The Hearty Fisherman

By Tony Dajer|Wednesday, July 01, 1992
RELATED TAGS: HEART DISEASE
There she goes, Doc. Eddie’s bluff, ebullient expression turned suddenly attentive, as if straining to hear distant, ominous hoofbeats.

It’s right there, he said, pointing delicately to a spot on his burly chest. His breathing sped up as he talked. That’s what it feels like at night.

I slipped my stethoscope under his finger. Only minutes earlier that afternoon, his heart rate had been a reasonable, if irregular, 85 beats per minute. Now it was 130, beating a tattoo as erratic as raindrops on a zinc roof. The racing heartbeat and shortness of breath that had plagued Eddie’s sleeping hours off and on for the past three months were making a special daytime appearance, as if to taunt the doctors who had tried to suppress them.

I’d met Eddie shortly after I’d begun working at a small-town clinic in upstate New York. He was a 58-year-old heavy-equipment operator by trade, and a year-round fisherman by conviction. When we shook hands, mine could barely enclose his. We never got down to business until he had told me his latest off-color joke.

Some time before I started working at the clinic, he’d developed a cough he couldn’t shake. A previous doctor there, noting Eddie was a pack-a-day smoker, had diagnosed bronchitis and prescribed antibiotics. But the cough worsened, and Eddie started feeling short of breath. A follow-up chest X-ray showed fluid in the lungs and an abnormally large heart, both signs of congestive heart failure.

Eddie’s condition had its roots in a heart attack he’d suffered ten years earlier that had scarred the tissue of his heart and caused it to work less efficiently. The problem was his heart’s left ventricle, the large chamber that receives oxygen-laden blood from the lungs and pumps it back out to the rest of the body. Because it had lost some of its squeezing power, it tended to accumulate a backlog of blood. To accommodate the higher blood volume, the ventricle had stretched. Even so, the extra blood sometimes backed up in the pipeline, engorging the vessels connecting the heart to the lungs, flooding the tiny air sacs in the lung tissue, and blocking oxygen absorption. Eddie had summed all this up as something’s cutting my wind.

At first his electrocardiogram had shown a regular heart rhythm with a few abnormal beats--nothing to write home about. His original doctor started him on a diuretic and a blood-pressure reducer, both standard therapy for congestive failure. But while Eddie improved a bit with these drugs, he still woke up at night gasping for breath. When his doctor subsequently picked up more irregular heartbeats, he asked Eddie to wear a Holter monitor, which is essentially a portable, 24-hour EKG. Two days later the results were in: atrial fibrillation, a type of heart rhythm disorder, or arrhythmia. That’s when Eddie was referred to me.

Atrial fibrillation--A-Fib in the jargon of the hospital--is nature’s way of telling us we really have four hearts, not one, and that they are connected not only hydraulically but electrically. The two larger heart chambers, called ventricles, do the heavy-duty work: the right ventricle receives deoxygenated blood from the veins, then pumps it through the lungs to the left ventricle, which squirts it out to the rest of the body. The two atria (each about one and a half inches in diameter) are the ventricles’ antechambers; they boost sluggish venous blood into the ventricles like fuel injectors.

More crucially, the right atrium contains a cluster of pacemaker cells that control the rate at which the heart beats by firing an electric signal 60 to 100 times a minute. The signal, I explained to Eddie, spreads through both atria like a ripple in a pond. It then hits the atrioventricular (AV) node, an electrical gateway between atria and ventricles that relays the signal in an orderly way into the larger lakes of the ventricles. When all goes well, the heart beats more smoothly and forcefully than any machine ever invented.

When I first went over this with Eddie, it was clear what kind of lake he was interested in. Are you a fisherman, Doc? he asked.

Only done it once, I apologized.

His eyes gleamed like a preacher in pursuit of converts. Oh, the steelhead are really biting now, Doc. We’ll get you out on the lake. You’ll have a freezerful of trout in no time--why, I had to give away a dozen just this past weekend.

If a normal heartbeat is like a ripple spreading evenly across a pond’s surface, then atrial fibrillation is what happens when a dozen splashing children jump in. The atria quiver rather than contract, and electrical impulses strike the AV node dangerously fast--up to 300 times a minute. Like any good gatekeeper, the AV node tries to let only one impulse through in a given fraction of a second (good thing, too: if the ventricles fibrillate, the result is sudden death), but it can’t completely dampen the speed or randomness of the signals. The result is a heartbeat that’s way too rapid and out of sync.

I drew Eddie a picture to show him what all this meant. See, when the left ventricle beats too fast, it doesn’t pump as well, so blood backs up, I explained. And with this ticker of yours, there’s a tendency for blood to back up already. Not only that, but your ventricle loses the boost from the left atrium, so you’ve got a double whammy.

Eddie forgot about his steelhead. He met my eye, then slowly asked, Does that mean the ticker’s shot, Doc?

Far from it, I said.

He looked relieved, then paused before asking his next question. And what about, you know, Doc? In our small town it was common knowledge that Eddie had a steady girlfriend. I tried to reassure him on that account, too.

That old heart attack weakened your heart, but it still has plenty of strength, I told him. It just needs to get itself coordinated again. First we’ll make sure that you don’t have another problem like an overactive thyroid revving up your heart. Then we’ll try a medication to see if we can’t slow things down a bit.

Eddie shifted his meaty frame on the exam table. He must have weighed close to 220 pounds. Okay, Doc, he said, but I’d better warn you: with me it always takes a double dose.

A-Fib, Eddie’s brand of arrhythmia, affects 1.5 million Americans, most of them over the age of 60. It’s a capricious problem, and it can be triggered by anything that jazzes up the heart, such as stress, exercise, or illness. It usually hits patients with other heart or lung problems, but in only a few can a single cause be pinpointed. In that sense, President Bush, whose arrhythmia was caused by an overactive thyroid gland, was lucky.

As for therapy, digitalis derivatives like Digoxin, which slow the conduction of signals through the AV node, are still the mainstay of therapy--200 years after the British physician William Withering first used digitalis obtained from foxglove leaves. With Eddie, none of the usual triggers turned up, so for the next three months I threw liberal doses of Digoxin and diuretics at his heart.

Oh, the pike are coming in by the barrelful now, Doc, he would tell me after getting up from the exam table and having a good stretch. When autumn peaked, that changed to, The salmon are so thick you can walk across them. But sooner or later his wind would feel short again. Since he wasn’t much of a complainer, I had to rely on Anne, his girlfriend, for the straight story.

He hasn’t been sleeping. Spends all night sitting up in his chair, came her refrain.

Up would go the doses again, but after a brief improvement, we’d be right back to square one.

Then came the afternoon his heart tripped into overdrive in my office, right before my very eyes. As I listened to his chaotic heartbeat, I could hear his breathing becoming wheezy and labored. By then he was on triple the normal daily dose of Digoxin. Something else, I felt, must be cutting his wind. Reluctant as he was to give up valuable fishing time, Eddie agreed to another round of hospital tests--a sure sign he too was worried.

But the tests came back normal. No sign of angina--his coronary arteries outside the areas damaged by his heart attack were clean. And despite his smoking, there was no damage from emphysema in the lungs. His entire problem was due to atrial fibrillation.

I tried another drug that can slow the heart rate but also weaken its pumping. Twelve hours later the new drug put Eddie in the emergency room with suddenly severe congestion.

No more rate-controllers for you, I told him the next morning. You need all the squeeze you can get. But there is another card we can play. Cardioversion.

Eddie looked at me noncommittally, not sure whether he was about to land the big one or an old boot.

Okay, Doc, he drawled in his broad upstate accent. What’s that in English?

Electric shock.

Oh. He would take convincing.

There are two reasons why it could help a lot, I said. First, your heart rate will come down to normal, so the ventricles will pump more efficiently. And second, the atria will resume pumping, instead of just quivering, so your heart won’t be losing up to a quarter of its output.

How does electric shock work? he asked.

Well, the electric charge overrides all the cells that are firing on their own--kind of shuts them all up at once--so the natural pacemaker can take over again.

Another pause. Are you sure it’ll work?

Eddie, you know there are no guarantees in medicine. Or fishing, for that matter. He gave me a pensive smile. But judging from the EKG, your atria are in reasonable shape. So once they’re back in sync they should stay there.

Is it dangerous?

There’s a slight chance it could trip a more dangerous heart rhythm. But we’ll be equipped to handle it.

Painful?

Don’t worry, we’ll pump you full of the good stuff.

His broad cheeks split into a grin. Okay. Anything you say, Doc.

There was another good reason to snuff out Eddie’s atrial fibrillation: it increases the risk of strokes. When the atria stop contracting smoothly, pools of blood can form and congeal into clots. If one breaks off and floats into the left ventricle, it might be pumped directly to a brain vessel, blocking blood flow and causing a stroke. Fifteen percent of strokes, nearly 75,000 strokes a year in this country, are the result of the rhythm disturbance. More insidiously, recent CT scan studies have implicated the arrhythmia in recurrent imperceptible strokes (which can lead to dementia) in almost a third of A-Fib patients. Fortunately, large studies have shown that aspirin or Coumadin, which are both anticoagulants that prevent clot formation, can reduce the A-Fib stroke rate. Unfortunately, because of the studies’ design, it won’t be known until December which is the better, safer drug. As for Eddie, he couldn’t breathe and he couldn’t wait.

For the next four weeks we gave him Coumadin to avert the danger of his heart’s inadvertently flipping clots to his brain. Then, a few days before Christmas, all was ready. Eddie checked into the hospital in the morning and was given a mild sedative. An hour later we wheeled him into the coronary care unit. Through an intravenous drip, the anesthesiologist administered a short-acting barbiturate. Just before he went out, Eddie winked at me. Doc, you know, if, well . . . tell Anne. You know.

Eddie, I replied, in twenty minutes, you’ll tell her yourself.

Right, Doc. Then he was asleep. The chaotic squiggle of his A- fib, interrupted by random spikes of ventricular contractions, filled the screen of the heart monitor.

The cardiologist charged up the two paddles that would deliver the electric shock to Eddie’s flailing heart, placing one under Eddie’s back and the other over his sternum. I almost said, Better make it a double charge. Then he announced, Ready. All clear, please.

The cardiologist squeezed the discharge buttons on the sternum paddle. Eddie’s body tensed, then relaxed, and the squiggle on the monitor screen went flat. I held my breath. Beat, I urged the suddenly straight line. Eddie lay still. Then, as if they’d never left, small waves of atrial contractions, followed faithfully by the high spikes of ventricular contractions, started marching in stately procession across the screen.

For five minutes we listened to Eddie’s contented snoring. Then he stirred. I walked around the bed and squeezed his shoulder. Eddie, it worked, I whispered, not sure he was awake.

His eyes fluttered open, then he took one look at the monitor and beamed. Lots of perch under that ice waiting to be caught, Doc.

In a month he was completely off diuretics. He hasn’t missed a
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