CARDIAC EFFECTS OF SLEEP APNEA
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The purpose of this paper is to examine research on the involvement of the heart and its processes in relation to sleep apnea. The reviewed material begins with a definition of sleep apnea and discusses the stages and prevalence of the disease along with cardiac complications associated with the different types of the disease. This is followed by a discussion of respiratory and hemodynamic changes associated with sleep apnea. The final section discusses methods and treatments for sleep apnea and the effects of these on cardiac effects. Sleep Apnea: Definition, Types and Prevalence According to Dealberto, Ferber and Garma (1994) sleep apnea may be defined as the temporary but complete closure of the throat during sleep which causes breathing to stop. Often a gasping or snorting sound is made when breathing resumes. In general, the authors report that symptoms include: loud snoring, fatigue, excessive daytime tiredness, morning headaches, and morning headaches. Diagnosis commonly requires overnight studies at a certified sleep facility. The American Sleep Apnea Association (1999) reports that the disease is very common, affecting over 12 million Americans. If left untreated, sleep apnea can cause high-blood pressure, cardiovascular disease, memory problems, weight gain, impotency and headaches. Sleep apnea can be classified as obstructive, central, or mixed, depending on the presence or absence of respiratory muscle effort (I
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dioxide and restoring oxygen to the blood. Blood chemistry returns to normal and the person goes back to sleep. The cycle then repeats.
There has been a good deal of research investigating the hemodynamic consequences of sleep apnea, the most common of which are the consequences of systemic hypertension, arrhythmias, pulmonary hypertension, left ventricular dysfunction and stroke (Noureddine, 1996). Most of this research has attempted to examine the consequences in more detail.
In some current research on sleep apnea, the hemodynamics associated with the condition have been found to be related to morbidity due to increased sympathetic activation (Rouche, Court-Fortune, Pichot, Duverney, Costes, Emonot, Vergnon, Geyssant, Lacour & Barthelemy, 1998). Further, Schafer, Hasper, Ewig, Koehler, Latzelsberger, Tasci and Luderitz (1998) found that hypoxemia and mechanical factors (e.g., increased negative thoracic pressure) are associated with the pulmonary hypertension that so often accompanies sleep apnea.
In addition to the foregoing studies, Nelsen and associates (1996), in a comparative study of people with and without sleep apnea, found elevated cardiac contractility in apneics. The authors concluded that:
These findings su
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Imran Khawaja, Information Clearinghouse, Tasci Luderitz, Oswald Kessler, Ferber Garma, APNEA Introduction, Apnea Association, Apnea Noureddine, sleep apnea, Barthelemy JC, MG Ancoli-Israel, imran khawaja, khawaja 1998, imran khawaja 1998, obstructive sleep, nasal cpap, obstructive sleep apnea, pulmonary hypertension, upper airway, sleep apnea syndrome, apnea information, apnea syndrome, effects sleep, sleep apnea information, effects sleep apnea,
Approximate Word count = 1555
Approximate Pages = 6 (250 words per page)
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