Pseudoephedrine for refractory bradycardia and hypotension in patients with autonomic dysfunction

Introduction: Hypotension related to autonomic dysfunction presents a particular challenge in patients on vasopressors who are refractory to conventional measures. We describe a case of autonomic dysfunction where utilization of pseudoephedrine successfully increased blood pressure (BP) and heart rate (HR) and aided in discontinuation of vasopressors. Description: A 46-year-old male with history of chronic intranasal cocaine use and C5-C7 incomplete quadriplegia complicated by neurogenic orthostatic hypotension (on outpatient midodrine) and bradycardia, was admitted to the ICU for worsening bradycardia (HR 48 to 55 bpm) and hypotension (BP 60/40 mmHg). The patient required dopamine at a rate of 7.5 mcg/kg/min and midodrine 10 mg every 8 hours to maintain mean arterial pressures (MAPs) above 65 mmHg and a HR above 60 bpm. Cardiology deemed the etiology to be secondary to autonomic dysfunction. On day two of ICU admission, dopamine was weaned to 5 mcg/kg/min, leading to HRs in the 50s and systolic BPs in the 70s. A recommendation was made to add pseudoephedrine 60 mg every 6 hours. After two doses of pseudoephedrine, the patient tolerated dopamine at a rate of 2 mcg/kg/min, maintaining MAPs above 70 mmHg and systolic BPs above 90 mmHg. Less than 24 hours after initiation of pseudoephedrine, the patient was able to be fully weaned off dopamine. After three days of pseudoephedrine, the dose was titrated down to 30 mg every 6 hours with stable hemodynamics, and subsequently discontinued by hospital day 7. Discussion: Pseudoephedrine is an α1- adrenergic receptor agonist and also stimulates β-adrenergic receptors, leading to vasoconstriction, bronchodilation, increased HR and contractility. It has a rapid onset of action within 30 minutes, and peak effect 1-4 hours after absorption. This case highlights the utility of pseudoephedrine for refractory bradycardia and hypotension secondary to autonomic dysfunction, where discontinuation of vasopressors is a challenge. Given our patient’s history of chronic hypotension and bradycardia secondary to spinal cord injury and incomplete quadriplegia, pseudoephedrine was successfully added to his current regimen of midodrine to facilitate discontinuation of dopamine.