Millions of individuals and families worldwide are familiar with the scenario: A family member drifts off to sleep, and within minutes begins to snore, perhaps quietly at first. Breathing becomes irregular; snoring grows louder. There may be a period of relative silence during which the individual’s chest wall appears to move as if he or she is breathing, but no snoring is heard. Suddenly there is an “explosion” of noisy breathing and motion as the individual arouses and possibly awakens.
This pattern may be repeated dozens or even hundreds of times per night, resulting in fragmented and non-restorative sleep for the snorer, and often a great deal of annoyance for the remainder of the household.
The above scenario describes obstructive sleep apnea, the most widely recognized of a group of ailments categorized as sleep disordered breathing. Obstructive sleep apnea (OSA) results from partial or complete blockage of the upper airway during sleep. The obvious result of this blockage is snoring. Other results are less obvious, but may carry far more serious health consequences. These can include restless and non-restorative sleep, shortness of breath, headaches, and excessive daytime sleepiness.
The medical community is now coming to realize that the changes in body chemistry and function that accompany these episodes of disordered breathing can have profound effects on the heart and blood vessels, potentially increasing the individual’s risk for heart disease, hypertension and stroke.
Obstructive sleep apnea (absence of airflow to the lungs lasting for longer than 10 seconds) and hypopnea (airflow reduced by more than one-half) results from complete or partial collapse of a narrowed upper airway.
In individuals without OSA, muscles that hold open the upper airway relax during sleep, but there is still sufficient opening to permit airflow with breathing. In persons with OSA, the airway is already narrowed, and when the muscles relax the airway can become blocked.
Obesity is a major risk factor for OSA, since a layer of fat may be deposited around the airway, causing partial narrowing even during waking periods. Other known risk factors for obstructive sleep apnea are male gender, age greater than 40 years, and structural abnormalities of the face, head, or neck, including increased neck circumference.
Results of these partial or complete airway obstructions can include a multitude of mechanical, hemodynamic, chemical, nervous, and inflammatory responses that have a negative effect for the heart and blood vessels. These effects last long beyond the restless night, and can over time damage an otherwise healthy heart or further compromise an already damaged heart.
Each time the individual with OSA struggles to move air through the narrowed or blocked airway, pressure changes within the chest can dramatically impair the heart’s ability to fill and pump. Also, stimulation of the nervous system causes release of chemicals that can significantly increase blood pressure and heart rate.
When the individual startles awake and the actual air movement of breathing resumes, there is a further dramatic increase in both blood pressure and heart rate. These heart rate and blood pressure changes are similar to those of the “fight or flight” response to fear or excitement.
In individuals with significant obstructive sleep apnea, these episodes can occur dozens or hundreds of times per night. In effect, the heart rate and blood pressure never really sustain “resting” levels.
At the same time that all these “fight or flight” chemicals are circulating to stimulate the heart, ineffective breathing is causing the oxygen level in the blood to drop. This mismatch of the heart’s oxygen need and what the lungs can provide can further stress the heart.
In a follow-up column next week, we can examine the daily toll that OSA has on health.
Gary Neidrick is the Director of Cardiopulmonary Services at Mount Nittany Medical Center.