When something exciting or dangerous happens, the nervous system just has to take its foot off the brake to get up to a hundred beats per minute (speeding up even more takes more active control).

  Each step in this signaling can go wrong. Every day people come into hospitals, have EKGs done, and learn that, indeed, something has gone wrong. Usually, they have a sense of a problem in advance, but not always. The heart can lose its rhythm when its atria, those top chambers of the heart, temporarily lose their beat. Most of us have felt this, especially, common wisdom holds, when having consumed a bit too much coffee. With too much coffee, the atria beat too soon. In doing so, they contract before they have filled and push too little blood into the ventricle.18 In your chest, this feels like no beat has happened at all. Then, on the next beat, the ventricles are filled with too much blood. You feel this second beat more strongly than normal. The overall effect is “no beat,” “too much beat.” A related problem occurs when the ventricles contract too soon, before they receive the signal from the sinoatrial node, producing a similar effect: too little blood, then too much. These minor arrhythmias, referred to as ectopy, can be terrifying. Fortunately, they are harmless.

  Another form of arrhythmia, atrial fibrillation, occurs in about one in twenty adults over sixty-five. With atrial fibrillation, the atria contract erratically and asynchronously. The muscle fibers in the atria are no longer under the control of the sinoatrial node and contract on their own, like a bag of uncoordinated worms. Without coordinated contraction, blood pools in the recesses in the atria and can clot; these clots can travel to the brain. In addition, because the signals from the sinoatrial node arrive at the atrioventricular node irregularly, the contractions of the ventricles, and hence the pulse, become irregular, sometimes rapid (with associated fatigue, palpitations, or even heart failure), and sometimes slow. The symptoms of atrial fibrillation can be as idiosyncratic as the contraction of the worms of the atria. Atrial fibrillation can happen as a result of aging, due to viral infection, or, most often, for reasons no one understands.19 In most cases, atrial fibrillation is treated by primitive medicine. The heart is shocked to stop it.20 When the heart restarts, the hope is that the rhythm will return to normal (no one understands why; this is just medicine’s version of rebooting the computer). If this does not fix the problem, part of the heart can be scarred—ablated—with the intent of preventing extra signals from causing one or another area of the heart to misfire.

  Just as the atria can become asynchronous, so too can the ventricles. But when the ventricles beat out of rhythm in ventricular fibrillation, the resulting problems are life-threatening. Even if the atria are firing poorly, a fair amount of blood drops down into the ventricles. But if the ventricles are misfiring, the whole heart spasms and fights against itself.21 With ventricular fibrillation, even slow pumping is not possible. Without the pump of the ventricles, no blood gets to the brain, and without intervention, death is certain.22 The first step in dealing with ventricular fibrillation is to shock the heart so as to stop the chaos; then, with the heart hopefully rebooted, the details of the problems can be considered.

  In short, the heart’s rhythm can flounder in several ways. Its beat is not easy for the body to keep. I describe this complexity because when surgeons started to contemplate the idea of an artificial pacemaker, the number of ways the natural pace of the heart could go wrong was not fully understood. What was understood was that the heart was electrical, and so, with this simple electricity as context, surgeons around the world began, on the eve of Gibbon’s success with the heart-lung machine, to attempt to create an artificial pacer, a pacemaker. The idea was simple: replace the aberrant natural stimulation of the heart with a more regular, artificial one; this was a solution with, it seemed, the potential to reso
lve many of the ways in which the electricity of the heart could go wrong. It was a simple fix for a diversity of electrical dilemmas.

  One of the men who most eagerly took on this challenge was Wilson Greatbatch. Greatbatch was a tinkerer and an inventor and, at least for a time, a professor of electrical engineering at the University of Buffalo in New York. He was no surgeon. He had not even thought very much about the heart until, in 1956, he made a mistake. The same year that Gibbon’s heart-lung machine began to be used at hospitals outside Jefferson College, Greatbatch was trying to build a device to record heart sounds for the Chronic Disease Research Institute. As he worked, he reached for a resistor to complete the circuits of the device. Absentmindedly, he installed a circuit of the wrong size, which caused his device to give off intermittent electrical pulses. It was a silly mistake, but rather than just rebuilding the device, Greatbatch paused. He was, he thought, onto something. He suddenly remembered conversations he had had in 1951, while an undergraduate in an animal-behavior lab at Cornell University, conversations in which researchers talked about the heart’s electrical activity and heart block. Maybe, just maybe, his artificial pulse would be enough to trigger the heart to beat. It could do so at any pace one might choose. It could remedy, at least temporarily, the various ways in which the heart’s beat could go awry.

  By the time Greatbatch made his mistake and grabbed the wrong resistor, doctors and researchers had been shocking hearts for two decades. In the 1930s, Albert Hyman developed a technique to quantify the electricity coming from the heart, and he measured it, accurately, at about one-thousandth of one volt. Hyman reasoned that, in a patient whose heart had stopped, a similar shock might resuscitate it. In this procedure, Hyman shoved a hollow gold-plated needle through a patient’s ribs into the right atrium of the heart. He then started his generator. In this way, Hyman saved many patients whose hearts had stopped. He also inspired a variety of tinkerers preceding Greatbatch to contemplate more sophisticated electrical treatments for the heart, perhaps even a long-term artificial pacemaker. If one could jump-start a heart, one might also be able to keep it running.