Use of dexmedetomidine to facilitate non-invasive ventilation
A 91-year-old female was admitted to the hospital after a syncopal episode. The patient had a past medical history of COPD, CHF, hypertension, depression, atrial fibrillation, fourth thoracic spine compression fracture, and pneumonia. Surgical and social histories were negative. Furosemide was given once per day at home and in the Intensive Care Unit to treat congestive heart failure, and the patient was given nebulizer treatments of albuterol, ipratropium, levalbuterol, and budesonide throughout her stay in the hospital to treat her COPD.\nThe patient's admission Glasgow Coma Scale was 13 and her baseline vital signs were heart rate of 101 beats per minute, tachypnea with a respiratory rate of 32 breaths per minute, a blood pressure of 156/65 mm Hg, and an oxygen saturation by pulse oximetry (SpO2) of 91%. Admission blood chemistry showed mild hyponatremia, and an elevated brain natriuretic peptide of 199 ng/L (normal < 99 ng/L). Admission chest radiography taken before bilevel positive airway pressure (BIPAP) showed focal pneumonia in the right lower lung, a widened mediastinum, and enlargement of the cardiac silhouette. Due to respiratory distress, the patient was transitioned from a 50% facemask to BIPAP (settings: FIO2= 50%, 8/4 cm H2O, 14 BPM) and became agitated shortly after. To mitigate her agitation, she was administered dexmedetomidine, without a bolus, at a starting dose of 0.2 μg/kg/hr, and continued on doses ranging from 0.2 to 0.5 μg/kg/hr titrated to a sedation scale. The patient received dexmedetomidine for a total of 40 h. After 1 h the dexmedetomidine was given, the patient was no longer agitated, with a Ramsey Score of three. Her vital signs showed no significant hemodynamic changes 2 h post-dexmedetomidine initiation, while her respiratory rate returned to normal (19 breaths per minute) and SpO2 increased to 97%. The patient did not experience bradycardia or hypotension, which are possible side effects of dexmedetomidine. The echocardiogram while on dexmedetomidine and BIPAP showed an ejection fraction of 60-65%, trace mitral and tricuspid regurgitation, and moderate to severe aortic stenosis. After discontinuation of the dexmedetomidine infusion, and given the previous agitation, haloperidol 1 mg every 6 h intravenously was given for an additional 2 days to maintain the non-agitated state. The total length of non-invasive ventilation was 3 days and 14 h. The patient was neither intubated nor received invasive mechanical ventilation, and was discharged from the hospital and ICU without other respiratory complications.