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Obesity is a risk factor for increased difficulty in most modalities of airway management. It decreases ease and effectiveness of face mask ventilation, supraglottic airway device use and front of neck airway techniques and probably makes laryngoscopy more difficult. When difficulty occurs, airway rescue techniques are more likely to fail in the obese patient. Obesity also increases the risk of aspiration and difficulty in lung ventilation, both of which may necessitate changes in anaesthetic technique. Most importantly, obesity reduces the time available for airway management before hypoxia supervenes. To worsen matters, obesity reduces the efficacy of pre-oxygenation and safe apnoea time is less prolonged with apnoeic oxygenation techniques than in the non-obese population. To compound these factors obesity is associated with obesity-specific (e.g. obstructive sleep apnoea, obesity hypoventilation syndrome) and non-specific co-morbidities (diabetes, asthma, hypertension). With increasing numbers of obese patients and increasing degrees of obesity in the surgical population it is essential that all anaesthetists are familiar with the potential complications of airway management in the obese and the techniques that may mitigate or manage risk.
The three parts of the respiratory control system are: sensors, central control and respiratory muscles. The different disorders of ventilation include hypoventilation syndromes and hyperventilation syndromes. The three main types of hypoventilation syndromes are: obesity hypoventilation syndrome, respiratory neuromuscular disorders and primary alveolar hypoventilation. Alveolar hyperventilation exists when PaCO2 decreases below 4.5 kPa. It is not the same as hyperpnoea which is increased minute ventilation with a normal PaCO2. Detailed history and clinical examination along with knowledge of coexistent disorders can provide clues to the cause of hyperventilation. An elevated pH is suggestive of a primary respiratory alkalosis; a low pH will show a metabolic acidosis. Widened A-a gradient suggests presence of a primary pulmonary disorder. Low bicarbonate suggests a chronic nature of the disorder and implies an organic cause. Transcutaneous PCO2 or arterial PCO2 during sleep studies can help to exclude psychogenic hyperventilation.
This chapter summarizes current knowledge about changes in pulmonary physiology associated with obesity. It describes the pathophysiology of obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS). In obese individuals with OSA, increased soft tissue deposition in the pharyngeal region and tongue contributes to a decreased upper airway size. The polysomnography (PSG) remains the standard for diagnosis and assessment of the severity of OSA. Expert consensus concluded that the degree of peri-operative risk for patients with OSA depends on the severity of the OSA and the type of surgery. Obesity hypoventilation syndrome is a diagnosis of exclusion and requires the absence of other reasons for chronic hypoventilation such as chronic lung or neuromuscular disease. Additional treatment options for OHS similar to those for OSA are available including pharmacotherapy. The significant potential cardio-pulmonary co-morbidities present in OHS patients mandate a high index of suspicion to identify these patients preoperatively.
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