| Class | Class Ib antiarrhythmic |
|---|---|
| Chemistry |
Aminoamide |
| Routes of administration |
IV, inhaled, subcutaneous |
| Absorption |
Oral bioavailability = 35% |
| Solubility |
pKa = 7.9; about 25% is not ionised at pH 7.4 |
| Distribution |
VOD= 0.9L/kg; 70% protein-bound |
| Metabolism |
Hepatic metabolism (90-95%) |
| Elimination |
Minimally renally excreted; half-life 10-20 minutes following IV bolus, closer to 45-90 minutes with subcutaneous infiltration |
| 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 |
Regional anaesthesia, by differential block (pain and temperature finres are blocked earlist). With higher doses, also motor block. In toxicity, CNS effects (visual disturbances, perioral mumbness, delirium,seizures, coma) and cardiovascular side effects (initially tachycardia and hypertension followed by bradycardia, negative inotropy, vasodilation and arrhythmias) Does not prolong the QRS, and actually shortens the QT. |
| Clinical effects |
Antiarrhythmic effect, analgesic and local anaesthetic effects. Lowers seizure threshold, causes CNS excitation. Does not prolong the QRS, and actually shortens the QT. |
| Literature reference |
Weinberg et al (2015) |
| CICM details of understanding | Level 1 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 1 from the first paper of 2019 Question 17 from the first paper of 2014 Question 9 from the second paper of 2012 |