Office Anesthesia Emergencies Flashcards

A patient under moderate sedation with midazolam and fentanyl develops a sudden decrease in SpO₂ to 88%, but chest rise appears adequate and airway sounds are clear. After supplemental oxygen is applied, saturation fails to improve. Which condition should be suspected first?

Answer: Methemoglobinemia

Methemoglobinemia causes SpO₂ readings to plateau around 85% on pulse oximetry regardless of supplemental oxygen, because the oximeter cannot distinguish oxyhemoglobin from methemoglobin accurately. Benzocaine and prilocaine are well-known triggers in dental settings. The treatment is IV methylene blue 1–2 mg/kg. Laryngospasm would present with stridor and poor chest movement; pulmonary embolism is rare in this acute sedation context; vasovagal syncope causes bradycardia and hypotension, not isolated desaturation.

During IV sedation, a 42-year-old patient receiving propofol develops peaked T-waves on the ECG monitor, then widening QRS complexes. Blood pressure remains stable. Which electrolyte abnormality is the most likely culprit?

Answer: Hyperkalemia

Hyperkalemia produces a classic progression: peaked T-waves → prolonged PR → widened QRS → sine wave pattern → ventricular fibrillation. In the dental office, this can occur in patients with renal impairment or those on ACE inhibitors/potassium-sparing diuretics. Hyponatremia causes neurological symptoms; hypocalcemia causes prolonged QT and tetany; hypomagnesemia typically causes torsades de pointes, not widened QRS progressing in this pattern.

A patient experiencing a life-threatening anaphylactic reaction has received intramuscular epinephrine 0.3 mg (1:1,000) in the lateral thigh, but symptoms are worsening after 5 minutes. The patient is on chronic beta-blocker therapy. What is the most appropriate next intervention?

Answer: Administer IV glucagon 1–2 mg and activate EMS

Beta-blockers competitively antagonize the beta-adrenergic effects of epinephrine, making anaphylaxis refractory. Glucagon acts through a non-adrenergic receptor pathway (adenylate cyclase via glucagon receptors), bypassing the beta-blockade and restoring bronchodilation and positive inotropy. A second dose of epinephrine can still be given, but glucagon is the critical adjunct in this scenario. Subcutaneous administration is no longer recommended over IM in emergencies; diphenhydramine is not a rescue agent for hemodynamic collapse.

Midway through an oral surgical procedure under deep sedation, the DAANCE-certified anesthesia assistant notices the capnograph waveform changes from its normal rectangular shape to a shark-fin pattern (slow upstroke, no plateau). Ventilation appears to be assisted adequately. What does this waveform pattern indicate?

Answer: Obstructive bronchospasm or reactive airway disease

The 'shark-fin' or obstructive capnograph waveform occurs when expiratory flow is uneven due to bronchospasm, COPD, or reactive airway disease — gas from different alveolar units empties at different rates, eliminating the flat plateau of the normal waveform. Esophageal intubation produces a flat capnograph or rapidly diminishing waveform. Complete obstruction yields no waveform at all. Hypoventilation from opioids slows the respiratory rate but does not alter the waveform shape in this characteristic manner.

A patient who received local anesthesia with 4% articaine (with 1:100,000 epinephrine) during IV sedation develops tinnitus, perioral numbness, a metallic taste, and then sudden muscle twitching approximately 8 minutes after injection. The team suspects local anesthetic systemic toxicity (LAST). Which statement about managing this emergency is MOST accurate?

Answer: Administer 20% lipid emulsion IV as the definitive antidote and avoid vasopressors containing epinephrine

20% lipid emulsion (Intralipid) is the definitive treatment for LAST, acting as a 'lipid sink' that sequesters the lipophilic anesthetic away from cardiac and neural tissue. The ASRA guidelines specify avoiding vasopressin and large doses of epinephrine in this setting because they worsen outcomes; if vasopressors are needed, small doses of epinephrine are preferred. Sodium bicarbonate is not a treatment for LAST. Lipid emulsion should be initiated at the first sign of cardiovascular compromise — not deferred until arrest. Hyperventilation lowers CO₂ and raises pH, which may slightly increase protein binding, but this is a supportive measure, not definitive treatment.

During recovery from general anesthesia in a dental office setting, an adult patient abruptly develops inspiratory stridor, paradoxical chest movement (chest retracts while abdomen rises), and a SpO₂ dropping from 97% to 80% over 60 seconds. Jaw thrust and supplemental oxygen provide no improvement. What is the correct sequence of interventions?

Answer: Positive pressure bag-mask ventilation → IV/IM succinylcholine if unresponsive → emergency cricothyrotomy if still unresponsive

This presentation is classic complete laryngospasm. Initial management is positive pressure bag-mask ventilation with 100% oxygen using firm continuous pressure — this can mechanically break the spasm in many cases. If unresponsive within 15–30 seconds, succinylcholine (0.1–1.5 mg/kg IV or 4 mg/kg IM if no IV access) is administered to relax the vocal cords. Cricothyrotomy is the last resort if all airway maneuvers fail. CPAP alone is ineffective in complete laryngospasm. Deepening sedation with propofol without controlling the airway first is dangerous and delays definitive treatment.