Beta Blockers Mnemonic for Effective Learning

β-blockers bind to Gs proteins and inhibit the formation of cAMP from ATP. This prevents intracellular flow of Ca2+ and leads to decreased Ca2+ currents by the sarcoplasmic reticulum of the heart. This translates into decreased heart contractility.

Beta-blockers decrease sinoatrial (SA) and atrioventricular (AV) node conduction velocity, which means they decrease dromotropy. It is for this reason that they can be indicated for supraventricular tachycardia (SVT), ventricular tachycardia, atrial fibrillation, and atrial flutter. It is also for this reason that they are generally contraindicated in patients with heart block, or AV conduction delay, regardless of 1st-, 2nd-, or 3rd-degree.

These drugs typically are NOT first-line antihypertensive agents. Beta-blockers work to decrease blood pressure in multiple ways. First, their beta-blockade leads to decreased chronotropy and inotropy, meaning that the heart has a lower cardiac output, contributing to lower blood pressure, and requiring less oxygen in the process. Secondly, beta-blockers decrease renin secretion, which in turn reduces extracellular volume, further lowering blood pressure, and also decreasing myocardial oxygen demand.

By inhibiting the chronotropic and inotropic sympathetic effects of β-adrenergic receptors, the workload of the heart is decreased. This leads to decreased O2 consumption (through decreased myocardial oxygen demand), making β-blockers an important medication class for treating angina.

Beta-blockers such as metoprolol, atenolol and bisoprolol are specifically used after myocardial infarctions and have been proven to decrease mortality and morbidity in these patients.