Class II antiarrhythmics: beta-blockers and the PR interval
Class II antiarrhythmic drugs (for rhythm disturbances) are beta-blockers, which block the effects of adrenaline and noradrenaline at beta-receptors in the heart, reducing sympathetic drive (the 'fight or flight' stimulation).
Remember
Beta-blockers slow the sinoatrial (SA) node, the heart's natural pacemaker, and the atrioventricular (AV) node, the electrical relay between the upper and lower chambers, so the heart rate falls and the PR interval (measured on the ECG from the start of the P wave to the start of the QRS complex), which mostly reflects the delay in the AV node, gets longer.
Mnemonic
Some Block Potassium Channels
- S Sodium
- B Beta-blocker
- P Potassium
- C Calcium
The first letters, in order, give the classes of antiarrhythmic drug, so the beta-blocker comes second, as Class II.
Sympathetic stimulation normally speeds the pacemaker and the AV node. A beta-blocker reduces that drive. In pacemaker tissue, phase 4 depolarisation is the slow spontaneous rise in membrane potential between beats, and it sets the heart rate. With less sympathetic drive that rise is slower, so the sinoatrial node fires less often and the heart rate falls.
The same reduction in drive slows conduction (the passage of the impulse) through the AV node. The PR interval on the ECG mostly reflects the delay in the AV node, so a slower AV node gives a longer PR interval. Beta-blockers lengthen the PR interval and reduce heart rate.
Sympathetic stimulation also raises cyclic AMP (a messenger molecule inside the cell), and cyclic AMP increases calcium entry. A beta-blocker weakens that chain, so cyclic AMP falls and less calcium enters.
Slowing the AV node helps in supraventricular tachycardia (a fast rhythm arising above the ventricles), which often depends on the AV node, because a slower node limits how fast impulses reach the ventricles. Beta-blockers such as bisoprolol, atenolol, metoprolol and propranolol can be used when the AV node needs to be slowed.
Key facts
- Main action
- Beta-blockers reduce sympathetic drive to the sinoatrial and AV nodes.
- Pacemaker effect
- Phase 4 depolarisation is slower in pacemaker tissue, so the heart rate falls.
- AV node effect
- Conduction through the AV node is slower, so the PR interval is longer.
- Drugs
- Beta-blockers such as bisoprolol, atenolol, metoprolol and propranolol can be used when the AV node needs to be slowed.
- Good evidence
- Class II drugs are effective, generally safe, and have good evidence in supraventricular tachycardia.
- Side effect
- Bradycardia (a slow heart rate) is one of the usual side effects.
Exam traps
- A shortened PR interval due to faster conduction through the AV node is the opposite of what a beta-blocker does, because beta-blockers slow AV nodal conduction and lengthen the PR interval.
- Widening of the QRS complex (a sign that depolarisation of the ventricles is slowed) belongs to sodium channel blockers such as flecainide in Class I, because beta-blockers act mainly on the nodes and do not typically widen the QRS complex.
- Verapamil and diltiazem (Class IV drugs) also slow AV node conduction by reducing calcium entry, but they block the calcium channel itself, whereas a beta-blocker acts earlier, by reducing the sympathetic drive that raises cyclic AMP.
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