What Untreated Sleep Apnea Means for Your Blood Pressure

The more we learn about sleep and sleep disorders, the more we realize that the symptoms of fatigue and sleepiness experienced by those with chronic sleep disruption are only the tip of the proverbial iceberg. In fact, poor sleep can exert its effects on nearly all medical conditions.
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By Mitchell Miglis, M.D.

The more we learn about sleep and sleep disorders, the more we realize that the symptoms of fatigue and sleepiness experienced by those with chronic sleep disruption are only the tip of the proverbial iceberg. In fact, poor sleep can exert its effects on nearly all medical conditions. Take obstructive sleep apnea (OSA). If left untreated, those with OSA have an increased risk of developing high blood pressure, high cholesterol, diabetes, heart attack and stroke.

For centuries, sleep was thought to be a passive state, however, we now know that nothing could be farther from the truth. There is a lot going on in our bodies while we sleep -- a complex interaction of neurotransmitters, hormones and regulatory nerve traffic -- resulting in dynamic physiological interactions.

Take for example, the role of the autonomic nervous system, the part of our nervous system responsible for regulating our body's automatic functions -- breathing, heart rate, blood flow, digestion, etc. The autonomic nervous system has two components: the sympathetic, or "fight or flight" component and the parasympathetic, or "rest and relaxation" component. When we fall asleep, our parasympathetic system takes over and as we progress into deeper stages of sleep, its effects become even more pronounced. Our breathing becomes more regular, our heart rate decreases and our blood pressure falls.

Then we enter rapid eye movement (REM) sleep, or dream sleep, and our sympathetic system intermittently takes over. While we dream, our blood pressure can swing dramatically and our heart rate and breathing become irregular. Those of us who can recall awakening from a particularly bad nightmare can attest to the nature of the fight-or-flight response: sweating, heart racing, we awaken with intense fear. These same physiological response would occur if we were attacked or chased by a predator.

How does this all relate to high blood pressure and cardiovascular risk in untreated sleep apnea? Researchers have established that resting blood pressure typically falls by 10 to 20 percent in most individuals during sleep. This is a normal physiological response, mediated by the parasympathetic component of the autonomic nervous system. However, in some individuals, termed "non-dippers," this does not occur. In others, so-called "reverse dippers," blood pressure actually increases by 10 to 20 percent. Non-dippers and reverse dippers are at higher risk for stroke than dippers are. And those with obstructive sleep apnea are much more likely to be non-dippers or reverse dippers.

In addition, whenever there is a sudden arousal from sleep, be it due to a nightmare or to upper airway obstruction from sleep apnea, there is a surge in sympathetic activity. As a result, there is a burst of adrenaline released into the bloodstream, blood pressure shoots up (sometimes extremely high), and -- especially if there is a corresponding drop in blood-oxygen levels as frequently occurs during an apnea -- heart rate can become irregular and dangerous arrhythmias, such as atrial fibrillation may develop.

Furthermore, it is thought that this apnea-induced sympathetic surge carries over into the waking state. Researchers have found that patients with sleep apnea have higher daytime levels of adrenaline and higher resting blood pressure than normal controls. They were, however, able to significantly lower the levels in those treated with continuous positive airway pressure (CPAP), the most common treatment for obstructive sleep apnea.

The relationship between sleep apnea and high blood pressure has now been well established in several epidemiologic studies. As with the adrenaline experiments, treatment with CPAP alone resulted in a small but significant reduction in resting blood pressure. There is also a well-established relationship between the severity of obstructive sleep apnea and the risk of developing (or worsening the risk of) diabetes, atrial fibrillation, stroke and heart attack.

Of course these risks are all related to the severity of sleep apnea -- how many apneas an individual has in a given hour of sleep and how often the blood oxygenation drops throughout the night. To fully assess an individual's risk, he or she should be evaluated by a sleep physician and most likely undergo a sleep study to evaluate for the presence and severity of OSA. If present, OSA is a very treatable condition, one that if addressed properly can help not only to improve a patient's level of daytime alertness, but also help to reduce the risk of developing many other significant health problems down the road.

Mitchell Miglis, M.D., is a sleep neurologist in the Stanford Neurology Department and the Stanford Center for Sleep Sciences and Medicine. He specializes in the relationship between sleep medicine and autonomic disorders. The center is the birthplace of sleep medicine and includes research, clinical and educational programs that have advanced the field and improved patient care for decades. To learn more, visit our website.

For more by the Stanford Center for Sleep Sciences and Medicine, click here.

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1. Narkiewicz K., Kato M., Phillips B.G., et al. "Nocturnal continuous positive airway pressure decreases daytime sympathetic traffic in obstructive sleep apnea." Circulation. 1999;100:2332-2335.

2. Peppard P.E., Young T., Palta M., et al/ "Prospective study of the association between sleep-disordered breathing and hypertension." N Engl J Med. 2000;342:1378-1384.

3. Nieto F.J., Young T.B., Lind B.K., et al. "Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study." Sleep Heart Health Study. JAMA. 2000;283:1829-1836.

4. Yaggi H.K., Concato J., Kernan W.N., et al. "Obstructive sleep apnea as a risk factor for stroke and death." N Engl J Med. 2005;353:2034-2041.

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