Hypertensive Emergency in the Context of SARS-CoV-2 Infection: Clinical Course and Management

Coronavirus Disease2019 (COVID-19) can increase sympathetic nervous system activity by inducing systemic inflammation and a cytokine storm. This can result in elevated blood pressure, increased heart rate, and vasoconstriction. A 67-year-old Black male was admitted to the emergency department with a chief complaint of shortness of breath for 2 days. On examination, he exhibited edema and symmetric palpable pulses in his lower limbs. His electrocardiogram revealed left axis deviation, sinus tachycardia, and ST-segment elevation. Reverse transcription-polymerase chain reaction confirmed COVID-19. Hydralazine (5 mg) was administered intravenously immediately. The patient was re-evaluated after 20 min during his stay in the emergency department. After two 5 mg doses of hydralazine, he developed reflex tachycardia. To control heart rate, IV hydralazine was replaced with oral atenolol (50 mg once daily), a β₁-blocker that reduces cardiac output. Subcutaneous enoxaparin 80 mg daily was given to prevent thrombotic complications in hospitalized COVID-19 patients. Acute hypertension and COVID-19-induced hypertensive emergencies in patients with preexisting hypertension are typically associated with a worse prognosis.