Propranolol

Heart rate reduction is the mechanism, not just a side effect. Check resting heart rate before starting and with dose changes. Reduce dose or hold if HR falls below a clinically acceptable threshold.

Blood pressure reduction is expected. Usually mild at psychiatric doses (10-80mg/day), but monitor in patients on concurrent antihypertensives or those prone to orthostasis.

Beta-blockade reduces cardiac output and sympathetic tone. Some patients report reduced energy or exercise intolerance. Usually mild at lower doses used in psychiatry.

β2 blockade causes peripheral vasoconstriction. Patients may notice cold hands and feet. Usually mild.

Propranolol's lipophilicity allows CNS penetration. Some patients report vivid dreams, nightmares, or disrupted sleep. Less common with hydrophilic beta-blockers (atenolol).

β2 blockade can provoke bronchospasm in patients with asthma or reactive airway disease, and can blunt response to β2-agonist rescue inhalers. Screen all patients for respiratory history before prescribing. When beta-blockade is needed in patients with respiratory disease, β1-selective agents carry lower risk.

Beta-blockade suppresses the tachycardia that normally alerts diabetic patients to hypoglycemia. Sweating (a cholinergic response, not adrenergic) is preserved. Counsel diabetic patients about this risk.

Abrupt cessation of chronic propranolol can cause rebound tachycardia, hypertension, and in patients with coronary artery disease, angina or myocardial infarction. Always taper gradually. Not clinically significant after single PRN doses.

The association between beta-blockers and depression has been taught for decades but more recent reviews suggest it may be overstated. Monitor mood, but do not avoid propranolol solely on the basis of depression history without weighing the clinical benefit.