A 52-year-old man with a history of myocardial infarction 3 months prior presents to his cardiologist with persistent hypertension (BP 158/94 mmHg) and recurrent anginal chest pain. His resting heart rate is 78 bpm. Metoprolol succinate 25 mg daily is initiated for cardioprotection and blood pressure control. One week later, he returns with new-onset fatigue, dyspnea with minimal exertion, and bilateral ankle edema. On examination: heart rate 48 bpm, BP 132/82 mmHg, bibasilar crackles on lung auscultation. Laboratory findings show BNP 520 pg/mL (normal <100). Repeat echocardiography reveals ejection fraction has declined from 45% to 38%. Which of the following best explains this acute clinical deterioration?
- A)Reflex tachycardia from unopposed alpha-adrenergic activity causing increased myocardial oxygen demand
- B)Acute hyperkalemia from beta-2 adrenergic blockade leading to conduction abnormalities
- C)Progressive coronary vasospasm triggering recurrent myocardial infarction in the periinfarction period
- D)Excessive afterload reduction with metoprolol succinate causing compensatory ventricular remodeling
- E)Negative inotropic effect of beta blockade precipitating acute decompensated heart failure in vulnerable myocardiumGABARITO
Explicação
Beta blockers produce negative inotropic effects by decreasing intracellular cAMP, reducing cardiac contractility. In a post-MI patient with marginal ventricular function (EF 45%), the sudden initiation of beta blockade can precipitate acute decompensated hear... Ver explicação completa e trilha adaptativa →