From Ask Dr Wiki
Mechanism of action
- Non-selective beta blockers antagonizes both beta1 and beta2 receptors thus inhibiting the effects of catecholamines on these receptors
- Cardiovascular effects include
- Reduced contractility
- Decreased heart rate
- Non-cardiovascular effects mediated through beta2 blockade include potential to increase peripheral vascular resistance or bronchospasm
Therapeutic uses
- Angina
- Arrhythmias
- Hypertension
- Hyperthyroidism
- Migraine
- Post myocardial infarction
- Tremor
Dose
- Initial dose: 40 – 80 mg PO daily
- Maximum dose: 320 mg PO daily
- Use lower doses in patients with renal dysfunction
Contraindications
- Hypersensitivity to beta blockers
- Asthma
- Heart block greater than first degree
- Insulin dependent diabetics with frequent hypoglycemic episodes
- Overt heart failure/cardiogenic shock
- Severe bradycardia
Side effects
- Fatigue
- Bradycardia
- Heart block
- Bronchospasm
- Depression
- Lipid abnormalities
- May mask the symptoms of hypoglycemia
- Rebound effect with abrupt discontinuation
- Precipitation of heart failure
- Impotence
Drug interactions (not inclusive)
- Medications that slow AV nodal conduction such as
- Digoxin
- Diltiazem
- Verapamil
- Amiodarone
- Other beta blockers
- Non-steroidal anti-inflammatory drugs
- Other medications that lower blood pressure
- Other medications that produce a decrease in contractility
- Medications that inhibit the CYP 2D6 enzyme
Comments
- Patients should be informed that they should not stop taking beta blockers abruptly because this can lead to a rebound effect.
- Diabetic patients should be informed that they need to monitor their blood glucose more frequently when starting a beta blocker since beta blockers can mask signs and symptoms of hypoglycemia
- Patients with bronchospastic lung disease should not receive beta blockers unless the benefits outweigh the risks
Pharmacokinetics
- Onset: 1-2 hours
- Half-life: 20 – 24 hours
- Elimination: renal
- Lipid solubility: low
