2024 FSA Podium and Poster Abstracts
P067: A CURIOUS CASE OF CENTRAL APNEA CAUSED BY DEXMEDETOMIDINE
Sae-In Kay, DO; Cosmin Guta, MD; University of Miami / Jackson Health System
Introduction/Background: Dexmedetomidine exerts hypnotic action through activation of central pre- and postsynaptic a2-receptors in the locus coeruleus, inducing a state of unconsciousness similar to natural sleep. The most common adverse reactions are hypotension, bradycardia, and dry mouth. Respiratory failure due to dexmedetomidine is rare, which is reported as seen in only 2% in population given <0.7 mcg/kg/hr. We report a rare case of central apnea potentially caused by dexmedetomidine in a 79 year-old who underwent outpatient TAVR under MAC with dexmedetomidine 0.4mcg/kg/hr.
Methods: This is a 79-year-old 54kg female with history of HTN, HLD, T2DM, atrial fibrillation complicated by stroke, and severe aortic stenosis who presented for elective TAVR under MAC. Preoperative transthoracic echocardiogram showed ejection fraction of 60-65%, normal biventricular function, moderate valvular aortic stenosis. EKG showed sinus rhythm. Cardiac catheterization showed normal cardiac output with normal cardiac index, PVR, and SVR. Labs were unremarkable. The patient was brought to the operating room and standard ASA monitors were applied. Supplemental oxygen via nasal cannula was applied. Preinduction right arterial line was inserted. Dexmedetomidine 25mcg bolus was given and infusion of 0.4mcg/kg/hr was initiated. Throughout the case, fentanyl total dose of 100mcg was given incrementally. During the valve deployment, which was two hours after dexmedetomidine infusion was started, patient became hypotensive to MAP of 50s, desaturated to 80s, and became apneic. Patient was obtunded and non-responsive to noxious stimuli. Dexmedetomidine infusion was promptly stopped. Manual bag valve mask ventilation was initiated with FiO2 100% and pressors were given. After 20 minutes since apnea, naloxone total dose of 1.6mg was given, however spontaneous ventilation never returned. Patient persistently remained unresponsive with absent gag reflex. Patient was emergently intubated with direct laryngoscopy MAC3 blade and ETT 7.0.
Results: Stroke alert was called, and patient was emergently taken to CT/CTA brain. The images showed negative acute intracranial processes. After CT, which was two hours after dexmedetomidine was stopped, patient started to become responsive and followed simple commands. Patient was left intubated and transported to cardiac intensive care unit for further management. Patient was extubated the next day and underwent full recovery with no further complications.
Discussion/Conclusion: Respiratory drive is controlled by chemoreflexes such as CO2 dependent central chemoreceptors in the brain stem and O2 dependent for peripheral receptors in the carotid body. Some animal studies demonstrate that a2 agonists in the carotid body inhibit hypoxia-induced chemoreceptor responses in vivo. In a small randomized cross over study with ten healthy male volunteers, sedation with dexmedetomidine was found to reduce 59% of hypoxic ventilation and 82% of hypercapnic ventilation compared to baseline.
Central nervous system depression with sedatives particularly opioids, cardiac disease such as heart failure and atrial fibrillation are known risk factors for central sleep apnea. In this case, we believe that combination of patient comorbidities and usage of both opioid and dexmedetomidine contributed to prolonged central apnea. Thus, dexmedetomidine should be used with caution in patients with high risk of central apnea, and when used with other sedatives such as benzodiazepines or opioids.