A state-of-the-art review in Intensive Care Medicine (August 2026) examines beta-blockade as a way to temper the sustained adrenergic response of critical illness, which can drive tachyarrhythmia, myocardial injury and organ dysfunction.
The authors find established benefit in acute myocardial infarction, tachyarrhythmias, hypertensive emergencies, thyroid storm and prevention of variceal bleeding. In septic shock, traumatic brain injury, acute heart failure and burns the evidence is limited or conflicting. The risks are loss of compensatory tachycardia, reduced cardiac output, hypotension and impaired perfusion.
They stress that effect depends on the drug and dose, the patient's haemodynamic reserve, timing, and whether a beta-blocker is being continued, stopped and restarted, or started new. There are no reliable markers to identify who will benefit.
For the emergency physician, the practical message is to separate the settings: treat thyroid storm and rapid AF with a beta-blocker where appropriate, but do not reach for one to slow the compensatory tachycardia of a septic or bleeding patient.
- Use beta-blockers where benefit is established: acute MI, tachyarrhythmia, hypertensive emergency, thyroid storm
- Do not slow a compensatory sinus tachycardia in sepsis, haemorrhage or hypovolaemia
- Assess volume status and cardiac output before rate control in the shocked patient
- Decide deliberately whether to continue, hold or restart a patient's long-term beta-blocker
- Prefer short-acting, titratable agents such as esmolol where haemodynamics are uncertain
Why it matters
It separates the settings where beta-blockade helps from those where its use is still experimental.
Don't overread it
This is a narrative review; it does not establish a role for beta-blockers in septic shock.
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