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Lidocaine's MOA is by blocking Na+ Channel

Mechanism of Action:

1. As an antiarrhythmic: Will block fast Na+ channels in their inactivated state(that is M gate is open while H gate is closed) results in an increased threshold for excitation and less excitability of hypoxic muscle.

Also will block the Na+ window current and will result in lowering of the action potential duration.

It is preferred in ventricular arrhythmias becasue:

  1. Less toxic than other drugs
  2. Has a rapid onset of action but wears off quickly on stoping iv
  3. Has no action on AV Nodal conduction velocity hence does not intensify the AV Block during treatment of ventricular arrhytmias due to digoxin toxicity
  4. Mainly preferred in ventricular arrhythmias associated with MI so that can help the hypoxic tissue

2. As a local anesthetic: Will enter nerve terminals in unionized form and become reionized inside the nerve terminal and this re-ionized form will block the Na+ Channel from inside so no entry of Na+ means no depolarization so no impulse, local anesthesia

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