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Primary respiratory depression, caused by the provision of anesthesia itself, refers to a deficit in ventilation or oxygenation or both. Respiratory depression may take the form of mechanical obstruction, caused by collapse of the oropharyngeal soft tissues or occlusion of the airway by the tongue or secretions. Central respiratory depression, characterized by hypopnea or apnea, can also occur either separately or concurrently.

      Typically, mechanical obstruction occurs more frequently and at lower anesthetic doses than central apnea does, and it occurs to some extent in susceptible persons. Obese patients, those with short thick necks, those with mandibular retrognathia, and patients with OSA are among the most susceptible groups. In severe cases, this may render these patients unsuitable for ambulatory anesthetic procedures. In most other cases, patient positioning can play a role in airway obstruction. Respiratory obstruction due to mechanical airway obstruction can be managed by careful suctioning, repositioning of the tongue in a forward position, and either a chin lift or jaw thrust maneuver. If necessary, the level of anesthesia may be lessened, as increasing levels of sedation contribute to the degree of airway impediment. Rarely, an oral or nasal airway may be needed to overcome the obstruction in the posterior pharynx and stent the airway open. Supplemental oxygen can be helpful to decrease any oxygen desaturation associated with mild to moderate obstruction, although oxygen by itself does not alleviate the mechanics of obstruction.

      Respiratory depression may also be “central,” characterized by a decreased respiratory rate or periods of apnea. Narcotic drugs are most often implicated because of their effects on the medullary respiratory center of the brainstem that results in decreased respiratory drive and decreased response to hypercapnia. At moderate levels of narcotic effect, the decreased respiratory rate is accompanied by a compensatory increase in tidal volume that prevents oxygen desaturation. At higher levels of narcotic sedation, respiratory depression can progress to apnea and respiratory arrest. A brief period of respiratory support in the form of supplemental oxygen via a face mask with cessation of anesthetic drug administration may be all that is necessary in terms of management – particularly with short‐acting drugs in a patient with good respiratory reserve. Whenever there is desaturation in a setting of frank apnea, however, the patient's ventilation should be assisted by a positive pressure face mask until spontaneous respiration resumes.

      Occasionally, mask ventilation with or without the placement of an oral or nasal airway will not be sufficient to overcome airway obstruction and provide oxygenation. In these cases, other means of establishing an airway and achieving effective ventilation should be employed. These include laryngeal mask airway (LMA) insertion or endotracheal intubation for administration of positive pressure ventilation with high oxygen flow. Because endotracheal intubation is a technically complex procedure and requires specialized equipment, it is subject to high rates of failure, especially in emergency situations. Intubation should only be considered in a patient who is hypoxemic and cannot be effectively mask ventilated. An LMA can be successfully used for the support of ventilation as an alternative to endotracheal intubation and has several advantages over the traditional endotracheal tube (ET). LMAs are quickly and easily inserted without the need for specialized equipment. Use of an LMA poses no risk of inadvertent intubation of the esophagus or mainstem bronchus or injury to the vocal cords. Airway stimulation is minimal and removal of the LMA can be easily accomplished once spontaneous respirations return. Regardless of the method used to establish an advanced airway, early recognition of the potential need, familiarity with the available equipment, and skill in their effective use are critical.

      In addition to respiratory depression or arrest caused by anesthetic drugs, other causes of respiratory complications include stroke or myocardial infarction (MI). The signs and symptoms of stroke or acute coronary syndrome can be significantly masked in a patient undergoing ambulatory anesthesia, and respiratory depression or arrest may initially be diagnosed as a case of oversedation. Any respiratory complication that does not respond to moderate interventions or progresses to a need for airway establishment and support of ventilation should be investigated for additional contributing factors or underlying conditions.

       Laryngospasm, Bronchospasm, and Acute Asthma

      A second group of respiratory complications that may arise in the course of outpatient anesthesia includes reactive airway conditions such as laryngospasm, bronchospasm, and acute asthma. One analysis of complications in ambulatory anesthesia identified laryngospasm, stridor, and obstruction as the most frequently observed adverse events, accounting for 40% of complications [15]. Acute asthma attacks are more frequent preoperatively and may be associated with patient anxiety. Laryngospasm and bronchospasm typically result from the combination of airway irritation and anesthetic sedation.

Acute asthma and bronchospasm are manifested clinically by audible wheezing (more prominent during expiration), tachypnea, shortness of breath, and are usually accompanied by decreasing oxygen saturation. They represent a hyperreactive process of the large airways that results in bronchoconstriction and obstruction to airflow. A number of factors may precipitate an asthma attack or bronchospasm, but in an oral surgical setting anything that causes airway irritation may be the predominant etiological factor. Some examples include the production of aerosols during a procedure or decreased clearance of secretions that can irritate the airway and stimulate coughing. Laryngospasm, in contrast, is an acute upper airway obstruction that presents with stridor (incomplete laryngospasm) or failure of ventilation (complete laryngospasm with total closure of the glottis). Obstruction of the upper airway due to foreign body aspiration may also present with acute stridor and should be ruled out clinically. Laryngospasm results in reflexive closure of the glottis upon irritation and is a protective airway reflex. It does not occur in awake patients or in patients during general anesthesia, but can occur in a mild or moderate stage of sedation [16].

      Acute asthma attacks may be managed with inhaled beta‐2‐agonist bronchodilator medications such as albuterol. These drugs are typically administered via a metered‐dose inhaler either with or without an additional spacer device. Patients who are awake and alert may be allowed to self‐administer the inhaled medication, while patients who are sedated may need assistance. In sedated patients, the use of a spacer may be particularly useful to assist delivery of the drug to the lungs and to prevent excess drug deposition in the oropharynx where it is has no therapeutic effect.

      Inhaled bronchodilators are also the first‐choice treatment for bronchospasm and are administered similarly. In intubated patients, these inhaled medications may be administered via ET or LMA, though the dosage must be greatly increased (up to 10–20 puffs) to account for the large amount of drug that coats the airway tube and does not reach the lungs. Both acute asthma and bronchospasm benefit from supplemental oxygen. In severe cases that do not respond to inhaled beta‐agonists, IV or subcutaneous epinephrine may be considered as a rescue therapy. The adverse effects of epinephrine – particularly tachycardia and increased blood pressure – limit its use for reactive airway disease. It should be used with extreme caution, if at all, in patients with underlying cardiac disease.

      The treatment of laryngospasm differs from that of asthma or bronchospasm. Because it occurs in patients who are at “lighter” levels of anesthesia, deepening the level

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