Researchers advise physicians: Don’t take sleep apnea lying down
Screen patients for CPAP
Controlling CHF comorbidity is an around-the-clock job, according to Canadian researchers. They recently found that while beta-blockers may keep hypertension under control during the day, the story may be completely different at night: Patients still can experience both higher levels of left-ventricular afterload and increased heart rate. These effects are a result of surges in systolic blood pressure occurring immediately after episodes of apnea.
The report indicates it may be helpful for physicians to recognize which CHF patients are at risk of experiencing sleep apnea, so continuous positive airway pressure (CPAP) treatment can be used to reverse the apnea and hypertension. At the researchers’ laboratory, 22% of CHF patients were found to have the nocturnal respiratory problem. Overall, experts say CHF patients may face a risk of sleep apnea 10 times than that faced by the healthy population.
"There’s no doubt in my mind physicians need to know about apnea in patients with congestive heart failure," says T. Douglas Bradley, MD, a pulmonologist at The Toronto Hospital and member of the research team.
"Medications reduce vascular resistance, but the mechanism on which they work probably is different than the mechanism that occurs during apnea," Bradley says. "The rises in blood pressure you see at night are not being blocked by these agents."
The team’s report is the latest in its series of studies on the relationship between CHF and apnea. It appeared in the Nov. 24 issue of Circulation, the Journal of the American Heart Association.
Eight patients receiving drug therapy for CHF and known to have obstructive sleep apnea were studied for two nights in a sleep center. None of the subjects were taking sedatives or had received previous CPAP therapy. The time spent asleep was divided into thirds, representing the time before, during, and after CPAP administration.
When sleeping subjects breathed on their own, Bradley and his group saw apnea occur. An event was followed by a rise in left-ventricular transmural pressure of 16 mm Hg. (This was calculated from the rise in systolic BP of 14 mm Hg and a 2 mm Hg drop in esophageal pressure during systole.) There were no significant changes in heart rate, BP, or respiration rate during diastole when patients’ breathing went unassisted.
When CPAP was administered, systolic BP was lowered 16 mm Hg and the esophageal pressure increased by 4 mm Hg. This meant a systolic left-ventricular transmural pressure 20 mm Hg lower than the pre-CPAP value. CPAP also lowered the heart rate by 5 bpm. Diastolic BP remained unchanged.
After CPAP, the heart beat at its reduced rate. The systolic left-ventricular transmural pressure times heart rate product increased, but it remained lower than the level before CPAP.
Bradley says the most severe episodes of apnea occur during rapid eye movement (REM), or dreaming sleep. In the course of a night, most people experience three to five cycles of REM, with apnea becoming progressively worse. However, in the sleep lab, patents rarely can reach dream sleep.
"Usually the sleep study is too invasive for REM sleep to occur," Bradley says. The patients in this study were monitored in stage 2 sleep. Monitoring began after subjects were asleep for an hour.
Did apnea contribute to CHF development?
Six of the eight subjects had idiopathic dilated cardiomyopathy. Bradley says that apnea may be a suspect in the development of the condition because of a 15-year span between the time people develop sleep apnea and show signs of CHF.
"We see obstructive sleep apnea affecting patients with an average age of 48. With heart failure, the average age is 63." So a CHF contributor may be happening long before patients ever show cardiac symptoms, he says. Asking patients about their quality of sleep can do a lot to determine if a follow-up sleep study should be ordered.
"Cardiologists should be asking patients how they are sleeping," Bradley says. "There are key questions that should only take two minutes to ask."
He suggests asking patients these questions:
o Do you have difficulty falling asleep or staying asleep because of shortness of breath?
o Do you feel tired or have to nap in the daytime because of tiredness?
o Do you snore habitually?
o Has anyone seen you stop breathing while you sleep?
For patients already diagnosed with CHF, apnea may not be suspected because the fatigue it causes may be automatically attributed to the heart failure.
"If a patient comes in and says he’s fatigued, it’s easy to say Oh, it’s just your heart failure,’ but if you dig a little deeper, you may see that it’s really sleep apnea."
"A good doctor can tell the difference between heart failure and sleep apnea," notes Gordon A. Ewy, MD, chief of cardiology at the University of Arizona Health Sciences Center and director of the Sarver Heart Center, both in Tucson. "But you have to be willing to consider it."
"It helps to know when the patient feels fatigue," says Marc Silver, MD, director of the Heart Failure Institute at Christ Hospital in Oak lawn, IL. "The patient may say Gee doc, I just wake up feeling all fatigued,’ then you can be very suspicious of sleep apnea," he says. "Then, ask more about if they are getting up at night to go to the bathroom. That will be indicating a different problem," he continues.
"If the patient is sleeping OK but is tired at the end of the day, you know something else is going on." But to make the differential diagnosis between cardiac and pulmonary problems causing the fatigue, Silver says the best evaluation tool probably would be the cardiopulmonary exercise test.
Bradley notes that at his facility in Toronto, all candidates for heart transplantation must first undergo a sleep study. He says some patients who have been found to have sleep apnea and received CPAP therapy showed enough improvement in cardiac performance that they could be removed from the transplant list.
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