It binds to sodium channels and slowly detaches from sodium channels.
Mechanism of action:
It is a sodium channel blocker. It suppresses phase 0 of action potential in purkinje fibers and fibers of the muscles of the heart.
Actions:
It does not affect greatly the action potential.
1. In this case, automaticity of the ectopic pacemaker is decreased by the promoted threshold potential (not by a reduction in the slope of phase 4 depolarization).
2. It causes a decreased conduction and excitability and promoted refractory period (pronounced in the depolarized tissue).
Pharmacokinetics:
It is absorbed orally and it has a half life of about 16-20 hours.
Therapeutic uses:
1. It is used in premature ventricular contractions, refractory ventricular tachycardia and supraventricular tachycardia.
2. It is used for the inhibition of sudden outburst of atrial fibrillation or flutter.
Adverse effects:
It may cause dizziness, blurred vision, anorexia, nausea, vomiting, impotence and in some cases may worsen preexisting arrhythmias.
Sunday, March 6, 2011
Mexiletine and tocainide
Phenytoin
Antiarrhythmic action
Its effects are almost same to that of lidocaine
1. It depresses unprovoked automaticity in atrial and ventricular tissues although it does no affect on intraventricular conduction.
2. It causes a promoted conduction through impaired purkinje fibers.
3. It is especially useful for ventricular arrhythmias related to digitalis toxicity or myocardial ischemia.
Its effects are almost same to that of lidocaine
1. It depresses unprovoked automaticity in atrial and ventricular tissues although it does no affect on intraventricular conduction.
2. It causes a promoted conduction through impaired purkinje fibers.
3. It is especially useful for ventricular arrhythmias related to digitalis toxicity or myocardial ischemia.
Lidocaine
It is a local anesthetic containing amide in structure.
Mechanism of action:
They act fast on sodium channels and also get detached from sodium channels rapidly. It shortens Phase 3 repolarization and blocks sodium channels and has the ability of shortening the duration of action potential.
Actions:
Due to short duration of action potential it prolongs diastole. On the other hand, it decreases the effective refractory period of purkinje fibers.
Therapeutic uses:
It is used for ventricular arrhythmias during open heart surgery, digitalis toxicity and myocardial ischemia.
It is used as local anesthesia.
Pharmacokinetics:
It undergoes first pass metabolism by the liver, so that is why it is given intravenously. In the liver, the drug is dealkalyted and approximately the entire drug is excreted by the liver.
Adverse effects:
It may cause paresthesias, hypotension, tremor, drowsiness, convulsions and respiratory arrest.
Administration and Dosage:
It is given IV with a loading dose of 150-200 mg in 15 minutes succeeded by maintenance dose of 2-4 mg/min.
Mechanism of action:
They act fast on sodium channels and also get detached from sodium channels rapidly. It shortens Phase 3 repolarization and blocks sodium channels and has the ability of shortening the duration of action potential.
Actions:
Due to short duration of action potential it prolongs diastole. On the other hand, it decreases the effective refractory period of purkinje fibers.
Therapeutic uses:
It is used for ventricular arrhythmias during open heart surgery, digitalis toxicity and myocardial ischemia.
It is used as local anesthesia.
Pharmacokinetics:
It undergoes first pass metabolism by the liver, so that is why it is given intravenously. In the liver, the drug is dealkalyted and approximately the entire drug is excreted by the liver.
Adverse effects:
It may cause paresthesias, hypotension, tremor, drowsiness, convulsions and respiratory arrest.
Administration and Dosage:
It is given IV with a loading dose of 150-200 mg in 15 minutes succeeded by maintenance dose of 2-4 mg/min.
Amiodarone
Amiodarone contains iodine and is structurally related to thyroxine. It shows the affects of all classes i.e. class I, II, III and IV.
Mechanism of action:
Amiodarone blocks the sodium channels in inactivated state. It also blocks the calcium channels but to a less extent. It also noncompetitively inhibits α- and β- adrenoceptors.
Actions:
Its dominant action is the increase in duration of action potential. It also causes an increase in effective refractory period in the atrial and ventricular muscles.
It causes an increase in PR, QRS and QT intervals.
It causes a decrease in sinus rate and AV conduction as well as systemic and coronary vasodilation.
Pharmacokinetics:
It is not well absorbed orally. It has a prolonged half life of about 20-100 days and distributes mostly into adipose tissues. Its full effects are seen after 6 weeks of start of treatment.
Therapeutic uses:
It is used in
1. Angina
2. Premature ventricular contractions
3. Ventricular tachyarrhythmia
4. Refractory supraventricular arrhythmias
5. Arrhythmias in patients with wolf Parkinson white syndrome
Adverse effects:
It may cause gastrointestinal intolerance (nausea, vomiting, and constipation), headache, dizziness, paresthesias, pulmonary fibrosis and blue skin discoloration (due to the increased concentration of iodine in the skin).
Mechanism of action:
Amiodarone blocks the sodium channels in inactivated state. It also blocks the calcium channels but to a less extent. It also noncompetitively inhibits α- and β- adrenoceptors.
Actions:
Its dominant action is the increase in duration of action potential. It also causes an increase in effective refractory period in the atrial and ventricular muscles.
It causes an increase in PR, QRS and QT intervals.
It causes a decrease in sinus rate and AV conduction as well as systemic and coronary vasodilation.
Pharmacokinetics:
It is not well absorbed orally. It has a prolonged half life of about 20-100 days and distributes mostly into adipose tissues. Its full effects are seen after 6 weeks of start of treatment.
Therapeutic uses:
It is used in
1. Angina
2. Premature ventricular contractions
3. Ventricular tachyarrhythmia
4. Refractory supraventricular arrhythmias
5. Arrhythmias in patients with wolf Parkinson white syndrome
Adverse effects:
It may cause gastrointestinal intolerance (nausea, vomiting, and constipation), headache, dizziness, paresthesias, pulmonary fibrosis and blue skin discoloration (due to the increased concentration of iodine in the skin).
Saturday, March 5, 2011
Disopyramide
Mechanism of action:
Similar to quinidine
Actions:
It also possesses properties of class III agents.
It has same actions as that of quinidine but it is more pronounced in causing anti-muscarinic actions. It causes peripheral vasoconstriction and produces negative inotropic effects.
It causes a prominent decline in myocardial contraction in patients whose left ventricular function has already been impaired.
Therapeutic uses:
Ventricular arrhythmias
Pharmacokinetics:
It is taken orally and about 50 percent of the drug is excreted without any change through the kidneys. It has been found that about 30 percent of the drug is metabolized in the liver into mono-N-dealkylated metabolite.
Adverse effects:
It causes anticholinergic effects such as constipation, dry mouth, retention of the urine and blurred vision. It may also cause hypotension.
Contraindications:
It is contraindicated for patients with
1. 2nd or 3rd degree AV block
2. cardiogenic shock
3. severe uncompensated cardiac failure
Dosage:
It is given 300-800 mg daily in divided doses.
Similar to quinidine
Actions:
It also possesses properties of class III agents.
It has same actions as that of quinidine but it is more pronounced in causing anti-muscarinic actions. It causes peripheral vasoconstriction and produces negative inotropic effects.
It causes a prominent decline in myocardial contraction in patients whose left ventricular function has already been impaired.
Therapeutic uses:
Ventricular arrhythmias
Pharmacokinetics:
It is taken orally and about 50 percent of the drug is excreted without any change through the kidneys. It has been found that about 30 percent of the drug is metabolized in the liver into mono-N-dealkylated metabolite.
It causes anticholinergic effects such as constipation, dry mouth, retention of the urine and blurred vision. It may also cause hypotension.
It is contraindicated for patients with
1. 2nd or 3rd degree AV block
2. cardiogenic shock
3. severe uncompensated cardiac failure
Dosage:
It is given 300-800 mg daily in divided doses.
Procainamide
It is a derivative of procaine which is a local anesthetic.
Mechanism of action:
Same as that of quinidine
Actions:
Cardiac effects:
Almost similar to quinidine.
It decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
However unlike quinidine it has less effecient antimuscarinic action.
Due to its ganglionic receptor blocking properties, it results in more pronounced negative inotropic effects than quinidine.
It instigates serious CCF in patients with already ventricular dysfunction.
Other effects:
It reduces peripheral vascular resistance and may cause hypotension due to its ganglionic blocking properties.
Procainamide is well-absorbed orally.
Its half life is 2 – 3 hours. Some of the procainamide is metabolized in the liver into N-acetylprocainamide (NAPA). NAPA has the same properties as that of class III agents as it prolongs the duration of action potential.
It is used in atrial and ventricular arrhythmias and ventricular arrhythmias which comes with acute myocardial infarction.
Adverse effects:
It may cause mental confusion, anorexia, nausea, urinary retention and hepatitis. After prolonged use, it may cause reversible form of lupus erythematosus like syndrome in 20-30 percent of patients. Its toxic dose may cause asystole or instigation of ventricular arrhythmias.
Its effects on CNS include depression, hallucination and psychosis.
Contraindications:
It is contraindicated in patients with AV block or systemic lupus erythematosus.
Dosage:
It is given up to 50 mg/kg daily in divided doses every 3 to 6 hours.
Mechanism of action:
Same as that of quinidine
Actions:
Cardiac effects:
Almost similar to quinidine.
It decreases ectopic pacemaker rate, conduction velocity (negative dromotropism) and excitability especially in depolarized tissue. By decreasing conduction velocity (negatively dromotropic) it causes a promoted effective refractory period in atrial, ventricular and Purkinje fibers.
However unlike quinidine it has less effecient antimuscarinic action.
Due to its ganglionic receptor blocking properties, it results in more pronounced negative inotropic effects than quinidine.
It instigates serious CCF in patients with already ventricular dysfunction.
Other effects:
It reduces peripheral vascular resistance and may cause hypotension due to its ganglionic blocking properties.
Pharmacokinetics:
Procainamide is well-absorbed orally.
Its half life is 2 – 3 hours. Some of the procainamide is metabolized in the liver into N-acetylprocainamide (NAPA). NAPA has the same properties as that of class III agents as it prolongs the duration of action potential.
Therapeutic uses:
It is used in atrial and ventricular arrhythmias and ventricular arrhythmias which comes with acute myocardial infarction.
Adverse effects:
It may cause mental confusion, anorexia, nausea, urinary retention and hepatitis. After prolonged use, it may cause reversible form of lupus erythematosus like syndrome in 20-30 percent of patients. Its toxic dose may cause asystole or instigation of ventricular arrhythmias.
Its effects on CNS include depression, hallucination and psychosis.
Contraindications:
It is contraindicated in patients with AV block or systemic lupus erythematosus.
Dosage:
It is given up to 50 mg/kg daily in divided doses every 3 to 6 hours.
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