Class I antiarrhythmics

Pasted image 20240317145409.png The key here is to separate the effects of sodium channels and potassium channels.

Sodium channel blockage = slow depolarization + wide QRS + long QT
Potassium channel blockage = prolonged APD + prolonged ERP. Both of these blocking effects can treat rapid cardiac arrhythmias. Class IA is 1+2, Class IC is only 1 (strongly). However, Class IB is different from the first two as it promotes potassium outflow, thus shortening APD and ERP and increasing ERP:APD ratio

Class III antiarrhythmics

Tip

Amiodarone has both Class I, II, III & IV actions!

Primary mechanism of action: antiarrhythmic effect via blockage of voltage-gated potassium channels → prolonged repolarization of the cardiac action potential
Secondary mechanism of action: inhibits β-receptors and sodium and calcium channels → decreases conduction through the AV and sinus node
Special uses: only antiarrhythmic agent with (almost) no negative inotropic effect → use in patients with reduced EF

Mechanism of action: activates Gi protein → inhibition of adenylate cyclase → ↓ cAMP → deactivation of L-type Ca²⁺ channels and activation of K⁺ channels → ↓ Ca²⁺ and ↑ K⁺ efflux → hyperpolarization → transient AV node block (short-acting, ∼ 15 seconds) → acute termination of supraventricular tachycardia
Indications
- Diagnosis and termination of certain forms of paroxysmal supraventricular tachycardias (e.g., AVNRT and orthodromic AVRT)
- Diagnosis of underlying AFib in supraventricular tachyarrhythmias
Adverse effects
- Chest pain, flushing, hypotension, bronchospasm
- Sense of impending doom
- AV block, asystole