| Indication |
For the treatment of ventricular pre-excitation and cardiac dysrhythmias |
| Pharmacodynamics |
Quinidine, a hydantoin anticonvulsant, is used alone or with
phenobarbital or other anticonvulsants to manage tonic-clonic seizures,
psychomotor seizures, neuropathic pain syndromes including diabetic
neuropathy, digitalis-induced cardiac arrhythmias, and cardiac
arrhythmias associated with QT-interval prolongation. |
| Mechanism of action |
Quinidine acts on sodium channels on the neuronal cell membrane,
limiting the spread of seizure activity and reducing seizure
propagation. The antiarrhythmic actions are mediated through effects on
sodium channels in Purkinje fibers. Quinidine may also act on the slow
inward calcium current (ICa), the rapid (IKr) and slow (IKs) components
of the delayed potassium rectifier current, the inward potassium
rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and
Ito. |
| Absorption |
Not Available |
| Volume of distribution |
- 2 to 3 L/kg
- 0.5 L/kg [congestive heart failure]
- 3 to 5 L/kg [cirrhosis of the liver]
|
| Protein binding |
80-88% |
| Metabolism |
Not Available |
| Route of elimination |
When the urine pH is less than 7, about 20% of administered
quinidine appears unchanged in the urine, but this fraction drops to as
little as 5% when the urine is more alkaline. |
| Half life |
6-8 hours |
| Clearance |
|
| Toxicity |
Not Available |
