A state-of-the-art review weighs when to counter the sympathetic surge of critical illness with beta-blockers. Excess, sustained adrenergic drive can cause tachyarrhythmias, myocardial injury and organ dysfunction, but that drive is also adaptive, maintaining perfusion.
The review finds established benefit in selected scenarios, acute myocardial infarction, tachyarrhythmias, hypertensive emergencies, thyroid storm and prevention of variceal bleeding, but limited or conflicting evidence, and real hazard, in septic shock, traumatic brain injury, acute heart failure and burns, where beta-blockade can blunt compensatory cardiac output and perfusion.
The practical message is to resist a blanket approach. Safety depends on the agent, dose, timing, the patient's haemodynamic reserve, and whether this is continuation of chronic therapy versus de novo initiation in shock. Favour a phenotype-driven, physiology-guided decision, and be cautious about starting a beta-blocker de novo in a haemodynamically fragile patient.
- Beta-blockade has clear benefit in AMI, tachyarrhythmias, hypertensive emergency, thyroid storm and variceal-bleed prevention.
- Evidence is limited or conflicting in septic shock, traumatic brain injury, acute heart failure and burns.
- It can blunt compensatory cardiac output and perfusion in fragile patients.
- Decisions hinge on agent, dose, timing and haemodynamic reserve.
- Be cautious starting a beta-blocker de novo in shock; continuing chronic therapy differs from new initiation.
Why it matters
It replaces an all-or-nothing instinct about adrenergic control with a context-specific decision.
Don't overread it
This is a narrative review with limited randomised evidence in heterogeneous ICU populations; it guides judgement rather than setting a protocol.
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