progesterone increase the sensitivity of the medullary respiratory centers, resulting in increased minute ventilation.5 These cumulative changes decrease the time to desaturation for the gravid female and induce a respiratory alkalosis.1,5 The lower esophageal sphincter tone is reduced secondary to progesterone,1 resulting in increased gastric reflux, delayed gastric emptying, and increased risk for aspiration.
TABLE 4.1 Checklist of Steps to Review Prior to an Emergent Obstetric Airway | ||||||||||||||||||||||||||||||||||||||||||||||||||||
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notch positioning, and head elevation. Use caution with NPA insertion in pregnant patients due to the risk of epistaxis secondary to increased vascularity of the nasal mucosa.13
for the emergent obstetric airway. Premedications are avoided given the increased risk of errors, delays incurred, and lack of evidence to support their use. Hypotension in pregnancy may not be evident until loss of 25% to 30% of the blood volume7,11; therefore, push dose pressors can be given prior to induction in patients with suspected hypovolemia; phenylephrine in 50 to 200 mcg IV pushes are considered safe for use in pregnancy. Asthmatic patients are at increased risk of bronchospasm due to mucosal edema; thus, ketamine can be used as an induction agent to improve respiratory insufficiency and bronchospasm in these patients.