propranolol

General Information

Propranolol is a nonselective beta-adrenergic receptor blocker used for multiple cardiovascular and neurologic indications (hypertension, angina, atrial fibrillation rate control, post-myocardial infarction mortality reduction, migraine prophylaxis, essential tremor, and others on label).

In psychiatric practice, propranolol is most commonly used off label for performance anxiety and for antipsychotic-associated akathisia, where it targets tremor, tachycardia, and physiologic arousal.

Propranolol generally does not treat the core cognitive features of generalized anxiety (worry/rumination); it should not replace psychotherapy or SSRI/SNRI-based plans when anxiety is persistent.

Safety is driven by cardiopulmonary screening: propranolol is contraindicated in bronchial asthma and in significant bradycardia or conduction block (label). It can also worsen hypotension and fatigue.

Beta blockade can mask adrenergic symptoms of hypoglycemia; coordinate care in diabetes and counsel patients who have recurrent hypoglycemia.

The propranolol compare view, propranolol evidence feed, and propranolol print page can support safe, time-limited prescribing discussions.

Propranolol is inexpensive and familiar to clinicians, which can lead to “refill momentum” for off-label anxiety use. Keep prescribing indication-specific (event-limited performance anxiety or akathisia treatment plans) and reassess frequently; when anxiety is chronic, prioritize psychotherapy and SSRI/SNRI strategies.

Mechanism of Action

Refer to the Glossary entry on Neurotransmitters for background on receptor systems involved in serious mental illness.

Nonselective beta-adrenergic antagonism reduces sympathetic physiologic responses (tachycardia, tremor, palpitations) and can blunt the physical feedback loop that escalates situational anxiety.

In akathisia, beta blockade can reduce subjective restlessness and motor agitation, but symptom control should be paired with antipsychotic dose/timing optimization.

Beta blockers can reduce exercise tolerance and cause fatigue; these effects may be misattributed to depression or medication “over-sedation” unless discussed proactively.

• Beta-1 and beta-2 adrenergic receptor antagonism.

Metabolism and Pharmacokinetics

• Highly lipophilic and almost completely absorbed, but undergoes high first-pass hepatic metabolism; on average ~25% reaches systemic circulation (label).
• Plasma elimination half-life is 3–6 hours; half-life can be prolonged in older adults and hepatic impairment (label).
• Metabolized via multiple CYP pathways (notably CYP2D6, CYP1A2, and CYP2C19) with direct glucuronidation; enzyme inhibitors can increase exposure (label).

Dosing and Administration

• Label dosing varies widely by indication (hypertension, arrhythmias, migraine prophylaxis). In psychiatric use, dose selection should be tied to the specific target symptom and the patient’s cardiopulmonary risk.
• Performance anxiety (off label): low single doses taken before a time-limited event are common; start low and confirm tolerability with a trial dose (monitor heart rate, blood pressure, and dizziness).
• Akathisia (off label): dosing strategies vary; use the lowest effective dose and reassess response alongside antipsychotic dose adjustments.
• Avoid abrupt discontinuation after sustained use, especially in patients with coronary disease risk; taper over days to weeks depending on dose and duration (label).

Monitoring & Labs

• Check baseline heart rate, blood pressure, and asthma/COPD history before starting.
• Monitor bradycardia, hypotension, dizziness, and fatigue after dose changes.
• Reassess mood and sleep after initiation; discontinue or adjust if adverse effects outweigh benefit.
• Taper rather than stopping abruptly after sustained use, especially in coronary disease risk.

Sources: FDA/DailyMed label; beta-blocker anxiety meta-analyses; akathisia trial evidence.

Adverse Effects

Interactions

• Additive bradycardia/hypotension with other rate-lowering agents (verapamil, diltiazem, digoxin) and with antihypertensives.
• CYP-mediated interactions: strong CYP2D6 inhibitors (e.g., fluoxetine, paroxetine, quinidine) and other enzyme modulators can increase propranolol exposure (label).
• Alcohol and sedatives can amplify dizziness and fall risk.

Other Useful Information

• For performance anxiety, emphasize “trial dosing” ahead of a high-stakes event and avoid use in patients with asthma, marked bradycardia, or conduction disease.
• For akathisia, combine propranolol with antipsychotic strategy changes (dose reduction, agent switch, timing changes) when feasible.
• If anxiety is generalized and persistent, prefer psychotherapy and SSRI/SNRI strategies; use beta blockers for targeted physiologic symptoms.

References

1. Propranolol hydrochloride tablets prescribing information — DailyMed (2025)
2. Propranolol for the treatment of anxiety disorders — Journal of Psychopharmacology (2016)
3. Beta Blockers FOR THE Treatment OF Anxiety Disorders — Journal of Affective Disorders (2025)
4. Neuroleptic Induced Akathisia — Propranolol Versus Benztropine — Biological Psychiatry (1988)