“Can’t we get that [intravenous] fluid to run any faster?” I asked.
RUTH ANN, MY HOUSEMATE AND FELLOW SECOND-YEAR FAMILY PRACTICE RESIDENT, HAD TOLD ME VIRGINIA WASN’T DOING WELL WHEN SHE SIGNED OUT TO ME THAT AFTERNOON IN 1990. THAT EVENING, I GOT THE CALL FROM THE THIRD-FLOOR CHARGE NURSE AT THE HOSPITAL; VIRGINIA WAS SHORT OF BREATH.
I had just finished changing from my work clothes of the day into blue surgical scrubs (with the pants always too short for my 44-inch-inseam legs) and running shoes, which I would wear until the morning. After three years of getting accustomed to working through the night, the first two as a medical student at UC San Diego and now at the Maine Dartmouth Family Practice Residency Program, I still hated it.
When I arrived at Virginia’s bedside a minute later, a respiratory therapist and nurse were already there; the therapist was giving her supplemental oxygen. Virginia, about 70 years old, thin, deeply wrinkled, pale, and tired from years of working harder than the rest of us to breathe, was using the accessory muscles in her neck and chest to help her get more air, just as a distance runner would.
Many people who smoke for years end up like her, with most of the airways and lungs permanently destroyed or clogged with mucus and a weak heart that often fails to keep up with the body’s demand for blood, causing fluid to back up into the lungs. Tonight, her heart was failing.
We were already giving her medicines to help her heart do its job. Lasix, a diuretic, reduces the work of the heart by diminishing the amount of blood it has to pump. Captopril decreases the resistance of the arteries into which the heart forces blood, simplifying the task of pushing blood forward. Digoxin increases the contractility of the cardiac muscle fibers, strengthening each heart contraction. Nitrates increase the flow of blood to the heart and diminish arterial resistance.
This night, Virginia needed more. She had been through this routine many times in the past and had made it clear she did not wish to return to the critical care unit, where she would have to go if we gave her intravenous “pressors,” which would further improve the contractility of her heart.
While I pondered this problem, Terry, the emergency room doctor, paged me. I called the ER.
“Hi, Jim. Gloria N.” — one of my fellow resident’s 52-year-old diabetic patient — “just arrived complaining of chest pain for two hours, and she has six to ten millimeter ST elevations in her inferior (EKG) leads." This meant she was having a heart attack. A blood clot was obstructing the circulation to the lower (inferior) wall of her heart. The inferior wall muscle was therefore dying. The remedy for this situation was and is intravenous tissue plasminogen activator (TPA), which dissolves the clot, restores the blood flow to the dying heart muscle, and therefore minimizes the heart attack (the amount of heart muscle that dies). I knew they could not wait for me to finish with Virginia to start the treatment, so I asked Terry to start the infusion and do me the favor of calling the cardiologist to come in. Usually, the resident on call is supposed to do everything, but Terry liked me and did as I requested.
I turned my attention back to Virginia. After thinking it over for a few moments, I arrived at an old-fashioned and now unconventional solution to the problem. I ordered an intravenous infusion of aminophylline, which in the body is metabolized into theophylline, a medication more often used to relax the bronchial smooth muscles of patients having asthma attacks, but which in this instance I would use to aid Virginia’s weakening heart muscle. She could receive this medicine on the medical floor, so she would not need to transfer to a critical care unit.
Virginia’s lungs needed help too. Her blood oxygen levels were going down as a result of the fluid in her lungs, a situation that additional supplemental oxygen can fix in most people. For those with smoke-damaged lungs, too much supplemental oxygen diminishes respiratory drive, which causes them to retain carbon dioxide. Carbon dioxide in high concentrations is a potent central nervous system depressant. We needed to improve her ventilation to prevent carbon dioxide retention. While the nurse started the aminophylline infusion, we decided to give Virginia intermittent positive pressure breathing (IPPB) until the theophylline (and some additional Lasix) took effect. We administer IPPB through a mask, which pushes air into the patient’s trachea and small airways to keep the airways open longer, facilitating the exchange of carbon dioxide for oxygen.
One hour later, Virginia had completed the transformation from dying to stable medical condition, so I left her bedside to see patients waiting for me in the emergency room. We residents took “call" every three to six nights, depending on which of three “services" we were covering. Family practice — which required covering outside phone calls, patients in the hospital, obstetrical patients, and emergency room visitors from our entire group practice — was the most demanding.
I finished in the ER about midnight, so I went upstairs to the Coronary Care Unit (CCU), where they were just bunging in Gloria N., who had suffered the heart attack and received her TPA. As Lola, the CCU charge nurse, wheeled Gloria’s gurney into the unit, I heard her command, “Cough, Gloria!” The color in Gloria’s face matched the off-white tones of the sheets covering her round, short body, so I knew she wasn’t obeying instructions. “This is a code,” Lola announced matter-of-factly to me and the rest of the CCU.
Code Blue, or Code 99, means cardiac arrest. The American Heart Association has devised protocols for the treatment of cardiac arrest based on the underlying electrical rhythm of the heart at the time. Those of us who carry certification in Advanced Cardiac Life Support (ACLS) have to demonstrate our knowledge of these protocols and other skills to gain certification.
The “crash cart" with the defibrillator, medications, and other essential equipment used during codes arrived within 30 seconds, along with the nurse manager, a phlebotomist, and several others whose jobs I didn’t know. Terry raced up from the ER to take charge. Residents did not run codes unless there weren’t any other ACLS certified personnel in the building. So we had about eight people surrounding Gloria in her cozy private CCU room, with the heart monitor shining its nearly flat line above us.
Terry dutifully followed the protocol for ventricular fibrillation, for which the most important treatment is electricity. Gloria’s heart teased us: on multiple occasions it responded to shocks by resuming a normal rhythm, only to gradually speed up to 120, then 140, and finally reenter ventricular fibrillation, in which the heart only quivers and does not contract in any organized way. Each time we shocked her, her body would jump violently, and she would blurt out "What's happening to me?” or just “Aaah!"
Codes cause great stress for everyone involved: codes try to restore life to someone who is dead and statistically has little chance to come back. In some academic institutions, strict rules prevail about who can give orders during a code. Larry, one of our surgical attending physicians in Waterville, Maine, was a former emergency room physician who had taught ACLS for many years before he decided to change careers and go back to do a surgical residency. During the first year of his residency, he was present at a code that an inexperienced internal medicine resident was running. The patient was dying, and Larry noted that the resident was neglecting to treat an underlying medical problem, which ensured that the patient would not recover. Larry spoke up, to which a supervising resident responded, “What are you?” conveying that Larry did not have the right to say anything during a code. Larry countered, “Anytime someone’s life is in danger, stress levels run high. You have to be willing to listen to helpful suggestions.” The comment later earned him a firm personal reprimand from the Chief of Surgery, who told him he had to be willing to watch people die so that residents could learn.
That attitude did not prevail at our hospital. I made note of the pattern and situation and made the diagnosis that saved Gloria’s life. “Can’t we get that [intravenous] fluid to run any faster?” I asked.
The heart has two pumps: the left and right ventricles. The right ventricle sends blood to the lungs, where the red blood cells exchange carbon dioxide for oxygen before the blood returns to the left atrium of the heart. From there, the blood goes to the left ventricle, which sends it to the rest of the body. In most people, the right coronary artery provides the circulation to the lower and back walls of the heart. The back wall of the heart is the free wall of the right ventricle. A heart attack involving the inferior wall can extend to the back wall, causing the back wall to stop functioning. This inactivates the right ventricle, which means the left heart doesn’t receive any blood to pump. The only way to get blood to the left side of the heart is to overload the veins so that blood spills forward through the lungs to get there. Sometimes this can require as much as two gallons of fluid.
Lola, who had the demeanor of a drill sergeant and did not respect residents but knew a good idea when she heard it, paused for a moment. Deciding to act on my suggestion, she left the bedside, found an inflatable cuff to wrap around the IV bag, and inflated the cuff, causing the fluid to rush into Gloria’s circulation. With each successive shock, Gloria’s recovery lasted a little longer, until after her 12th shock, her heart rate rose gradually, degenerating again into ventricular fibrillation. As her “tank” filled with fluid, her heart rate slowed down and stabilized.
During all of this, the elderly woman in the next room was dropping her heart rate 60s.. .50s.. .40s. less than three minutes after we finished with Gloria, the woman arrested. I wondered if all the women in the hospital with heart disease had held a meeting that afternoon and decided to die on my watch.
This code ended quickly. A couple of doses of atropine (which blocks a specific neurotransmitter receptor and thereby prevents the vagus nerve from slowing the heart rate) resulted in a restoration of her normal heart rhythm. I don’t know what happened to her after that, but I’m sure she ended up with a pacemaker to prevent another similar episode.
Virginia and Gloria didn’t get into any more trouble that night. After I finished my paperwork, I received no phone calls nor pages from the ER, so I sneaked into our tiny on-call room with its bare white walls and small hospital bed, slid under the faded maroon blankets, and slept for three hours before beginning another full day’s work.
When I wandered into the CCU the next morning with my usual post-call nausea and headache, Gloria was sitting up in bed talking to Brenda, my favorite CCU nurse. Both were all smiles, and Brenda was saying, “God must have been watching over you last night.”
“He’s always watching over me,” Gloria replied.
“But last night He must have been using binoculars!”
Firmly agnostic, I didn’t join the conversation but admired how well Gloria looked. From that day forward she quit smoking, adhered strictly to her diabetic diet, exercised daily, and in the next few months lost 25 pounds. Her weight loss fixed her diabetes. I drove by her house every day on the way home from the hospital, and I often saw her sitting on her front porch with her neighbors or children, healthier than she’d been before her heart attack. And I felt responsible.
As a family practitioner, I rarely get the opportunity to see such a dramatic example of someone who is alive and walking because I was there. Every time I saw her, I would hear the words of Karen, my supervising attending physician that night. After arriving in the CCU, reviewing the situation, and hearing the ER physician say, “I wonder which of the medicines finally cured her?” Karen answered, “It was the fluid."