Multiple drugs

Abstract

Hypotension, hypertensive hypertrophic obstructive cardiomyopathy crisis and lack of efficacy: case report An 81-year-old woman developed hypotension following treatment with hydralazine, lisinopril, verapamil, labetalol and nicardipine for blood pressure control and hypertensive hypertrophic obstructive cardiomyopathy crisis following treatment with hydralazine, lisinopril, verapamil, hydrochlorothiazide, labetalol and nicardipine. Subsequently, she had exacerbation of the hypertensive hypertrophic obstructive cardiomyopathy crisis following administration of epinephrine, norepinephrine, phenylephrine and vasopressin to maintain adequate blood pressure and exhibited lack of efficacy during treatment with atropine and epinephrine for bradycardia [dosages not stated; not all routes stated]. The woman, who had type II diabetes mellitus, poorly controlled hypertension and stage III chronic kidney disease, admitted to the hospital with haemorrhagic lacunar intraparenchymal haematoma and non-hyperacute right cerebellar and basal ganglia stroke. An arterial line for invasive monitoring was placed and she was treated with oral hydralazine, hydrochlorothiazide, lisinopril, verapamil, nicardipine drip, IV hydralazine and IV labetalol to achieve targeted blood pressure. Initially, she achieved blood pressure control. However, she developed hypotension and experienced clinical heart failure. Therefore, vasopressor therapy with epinephrine, norepinephrine, vasopressin and phenylephrine was commenced. Subsequently, she was shifted to the ICU due to hypoxia and treatment resistant hypotension. Her vasopressor support escalated rapidly to maintain adequate blood pressure. But, she developed acute kidney injury due to shock and pulmonary oedema that required noninvasive positive pressure ventilation. Her transesophageal echocardiogram demonstrated moderate to severe asymmetric septal hypertrophy with moderate concentric hypertrophy of left ventricle (LV), left ventricular outflow tract (LVOT) outflow tract obstruction, 80% LV ejection fraction, systolic anterior motion of mitral valve with severe mitral regurgitation and calcification of the mitral leaflet and annulus. Based on these findings, she was diagnosed with hypertensive hypertrophic obstructive cardiomyopathy crisis secondary to aggressive blood pressure control therapy. Thereafter, her ICU stay complicated by bradycardia with junctional escape rhythm possibly due to metabolic derangements caused by verapamil that she received 24 hours prior to the rhythm change. Epinephrine and atropine were given for bradycardia. But, her heart rate (HR) was found to be 45 beats/minute, which was refractory to epinephrine and atropine. Thus, the woman underwent right internal jugular transvenous pacing wire placement into the right ventricle and her bedside echocardiography showed increase in the HR. Her continuous cardiac output monitoring confirmed improvement in her cardiomyopathy. Subsequently, norepinephrine was weaned off and she did not require any vasopressors or inotropes to maintain mean arterial pressure more than 65mm Hg. She tolerated diuresis and had resolution of acute kidney injury. After discontinuation of vasopressors and initiation of metoprolol, her optimized LVOT gradient reduced to 15mm Hg and she had complete resolution of the hypertensive hypertrophic obstructive cardiomyopathy crises [duration of treatments to reactions onsets not staed].