The jangling phone punches through my deep sleep at 3 a.m. "Sorry to bother you," says Jean-Claude. "Sixty-five-year-old, doesn't look so hot. Might need intubating."
"On my way," I croak softly into the phone. Jean-Claude is one of my best residents, and he never cries wolf. I pull on sneakers, run a comb of fingernails across my scalp, and hurry to the emergency room.
Flat on his back, the 65-year-old Asian man looks near death, his eyes closed, his chest pumping like a manic bellows. The hissing oxygen mask muffles everything. The man's legs are a mottled, lacy blue. No oxygen is circulating.
Jean-Claude holds up Mr. Lee's chest X ray. "Increasing shortness of breath over the past 24 hours," he says. "Whiteout, both sides. Overwhelming pneumonia, probably sepsis too. I started Levaquin."
I know the antibiotic will take too long to have an effect. I glance at the pulse oximeter monitor. The reading — 79 percent —shows how much oxygen is in his blood. Anything under 90 percent is bad; less than 80 percent is dire.
"Blood pressure?" I ask.
"It's 205 over 100," Eric, an experienced nurse, answers over his shoulder. "A little high."
Translation: a lot high. The early morning fog blows off my brain. Sepsis lowers blood pressure, so whatever this man has is not sepsis. I slap a stethoscope on his chest. His lungs wheeze, but they do not rumble, as they would with pneumonia. I tap his chest. What I hear is not the dull thud that would indicate a chest filled with pus.
"Fever?" I ask Jean-Claude.
"No," he answers.
"Jesus," I mutter, "he's in failure." I grasp the top of the stretcher, press the hydraulic handle, and jackknife Mr. Lee's torso into a vertical position, which will make it easier for him to breathe.
"Eric," I shout across the room. "Give me some sublingual nitros. And 80 of Lasix. He looks like he's in failure."
Jean-Claude's face falls. "But the chest film showed a whiteout. Bad pneumonia," he stammers.
"Don't beat yourself up," I tell him. "Failure can look like anything—and fool anyone."
When the heart cannot pump well enough to meet the body's metabolic demands, we call it congestive heart failure, or more broadly, heart failure. The numbers are daunting: Heart failure afflicts 5 million Americans, and each year it precipitates 900,000 hospitalizations and kills 300,000 people. More people over 65 succumb to it than to any other disease.
There are dozens of ways a heart can fail. Two of the most common pathways affect the left ventricle, the chamber in the heart that pumps oxygen-rich blood out to the body. Either the left ventricle is too weak to squeeze (so-called systolic failure) or it is too thick and stiff to relax (diastolic failure). Focus on the systolic failure dominated medical thinking 20 years ago. The failure was ascribed to heart attacks that kill muscle and weaken the pump. Two decades of modern cardiac imaging and sophisticated studies have shown that as many as half of all heart failure cases are caused not by the left ventricle's inability to squeeze but by its failure to relax. High blood pressure—not heart attack—is the culprit. At the end of each heartbeat, the left ventricle must re-prime itself with about three ounces of blood. In patients with hypertension, years of blood straining against constricted arteries causes the ventricle, just like any other muscle, to bulk up. The heart chamber grows too small and too stiff to fill completely during diastole, the heart's relaxation-and-filling phase. The result is an Arnold Schwarzenegger heart: all beefcake.
Whatever the cause, the ultimate effect is the same. As cardiac output falls, the kidneys try to make up for the reduced blood flow by retaining fluid, thus boosting blood pressure. When pressure in the heart rises too much, blood backs up into vessels in the lung. Eventually, fluid leaks out of lung capillaries, choking life-giving air sacs around them.
If the right side of the heart—the part that takes in the oxygen-depleted blood from veins—also weakens, pressures in the venous system surge, making it hard to return the deoxygenated blood to the heart. As a result, the legs and abdomen swell with fluid. This is classic congestive heart failure.
But this patient's heart, on X ray, appears of normal size. So do his legs.
"If the blood pressure is low," I tell Jean-Claude, "as in no heart muscle left, then you have a problem. But if it's high, like now, there's room to maneuver: Slam that pressure down."
Eric drops a tiny nitroglycerin pill under the patient's tongue. I smile at Jean-Claude: "Nitro is magic medicine. First it dilates arteries, dropping blood pressure and making it easier for the heart to pump out excess fluid. The dilation also helps the coronary arteries—the vessels that feed the heart itself—send more blood to that poor struggling myocardium."
The nitro will hit the bloodstream almost instantly. Eric hangs an intravenous nitroglycerin drip. "Double it till that 205 hits 110. We'll ease him back into the land of the breathing."
Jean-Claude pushes 80 milligrams of Lasix, a potent diuretic, into the patient's IV. By forcing the kidneys to excrete more fluid, the drug decreases the amount overflowing into the lungs. Ten minutes later, blood pressure is down to 150 systolic, the pulse oximeter reads 87 percent, and the legs are turning pink.
Jean-Claude studies the monitors and listens to the patient's lungs again. "You know," he says slowly, "I still can't hear rales. This doesn't make sense."
Rales are the crackly sound that fluid-filled lungs make. Although known as the classic physical finding in heart failure, they are found in barely half of all cases.
"That's nothing," I tell him. "Some patients come in wheezing as if they're having an asthma attack. Others complain only of a nighttime cough. Many just have a vague sense of not being able to catch their breath. Heart failure will blindside you."
"What about the chest film?"
Fluid is so much denser than air that leakage into the lungs should make a chest X ray look abnormal. But life is never so simple. I shake my head. "Normal in a third of cases."
"So how do you make the diagnosis?"
"High index of suspicion. Learn the atypical presentations. Chase down any shortness of breath or undue fatigue. "
Jean-Claude is correct to wonder. Heart failure remains remarkably difficult to recognize. In one study of primary-care clinics, only a third of men and less than a fifth of women were accurately diagnosed with heart failure. Shortness of breath is a very common complaint— and, apparently, all too often attributed to a patient's being overweight or out of shape. Even in the emergency room, where more technology is available and patients are sicker, the misdiagnosis rate runs around one in eight.
Help might be on the horizon. New blood tests that detect B-type natriuretic peptide, a protein secreted by the ailing heart, are entering clinical use and might improve diagnostic accuracy. Moreover, the rethinking of heart failure has led to more aggressive use of blood-pressure-lowering medications. For example, doctors are prescribing drugs that block or inhibit angiotensin converting enzyme, a substance in the blood that helps blood vessels constrict. Doctors are also turning to drugs that block the receptor for adrenaline, a hormone that makes the heart beat faster and raises blood pressure. Known as beta-blockers, these drugs were once anathema because they dampen the heart's squeeze. Finally, therapeutic doses of the B-type peptide, in early trials, have shown promise as a natural alternative to nitroglycerin and Lasix.
Jean-Claude watches as the patient drifts into a nap. Shaking his head, he says, "I'm going back to med school."
"Nah," I say. "That's where they misled you in the first place."
