The Heart Healers (28 page)

As we compared their success to our failure, we discovered that we had ignored three huge practical limitations. Patients with acute myocardial infarction were scattered throughout the hospital so the resuscitation team was often starting CPR minutes, not seconds, after sudden death. More delay was caused by the lack of available devices at the site of the cardiac arrest to support advanced CPR. Macabre cynics suggested that if you want a defibrillator to save you, go stand beside it as you conk out. Finally few doctors or nurses were trained in the fundamentals of CPR. Our programs bore the universal hallmarks of failed enterprises: too disorganized, too little, and too late.

Londoner Dr. Desmond Julian’s frustration boiled over into print:

Many cases of cardiac arrest associated with acute myocardial ischemia could be treated successfully if all medical, nursing and auxiliary staff were trained in closed chest cardiac massage and if the cardiac rhythm of patients with acute myocardial infarction were monitored by an electrocardiogram linked to an alarm (sounded and recorded) at the onset of an important rhythm change … The appropriate apparatus would not be prohibitively expensive if these patients were admitted to special intensive care units. Such units should be staffed by suitably experienced people throughout 24 hours.

We had the tools, but we did not have the system. This was not a problem requiring a flash of intuition. It was a problem of organization. We needed a Henry Ford to come in and set things straight. Henry Ford’s revolutionary outside-of-the-box idea had been to bring his cars to the workers rather than workers to cars. Desmond Julian was proposing to do the same for heart attack victims.

Two years later, like the goddess Athena emerging from the forehead of her father Zeus, Julian’s imagined unit suddenly burst forth full grown from the convergence of four separate streams: defibrillators, pacemakers, new TV monitors, and CPR. In the United States, a single determined individual in a small private hospital in Kansas City acquired a grant from the Hartford Foundation to create a coronary care area, then cajoled his hospital’s administrators to dedicate the space for the first functioning CCU with a mobile crash cart with emergency supplies and drugs, a defibrillator, and an external pacemaker. An unthinkable preposterous idea, that sudden death due to heart attack could be a routinely treatable condition, was slouching toward Kansas City to be born.

Dr. Hughes Day opened the first CCU in small private 200-bed Bethany Hospital. The unit consisted of four private rooms adjacent to a seven-bed intensive care unit. At almost the same time as Day established his CCU in Kansas City, Londoner Desmond Julian, thoroughly frustrated in his attempt to establish a unit in England, moved to Australia to establish a CCU there. Within a few years Dr. Bernard Lown at the Peter Bent Brigham Hospital in Boston, Massachusetts, initiated a critical shift in emphasis, from resuscitation after cardiac arrest to monitoring for precursors of cardiac arrest. Other centers around the country began to report huge declines in the heart attack mortality rate after the opening of their CCU.

Nonetheless our greatest advance in treatment of heart attacks was met with the naysaying establishment’s holier-than-thou hostility, just like the days when the establishment condemned the innovators of cardiac surgery. Julian’s first report of his CCU experience was briskly dismissed by the prestigious
British Medical Journal
with just the right whiff of Anglican condescension, saying it was “irresponsible to suggest that all patients with myocardial infarction should be admitted to wards in which they could receive intensive care.” Harvard professors Bloom and Peterson complained that randomized trials were needed to prove the efficacy of CCUs. But to those of us on the firing line, we had ample, firsthand experience that CCUs saved lives, and you don’t need a randomized trial to know if a parachute works.

With resuscitation becoming routine in every town across the nation, Woody Allen could offer a twist on our miraculous new capability, saying, “I don’t want to achieve immortality through my work. I want to achieve it through not dying.”

We finally had our first major breakthrough in the treatment of the nation’s number one killer. But as we reduced death from electrical complications in the CCU, a new problem emerged. Many of my patients that we saved from the electrical complications of heart attack survived with such extensive damage to the heart muscle that they died of heart failure. We now needed a way to assess and treat heart failure at the bedside.

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IN THE MAYO
Clinic cath lab, my mentor Jeremy Swan had been an expert in measuring cardiac function. We can quantify the function of the heart using two measurements. We measure the volume of blood the heart ejects in a minute, called cardiac output. Cardiac output tells us how well the heart is doing in supplying oxygen to vital organs. Our second measurement is pulmonary capillary pressure, which tells us the effect of heart failure on the lungs. When this pressure rises, it causes lung congestion and shortness of breath. In a failing heart, cardiac output falls and the pulmonary capillary pressure rises. Jeremy wanted to make these two measurements at the bedside of heart attack patients so that we could continuously assess the effect of our treatment of heart failure.

Jeremy knew that he could use X-ray imaging to help him insert a catheter into an arm vein, advance it to the right atrium, cross the tricuspid valve into the right ventricle, cross the pulmonary valve into the pulmonary artery, and then push it out to its capillaries. Although it sounds complex, a first-year cardiology fellow learns the procedure easily if the catheter is visible on an X-ray monitor. In the CCU, however, there was no X-ray system to illuminate the path through this cardiac catacomb, and catheters pushed blindly simply coiled up sleepily in the right atrium. Maneuvering a catheter into the pulmonary artery was an impossible, insoluble problem.

One weekend, pondering this dilemma as he sat on Santa Monica beach watching sailboats, Jeremy had a fit of Irish intuition. He wondered if a catheter equipped with a tiny sail could bob along in the current of blood flowing from the right heart out into the pulmonary artery. Why not? He knew he could pass the catheter into the right atrium. Then if he could unfurl the sail, it would be like those sailboats … the sail would capture the force of the blood, and flow like a Mary Poppins umbrella out into the pulmonary artery.

As a consultant to Edwards Laboratories, he took his idea to their engineering group. The engineers took no time to agree: constructing a catheter with wires and sails was virtually impossible. But as the discussion wandered, someone made a second intuitive leap: maybe the same result could be accomplished with a balloon. “Balloons will float, used to do it when I was a kid,” one of the engineers said.

Edwards Laboratories knew exactly how to put balloons on catheters. They were inflating balloons on the ends of catheters to keep them from pulling out of the urinary bladder, and to drag clots out of blood vessels. Jeremy Swan’s intuition, put into highly improbable juxtaposition with a completely unrelated technology, had created an entirely new idea.

Edwards Laboratories Director of New Product Development David Chonette got some infant feeding tubes, affixed an inflatable balloon to the shaft, and delivered it to newly arrived Czechoslovakian immigrant Dr. Willie Ganz in the cardiovascular animal laboratory research laboratory. On his first try the catheter shot instantly into the pulmonary artery, carried by the force of blood flow behind the inflated balloon. In a few seconds that afternoon, Jeremy’s vision had morphed from laughable fantasy into feasible possibility.

When I arrived from Boston, our first-year cardiology fellow and I decided to try it in our Myocardial Infarction Research Unit. We chose Samuel Bernstein, a comatose eighty-year-old man in shock following a heart attack, who we felt would not survive the day.

In those days there was no institutional review board to approve our testing of the new catheter. Like Lillehei with Bakken’s improvised pacemaker, we just walked up to his bedside and did it. When my fellow and I advanced the catheter into Mr. Bernstein’s right ventricle, his heart reacted with intense fury, ventricular tachycardia (literally, very rapid beating of the ventricles). In a sick heart, ventricular tachycardia often degenerates into ventricular fibrillation, the rhythm of sudden death. Terrified, I imagined that my decision to test the new device might cause our patient’s sudden death. After what seemed an interminable period—I am guessing maybe fifteen seconds—his heart reverted back to normal rhythm. Mr. Bernstein passed away from his disease late that evening, never aware of the brief, ultimately inconsequential episode at his bedside.

My decision to use the catheter more than forty years ago, however, still haunts me. In the guise of advancing science and our understanding of managing heart failure at the bedside, I had put a patient at immediate, life-threatening risk. That afternoon, like Dwight Harken, I went home, got into bed, and cried. In those fifteen seconds of panic, I had experienced an epiphany. Yes, by the ethical standards of that era I had done nothing wrong. Yes, my patient was near inevitable death, and suffered no adverse consequence. Yes, I had noble intent. And yet, should I really have sole authority over whether or not to use an untested device in my research? Should not a group of peers independently assess risk vs. benefit in advance, and as my research proceeded? Worse, my patient had not participated in the decision to use the new device; he had not given his consent. My experience illuminated the terrible flaws in the professional ethic of that era. My personal penance has been to serve on our Institutional Review Board since its inception, the obligation of those who dedicate their career to clinical research.

I went back to the animal laboratory. I wanted to use a continuous X-ray to see what happened when the catheter entered the right ventricle. What I saw amazed me. The balloon was mounted about an inch or more from the catheter tip. When I inflated the balloon, the segment beyond the balloon began to thrash about in the flowing blood just like a balloon in a wind tunnel, whacking away at the heart’s inner surface. Each impact of the catheter tip on the heart’s inner surface induced an extra beat. In a sick heart, one of those extra beats would induce the ventricular tachycardia, the common predecessor of ventricular fibrillation and sudden death. So we asked the Edwards Laboratories’ engineers to move the balloon all the way out to very tip of the catheter. Now when we inflated the balloon it actually bulged around the tip. The bulging balloon was a perfect soft cushion, a pillow, which hid the catheter’s rigid tip and eliminated ventricular arrhythmias.

That little technical tweak turned out to be a huge breakthrough in bedside management of acute heart failure. We found that we could measure the severity of lung congestion, and we could also assess the effect of our cardiac drugs on the congestion. We discovered that our measurement was far more sensitive than either our stethoscopes or the chest X-ray, which often did not reflect the benefit of our therapy until the following day. Equally important, nurses could make the continuous measurements in our absence, and immediately notify us of important changes.

Now we desperately wanted that second measurement: cardiac output. The solution to our problem emerged from Communist Czechoslovakia. In Prague, at about the same time that Jeremy was sitting on Santa Monica beach, cardiac physiologist Dr. Willie Ganz was pondering how to escape. He had a lot of experience in survival, first as a youth in the World War II Budapest underground and later as a survivor of incarceration in a Nazi labor camp. In 1966 at age forty-seven, Willie, his wife, and their two small sons made a daring escape across the Austrian border, finally wending their way to the Jewish community of Los Angeles. Willie brought with him no worldly goods, but he did have one possession of inestimable value: he had developed a method of measuring cardiac output.

Incorporating Willie’s method into a catheter presented huge technical problems, but after two years of alternating exhilaration and frustration, I could measure cardiac output in critically ill patients. I found that my patients’ prognosis depended on these two measurements. When both were normal, the mortality rate was 1% whereas when both were abnormal 60% died. When only one of the two was abnormal, the mortality rate was 10% and 20% respectively. Four years later, after treating hundreds of patients in our Myocardial Infarction Research Unit, I was able to describe the effects of all the then-available therapies for disordered cardiac function. My mentees and I had created a solid basis for treating heart failure in acute myocardial infarction, which I described in
The New England Journal of Medicine
. The method, dubbed the Forrester classification, revolutionized critical care medicine.

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ALEXI KROON’S HEART
muscle was failing to deliver sufficient output to maintain the function of his vital organs. His heart was failing. In its most severe form, when the heart cannot even maintain a normal blood pressure, the condition is called cardiogenic (literally, heart-caused) shock. When a sudden obstruction of a coronary artery causes cardiogenic shock, the mortality rate skyrockets. I was looking at a young man with no prior symptoms who was dying of heart failure before our eyes. We needed a way to continuously monitor his heart muscle function as we used both drugs and a mechanical pump to supplement his cardiac output.

As Alexi moved in and out of consciousness we passed the balloon catheter into his heart. His cardiac output, the volume of blood the heart pumps out in a minute, had fallen to less than half normal. His pulmonary capillary pressure, the pressure in the small blood vessels of the lungs, was elevated into the range that causes severe pulmonary congestion. With about 30% of his heart muscle damaged, his brain compromised by diminished blood flow, Alexi was dying in front of us. Without effective treatment his chance of dying within the hospital was 80%. But unlike my days in Philadelphia, this time I was not helpless.