| Class | Class Ic antiarrhythmic |
|---|---|
| Chemistry |
monocarboxylic acid amide |
| Routes of administration |
Oral |
| Absorption |
Excellent GI absorption (90%); bioavailability is ~ 95% |
| Solubility |
pKa = 9.3; mainly water soluble at physiological pH |
| Distribution |
VOD = 8.7 L/kg; 40% protein-bound |
| Metabolism |
70% of a dose undergoes hepatic metabolism (and some people are slow metabolisers) |
| Elimination |
30% is excreted renally as unchanged drug; half-life is about 20 hours |
| Time course of action |
Duration of action is similar to half-life |
| Target receptor |
Nav1.5 subunit of the fast voltage-gated sodium channels |
| Mechanism of action |
Acts by blocking voltage-gated sodium channels, particularly during Phase 0, thereby increasing the duration of Phase 0 without much effect on the total duration of the cardiac action potential |
| Clinical effects |
Antiarrhythmic effect, analgesic and local anaesthetic effects. Prolongs the QRS but not the QT. Increases mortality in heart failure patients |
| Literature reference |
TGA PI |
| CICM details of understanding | Level 3 |
| Mentioned around Deranged Physiology |
Class I antiarrhythmic agents and classification of antiarrhythmic agents, as it is not special enough to warrant its own entry. |
| Related SAQs |
Question 9 from the second paper of 2012, diffusely. |