Breathless – sleep apnea
An insidious–and often undiagnosed–sleep disorder robs a woman of her ability to take in oxygen
BEATRICE STOOD FIVE FEET one and weighed just about 280 pounds. I marveled that she could move at all.
Bob, my resident, described her case: “Thirty-four-year-old woman complaining of shortness of breath with exertion, cold symptoms, cough, extreme weakness, and fatigue for three weeks. Her doctor prescribed codeine for the cough. And oh, I forgot–her O-2 sat is 70 percent.”
O-2 means oxygen. Sat means saturation. It’s an easy figure to get from the pulse oximeter, a probe placed on the finger to measure how much oxygen is being carried by hemoglobin in the bloodstream. Normal oxygen saturation is 98 to 100 percent.
“Seventy percent?” I scoffed. “Not possible.”
The resident shrugged. “The nurse double-checked. Here’s her blood gas.”
I did a double take. The results not only confirmed the low oxygen level but also showed that her carbon dioxide level was twice as high as normal. Beatrice’s lungs seemed to have quit working. Together, we walked over to her.
Now the pulse oximeter read 98 percent; the oxygen she was breathing through a mask had bumped it up.
“Beatrice, have you or anyone in your family ever had a blood clot in the lungs?” I asked.
“Oh yes,” she answered. “When my sister was pregnant, she passed out cold while she was in the shower. Big clot in the lungs. They kept her on heparin for the rest of her pregnancy”
A blood clot could explain breathing difficulties, but it wouldn’t explain Beatrice’s sky-high carbon dioxide levels. Even if a blood clot was interfering with oxygen exchange in the lung, any excess carbon dioxide would be shunted off to other parts of the lung and exhaled. Still, I wanted to be sure. “Let’s get her up to CT now.”
The scan came back a frustrating maybe, so we hustled her up to the duplex scan–a combination of ultrasound waves and Doppler sound analysis–to hunt for a clot in the large veins of the thigh. Clots tend to form there, and when they break up, chunks of them can move up into the lungs.
Forty-five minutes later, the duplex lab called. “You should come get her,” the technician said. “She doesn’t look so great, but the duplex is normal.”
When Bob wheeled Beatrice back down, her head was rolling from side to side, and her eyes were unfocused.
A hot jet of fear hissed through me. The nurses swarmed around Beatrice.
“Call anesthesia, please,” I finally said to the ward clerk across the room.
My resident stepped up. “Blood gas?”
He quickly found the wrist artery, drew the sample, and raced upstairs. He returned, amazed by the results. “Her [CO.sub.2] is 131.”
It had doubled again. From what the blood told us, Beatrice had, for all intents, stopped breathing.
The anesthesiologist sedated her and slipped a breathing tube down the trachea. Bob and I scurried around, checking blood pressure, oxygen level, and tube placement. Then we ran through diseases that assault muscle function: Guillain-Barre, myasthenia gravis, Eaton-Lambert. But those disorders usually progress over hours or days. Beatrice had stopped breathing in minutes.
To our relief, she seemed to stabilize on the ventilator, which mechanically forced air into her lungs. We got her upstairs to the intensive care unit. Soon she was sleeping soundly It would prove to be the soundest sleep she’d had in months.
In The Posthumous Papers of the Pickwick Club, published in 1837, Charles Dickens described an extremely obese boy who couldn’t help falling asleep during the day Early in this century, William Osler coined the term Pickwickian syndrome to describe rotund people who cannot keep their eyes open long enough to carry out normal daily activities. Nobody understood the condition until the early 1970s, when studies of nighttime breathing patterns turned up the answer.
During deep sleep, the soft palate and tongue relax completely, but they normally do not shut off the back of the throat. Snoring is what happens when they come close. In obese people the fat bulks up all tissues, thus narrowing airspace in the throat and making it easier to close off the airway completely during sleep. The technical term for these interruptions is “obstructive sleep apnea.” Apnea means “lack of breathing.” When the pharynx is blocked during sleep, survival reflexes howl, and the person wakes up. But falling back to sleep starts the cycle all over again. Some unfortunates may wake up an astonishing 400 times a night.
In Beatrice’s case it took us two days to eliminate other possible diagnoses, such as pneumonia or lung collapse. Pulmonologists finally decided Beatrice had obstructive sleep apnea. But it was more severe than any they had ever seen.
An estimated 12 million Americans currently suffer from obstructive sleep apnea. One of the biggest risk factors is obesity. And obesity is becoming a major health problem. From 1991 to 1998, the prevalence of obesity in this country leaped 50 percent, from 12 to 17.9 percent. So steep is the associated increase in sleep apnea that sleep labs can’t keep up with the demand for diagnostic testing. Yet some researchers estimate 80 percent of sufferers are undiagnosed.
Sleep apnea robs patients of more than rest. Researchers have found that sufferers have six times more automobile accidents than the rest of the population. One expert equates driving under the stuporous effects of sleep apnea with driving drunk. Most telling, patients with more than 20 sleep-apnea episodes per hour have a mortality rate of 37 percent over eight years.
Among these patients, hypertension and heart abnormalities abound, for unknown reasons. In Beatrice’s case, constant cardiac monitoring turned up abnormally long pauses between heartbeats. This is a common finding in older patients but rare in a 34-year-old. A permanent pacemaker had to be installed to stabilize Beatrice’s heartbeat.
On the third day, she was taken off the ventilator and started on a machine equipped with a mask that would generate enough pressure within her airway to keep it from closing shut. The mask is one of the most effective treatments for sleep apnea. The big disadvantage is that patients must sleep with the machine attached. Some opt out. Other treatments involve surgery to trim the palate or remove a portion of the tongue. These treatments work, but patients also tend to gain weight, adding to the original problem. The most effective remedy is a huge weight loss: One study found that a 10 percent drop in weight will confer a 50 percent drop in apnea episodes. But few patients have the willpower to shed that many pounds.
After several days on the mask, Beatrice was sleeping better, but her blood gases were still out of whack. Her doctors finally realized the main problem: She was suffocating from her own weight. Her chest could not expand enough to move carbon dioxide out and air in.
That was why her blood gas levels had looked so unusual. That was also why giving her oxygen had made her worse. The respiratory center in the brain stem is built to respond not to the level of oxygen in the blood but to the level of carbon dioxide. Even a small rise in carbon dioxide prompts the lungs to speed up breathing. Over time, however, persistently high carbon dioxide levels can blunt the reflex. The brain comes to sense that carbon dioxide levels are chronically out of whack, so it decides to run itself based on the oxygen level. This is called the hypoxic drive, and it is common in emphysema sufferers. When a well-meaning doctor slaps oxygen on a patient with low blood oxygen, the hypoxia goes away. The brain stem gets the message that oxygen is plentiful, so it stops signaling the chest to expand. To make matters worse, that signal also prompts the system to misdirect blood laden with carbon dioxide back into poorly functioning areas of the lungs. This error in trafficking causes carbon dioxide to build up in the blood, and the skyrocketing level interrupts the function of the respiratory center so profoundly that it fails to respond when oxygen levels plummet again.
Beatrice stayed in the hospital for a month. The surgeons opened a hole in her throat so she could breathe on a ventilator while she slept. And she was started on Orlistat, a drug that interferes with fat absorption. Most important of all, Beatrice began to exercise. Losing weight was a matter of life or death.
Six months later, I was in the ER. At 3 A.M., the nurses woke me up. “Thirty-four-year-old woman. Tracheostomy tube fell out.”
I shuffled sleepily into the cubicle to meet the patient and her mother.
“He’s the one, Beatrice–the one who helped you that first time.”
I peered more closely at the moderately plump young woman. “Beatrice?”
She placed a finger over the trach hole and spoke. “It’s me, doctor. I don’t remember you, though. Those first days are a big blur.”
“How are you?” I blurted, finally recognizing her smaller self.
“Doing great!” She beamed. “I’ve lost 75 pounds, I’m exercising every day, and I just feel good.” She pointed to her throat. “They say in another month or two I maybe able to come off this.” She flashed a triumphant smile.
Then, with the help of a nimble-fingered resident, I pushed and twisted the plastic sleeve of the tube into the tracheostomy port until it clicked home.
I took a step back to admire her.
She winked. “This is the new me.”
The case described in Vital Signs is based on a true story. Some details have been changed to protect the patient’s privacy.
Tony Dajer is the assistant director of emergency medicine at New York University’s Downtown Hospital. This was an extreme case of sleep apnea, says Dajer, but the condition can often go undetected. Like the patient in this article, people “don’t even realize their sleep is interrupted. Most go back to sleep quickly, but they wind up clobbered by fatigue.” Dajer is at work on a book about medical mistakes.
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COPYRIGHT 2000 Gale Group