by imaging studies (computerized tomography, magnetic resonance, or fluoroscopy). Recurrent apnea will lead to intermittent hypoxemia, hypercapnia, and sleep fragmentation, with secondary increase of the sympathetic tone. OSA represents an independent risk factor for cardiovascular morbidity and mortality. A plausible explanation seems to be the increased oxidative stress secondary to alternate hypoxia/reoxygenation. The oxidative stress causes systemic inflammatory response with activation of endothelial cells, leukocytes, and platelets that culminates in early signs of atherosclerosis. OSA is one of the leading causes of systemic hypertension, left ventricular hypertrophy, pulmonary hypertension with right ventricular failure and congestive heart failure, cardiac dysrhythmias, ischemic heart disease, and stroke.
patients who are unable to tolerate CPAP. The mechanism of action is similar to the jaw-thrust technique. Surgery is reserved for severe OSA or lack of response to CPAP. The main objective of any surgical technique is to enlarge the upper airway. Adenoidectomy, tonsillectomy, nasal polypectomy, septoplasty, uvulopalatopharyngoplasty, maxillomandibular advancement and hyoid expansion are all procedures used to alleviate the symptoms of OSA
surgically. If these are unsuccessful and the obstruction is severe, the last option is tracheostomy. As adjuvant therapy, the following may be helpful: losing weight, position therapy, topical application of soft tissue lubricant, and the use of acetazolamide to increase respiratory drive to compensate for the metabolic acidosis caused by hypoxia.
TABLE 75.1 SIGNALS REQUIRED FOR POLYSOMNOGRAPHY (HYPOPNEIC AND APNEIC EVENTS ARE ASSOCIATED WITH AROUSAL FROM REM SLEEP, OXYHEMOGLOBIN DESATURATION, POSSIBLE ARRHYTHMIAS AND HIGH BLOOD PRESSURE.)
TABLE 75.2 APNEA-HYPOPNEA INDEX (AHI) AND SEVERITY OF OBSTRUCTIVE SLEEP APNEA (OSA)