EDDY BUCZYNSKI

In 1975, as a newly minted cardiologist fresh from Harvard's Peter Bent Brigham Hospital, I started into private solo practice in Worcester, Massachusetts. From my small office on the fourth floor of a relatively new medical office building, I could look directly across busy Belmont Street, Route 9, to the Memorial Hospital emergency department. As part of my staff appointment at Memorial, I was the director of the new coronary care unit. If I walked briskly, and traffic was not too heavy, I could make the journey from the office to the emergency room in roughly two and a half minutes, depending on the traffic coming down the hill. I consulted on a lot of patients with new onset or rapidly worsening (acute) heart failure for the ER team.

Heart failure (HF) is not a specific disease. HF is what medical doctors call a syndrome, a collection of various patient complaints (symptoms), evidence on physical examination (signs), and laboratory abnormalities (on blood tests, electrocardiogram, and imaging studies) that cluster together. The HF syndrome includes a broad spectrum of clinical problems that plague individuals who have impaired heart function. The heart is a pump; its mechanical functions are limited to filling and emptying. Nonetheless, a long list of specific diseases can cause impairment of either its filling, its emptying, or both. If and when the consequences of that reduced cardiac function come to dominate a patient's life, then he or she has the heart failure syndrome.

The 1970s and 1980s saw great progress in heart failure research. Laboratory and then clinical data established compelling evidence that the same physiological responses that are activated to retain salt and water under a variety of circumstances like dehydration, gastrointestinal fluid loss (vomiting or diarrhea), or bleeding are also highly activated in heart failure. Collectively, those responses are known as the renin-angiotensin-aldosterone system (RAAS). This occurs because the heart is not adequately filled or emptied, and the systemic arterial circulation is underfilled. The relative underfilling that occurs with heart failure stimulates the same RAAS responses that depletion of the circulating blood volume from dehydration or bleeding does. Think of it this way: it's as if you set your home thermostat on the living room wall to a comfortable seventy degrees. Then, when the house temperature was steady at seventy degrees, you take the thermostat off the wall and put it in the refrigerator (without cutting the wires!). Now the relocated thermostat gets a totally inappropriate input because it's cold in the fridge and will fire up the furnace to make the house hotter and hotter. The problem is identical with heart failure; the RAAS is inappropriately activated, like the thermostat in the refrigerator. Patients crave salt and water, and they retain both avidly, like the house getting hotter and hotter. Eventually, the patients become congested. They can't breathe comfortably because of congested lungs, and they gain weight from fluid retention in swollen (edematous) legs and ankles. In clinical trials, drugs that blocking the RAAS response (cutting the thermostat wires) produced important improvements in survival for long-term (chronic) heart failure patients.

On the other hand, acute heart failure remained a serious problem. A heart failure patient's clinical history is usually a variation on a theme, but every heart failure patient has his or her own individual story with memorable unique details. There is some underlying heart disease — high blood pressure or a previous heart attack. There's a week or two of feeling thirsty and not sleeping well, often in conjunction with some unusual personal stress — maybe a death in the family or a divorce. At first, the patient can't lie flat. He props himself up on two or three extra pillows, or he takes to sleeping in a chair or trying to catnap while sitting at the kitchen table. Then comes a particularly difficult night, the onset of acute heart failure. The patient wakes up short of breath, coughing. Some make it through the night and come to the emergency room in the morning. Some struggle on through the morning and try to take a nap after lunch only to realize that the symptoms are still there. Others don't come in until they get frightened when their sputum turns frothy and pink.

Eddy Buczynski's story was typical; it was also deeply personal for me. Eddy was the all-round manager of the building where I had my new office. He was a wonderful guy. Early on winter mornings, wrapped in his knit scarf, he made sure the plowing service cleared the parking lot, and then he opened a can of cat food for the neighborhood stray and let him chow down in the warm stairwell. He gave the older patients, particularly the ladies, a hand up the three short steps into the building. In the summer, he picked up any refuse that blew over from the convenience store across the street.

"Hi, Doc. You want the place to look professional, right?" he would say, smiling.

Eddy was five foot nine and about 225 pounds, balding, in his early sixties, with adult-onset diabetes and bad high blood pressure. After I had been there a few months, he showed up as a patient. His incredible affection for stuffed cabbage and kielbasa challenged his motivation, but we worked at keeping his problems under control.

Then, the following winter, Eddy's wife got sick. Very sick. After several years in remission, her breast cancer had returned with a vengeance. She was clearly going to die. Eddy paid no attention to himself or to taking his own medications; his life was limited to taking care of the building and taking care of his wife. After a few weeks of this, on a Monday morning, he stopped me on my way into the office, saying, "Doc, I gotta see ya today!"

We rode up together on the elevator. His shoes were untied, and he was sweaty. Sitting on the exam table, his blood pressure was high again, and he was short of breath. When he took a deep breath, I could hear crackles and wheezes at the bases of both lungs. His jugular veins were distended, and his ankles were swollen.

The acute heart failure patient literally starts to drown in his or her own bodily fluids. The heart's left ventricle can no longer support the circulation...