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Beta-Blocker in Acute Decompensated Heart Failure

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Beta-Blocker in Acute Decompensated Heart Failure

A 72-year-old man with HFrEF (EF 28%) on carvedilol 12.5 mg BID, sacubitril/valsartan, spironolactone, and furosemide presents with 3 days of worsening dyspnea. He is orthopneic, has bibasilar crackles to mid-lung, JVP elevated, and 2+ bilateral edema. BP 98/62 mmHg, HR 88 bpm, SpO2 90% on room air. Creatinine 1.9 mg/dL (baseline 1.3), potassium 5.1 mmol/L. He gained 4 kg. He is not in cardiogenic shock, has no altered mentation, and is making urine. The resident asks whether to stop carvedilol, hold sacubitril/valsartan, and whether spironolactone should continue given the potassium.

1. Should carvedilol be discontinued, held, or continued? Justify using the physiology of decompensation.

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Continue carvedilol at the current dose in this patient. He is not in cardiogenic shock, is hemodynamically stable (BP 98/62, HR 88, adequate mentation, making urine), and beta-blockade is a mortality-reducing therapy in HFrEF. Abrupt discontinuation risks rebound tachycardia, ischemia, and arrhythmia, and is associated with worse outcomes. The exam distinction: beta-blockers are held or reduced in cardiogenic shock, severe hypotension, symptomatic bradycardia, or worsening congestion attributable to the beta-blocker. Here the decompensation is volume/afterload-driven, not beta-blocker-driven. The correct action is to treat the congestion (increase diuresis) rather than withdraw a disease-modifying drug. Nuance: if hypotension becomes limiting or the patient develops low-output signs, reduce the dose; do not stop abruptly. Down-titration, not discontinuation, is the fallback.

2. Address the sacubitril/valsartan and spironolactone decisions, including the potassium and creatinine changes. What monitoring would you order?

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Sacubitril/valsartan: Hold or reduce during acute decompensation with hypotension (BP 98/62) and AKI (Cr 1.9 from 1.3). ARNI/ACEi/ARB are typically held in acute decompensated HF with hypotension or worsening renal function, then restarted once euvolemic and stable. Do not restart until BP and renal function recover. Spironolactone: K 5.1 with AKI is a relative contraindication. MRA raises hyperkalemia risk, especially with reduced eGFR and concurrent ARNI. Hold spironolactone until K < 5.0 and renal function improves; recheck K and Cr in 24–48 h. Monitoring: daily BMP (K, Cr, Mg), daily weights, strict I/O, renal function before/after diuretic escalation, and reassess BP. Consider whether loop diuretic dose needs increase for the 4 kg gain. The teaching point: in ADHF, hold RAAS/MRA agents that worsen hypotension/hyperkalemia/AKI, but continue beta-blockers unless shock or rate-limiting bradycardia.