OSA represents the most severe stage of the spectrum of sleep – disordered breathing.
It is generally agreed that an apnea, defined as a cessation of airflow, has to exceed 10 seconds duration to be considered significant.
Hypopnea is usually defined as a reduction in airflow or respiratory effort for more than 10 seconds accompanied by a desaturation of 3% or more & /or electroencephalographic evidence of arousal(4).
The apnea hypopnea index (AHI) is the number of apneas & hypopneas per hour of sleep and is used more or less interchangeably with the term respiratory disturbance index. The apneas may be obstructive, central or mixed.
OSA presents with symptoms of chronic loud snoring and daytime sleepiness. In middle – aged adults, OSA increases the risks of cardiovascular morbidity, mortality, cognitive dysfunction, and reduced quality of life. Although OSA is likely to be more prevalent in the older adult, several studies show an association between OSA and increased daytime sleepiness, cognitive dysfunction, nocturia, and reduced quality of life. A high index of suspicion, careful clinical history, and appropriate sleep testing is necessary for the diagnosis of OSA.
Obesity is considered one of the main risk factors for the development of OSA, although anatomic factors contributing to a narrow UA also have a significant part. Skeletal and soft tissues of the pharynx may narrow the UA lumen, thereby contributing to pharyngeal collapse. Important skeletal structures include the mandible, hard palate of the maxilla, and position of the hyoid bone. Contained within the confines of these skeletal structures are soft tissues of the pharynx, including the lateral pharyngeal wall, adenotonsillar tissue, tongue, uvula, and pharyngeal fat pads. Excess soft tissue in the pharynx or a small bony cage due to the skeletal structures can narrow the UA lumen in patients who have OSA.
This sleep breathing disorder is thought to contribute to, or be a cause of systemic and pulmonary hypertension, atherosclerosis, coronary artery disease, heart failure, atrial fibrillation, and stroke. The mechanisms underlying cardiovascular disease in patients with OSA are still poorly understood. The pathogenesis is likely to be a multifactorial process involving a diverse range of mechanisms, including sympathetic nervous system overactivity, selective activation of inflammatory pathways, endothelial dysfunction, and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism.
Obstructive sleep apnea (OSA) may independently, or in association with other cardiovascular triggers (such as ischemic heart disease or heart failure), predispose patients to the development of arrhythmias. The Sleep Heart Health Study demonstrated that individuals with severe sleep disordered breathing had two – to four –fold higher odds of developing complex arrhythmias than those without sleep disordered breathing. These arthythmias primarily occur during sleep hours and include either brady – or tachycarrhythmias. The mechanisms by which obstructive sleep apnea contributes to arrhythmogenesis may include increased sympathetic nerve activity, reflex increases in vagal tone, hypoxemia, or by decreasing arrhythmia threshold.
Obstructive sleep apnea is associated with considerable immediate hemodynamic changes. The apnea event leads to increased work of breathing, recurrent episodes with considerable negative intrathoracic pressure, hypoxia or reoxygenation, and fluctuating autonomic activity. Heart rate and blood pressure oscillate considerably across the cycle. The relative contribution of these changes to the development of cardiovascular disease is unknown. Nevertheless, increased oxygen demand and reduced oxygen supply (i.e., hypoxemia during episodes with sleep disordered breathing) may trigger an attack of angina pectoris in patients with CAD who already have reduced coronary flow reserve. OSA is also associated with longterm alteration of cardiac structure, hemodynamic reflex function, and vascular structure and function. The disorder leads to immediate and sustained sympathetic activation. Baro-and chemoreceptor responsiveness is altered and vascular reactivity, in terms of responsiveness to hypoxemia or vasoconstrictors, appears to be elevated.
Preoperative evaluation of any patient should include an assessment of the likelihood of OSA. In previously diagnosed patients, a copy of the diagnostic and therapeutic sleep studies should be reviewed thoroughly. Information such as the apnea –hypopnea index, oxygen saturation, associated arrhythmias, sleep architecture, effect of body position, treatment modality (continuous positive airway pressure [CPAP], bilevel positive airway pressure, an oral appliance, or upper airway surgery), type of interface (nasal or fullface mask), pressure requirement, and need for supplemental oxygen should be reviewed thoroughly to understand the nature and severity of the patient's OSA. This information provides an important guide for peri–and postoperative management.
Choice of anesthetic technique is important. The problems of airway maintenance intra – and postoperatively and suppression of arousal responses can be circumvented by use of regional techniques. If the surgical procedure lends itself to them and the patient is otherwise suitable they should be considered, bearing in mind the necessity for airway management should the regional technique result in unconsciousness or respiratory paralysis. If general anaesthesia is necessary then the following considerations apply.
Preparation for a possible difficult intubation should be made along with strategies to manage what may be a difficult airway intraoperatively if the patient is not to be intubated. The choice of induction and maintainance agents is probably not important although it would seem sensible to avoid large doses of longer acting drugs, especially neuromuscular blocking agents. Opioids should be used judiciously although the availability of CPAP will obviate potential difficulty postoperatively, particularly if the patient is already familiar with it. The issue of familiarity is important, sa the early postoperative period is not the ideal environment for introduction of CPAP therapy, particularly if the patient is restless, in pain or hypoxaemic.
In theory, before discharging a patient after surgery, it should be known how well the paient can sleep in their usual way (typically flat in a normal bed, in their preferred sleeping position, and without supplemental oxygen or intravenous or intramuscular narcotic agents) and to know that their sleep apnea is not any worse than preoperatively. In reality, postoperative monitoring is never set up to simulate the home environment. Some monitoring situations tend to improve the sleep apnea (head of bed elevation, use of supplemental oxygen, use of steroids, frequent patient checks and alarms that disturb sleep and reduce deep sleep), whereas others tend to worsen the apnea (laying supine, receiving intravenous or intramuscular narcotics). Given the limitations that the monitored setting is not really like the home, the importance of the postoperative observation period is to document the presence or absence of sleep apnea and oxygen desaturation in the patient while sleeping without supplemental oxygen. The need for postoperative monitoring depends on the procedure performed and associated comorbid conditions. The hospital policies and protocols and quality of the hospital nursing care also have an impact on the level and type of postoperative monitoring. For example, some facilities can perform continuous pulse oximetry in the extended recovery unit or regular nursing unit, whereas others require an ICU to administer this same level of care. It is this author's opinion that most patients with mild or moderate sleep apnea undergoing nonairway surgery or nasal surgery only may safely be done as an outpatient, whereas those with severe sleep apnea may require some observation, preferably with some time asleep, before discharge. Most patients with mild obstructive sleep apnea hyponea syndrome undergoing UPPP or other pharyngeal airway surgeries should at least be observed for several hours before discharge, whereas those with moderate or severe obstructive sleep apnea hypopnea syndrome should stay in some type of observation unit for a longer period of time, typically to include an observation of sleep.
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