These are potassium channel blockers.
Actions:
They reduce the outward flow of potassium during repolarization phase of cardiac cells.
They have the ability of increasing the duration of action potential without changing Phase 0 of depolarization or the resting membrane potential.
They also have the ability of prolonging the effective refractory period.
Class III antiarrhythmic agents have the potential of induction of arrhythmias.
Sunday, March 6, 2011
Esmolol
It is one of the very short acting β-blocker.
Therapeutic uses:
It is used intravenously in acute arrhythmias that occur in surgical and emergency situations.
Therapeutic uses:
It is used intravenously in acute arrhythmias that occur in surgical and emergency situations.
Metoprolol
It is selective β1 blocker.
Therapeutic uses:
1. Hypertension
2. Angina pectoris (increase endurance to exercise)
Safe in patients with diabetes or peripheral vascular disease. It decreases the risk of bronchospasm.
Therapeutic uses:
1. Hypertension
2. Angina pectoris (increase endurance to exercise)
Safe in patients with diabetes or peripheral vascular disease. It decreases the risk of bronchospasm.
Bretylium
Mechanism of action:
1. It is an adrenergic neuronal blocking agent. It is collected in adrenergic nerve terminals, where it stimulates norepinephrine release firstly but then causes inhibition of the release of norepinephrine in response to neuronal stimulation.
2. It also has direct electrophysiologic effects on heart.
Actions:
1. Promoted duration of ventricular action potential and effective refractory period is more pronounced in ischemic cells.
2. It also causes an increase of action potential duration and effective refractory period of atrial muscle and AV node.
3. Some positive inotropic effect is also observed from initial release of norepinephrine.
Therapeutic uses:
It is used for those life threatening ventricular arrhythmias which are unresponsive to other therapy.
Adverse effects:
Orthostatic hypotension (adrenergic neuron blocking mechanism), Nausea, vomiting
1. It is an adrenergic neuronal blocking agent. It is collected in adrenergic nerve terminals, where it stimulates norepinephrine release firstly but then causes inhibition of the release of norepinephrine in response to neuronal stimulation.
2. It also has direct electrophysiologic effects on heart.
Actions:
1. Promoted duration of ventricular action potential and effective refractory period is more pronounced in ischemic cells.
2. It also causes an increase of action potential duration and effective refractory period of atrial muscle and AV node.
3. Some positive inotropic effect is also observed from initial release of norepinephrine.
Therapeutic uses:
It is used for those life threatening ventricular arrhythmias which are unresponsive to other therapy.
Adverse effects:
Orthostatic hypotension (adrenergic neuron blocking mechanism), Nausea, vomiting
Propranolol
It is helpful in myocardial ischemia. It decreases mortality rate by reducing ventricular arrhythmia.
Mechanism of action:
It acts on both β1 and β2 adrenoceptors i.e. cause their blockage.
Actions:
It has both negative inotropic and chronotropic effect resulting in the decrease of cardiac output.
It also decreases SA and AV nodal activity.
It shows promising effects in angina by decreasing cardiac output, work load on the heart and oxygen consumption of the heart muscles at rest and in physical activity.
In the first instance, it produces anti-hypertensive effects by reduced cardiac output associated with bradycardia. And its long term use inhibits renin secretion, which results in reduced peripheral resistance leading to anti-hypertensive effects.
Due to β2-blockade, it causes an elevated airway resistance.
It causes an increased sodium retention.
Antiarrhythmic action:
Its effects are due to β-adrenoceptor blockade but also due to a direct membrane effect. It
1. Suppresses SA nodal firing
2. Reduces automaticity in purkinje fibers
3. A substantial promotion in effective refractory period of AV node
Therapeutic uses:
1. Chronic form of angina pectoris
2. prophylaxis of myocardial infarction and migraine
3. Hypertension
4. Hyperthyroidism
Antiarrhythmic uses:
It is used for:
1. Atrial flutter or fibrillation
2. Sudden outburst of supraventricular tachycardia
3. Ventricular arrhythmias due to:
a. increased adrenergic activation
b. Toxicity caused by digitalis
Adverse effects:
Sedation, depression, cardiac failure, nausea, vomiting, bronchconstriction, diarrhea, rashes, fever, impaired metabolism (Due to reduced glycogenolysis and glucagon secretion caused by β-blockade)
Mechanism of action:
It acts on both β1 and β2 adrenoceptors i.e. cause their blockage.
Actions:
It has both negative inotropic and chronotropic effect resulting in the decrease of cardiac output.
It also decreases SA and AV nodal activity.
It shows promising effects in angina by decreasing cardiac output, work load on the heart and oxygen consumption of the heart muscles at rest and in physical activity.
In the first instance, it produces anti-hypertensive effects by reduced cardiac output associated with bradycardia. And its long term use inhibits renin secretion, which results in reduced peripheral resistance leading to anti-hypertensive effects.
Due to β2-blockade, it causes an elevated airway resistance.
It causes an increased sodium retention.
Antiarrhythmic action:
Its effects are due to β-adrenoceptor blockade but also due to a direct membrane effect. It
1. Suppresses SA nodal firing
2. Reduces automaticity in purkinje fibers
3. A substantial promotion in effective refractory period of AV node
Therapeutic uses:
1. Chronic form of angina pectoris
2. prophylaxis of myocardial infarction and migraine
3. Hypertension
4. Hyperthyroidism
Antiarrhythmic uses:
It is used for:
1. Atrial flutter or fibrillation
2. Sudden outburst of supraventricular tachycardia
3. Ventricular arrhythmias due to:
a. increased adrenergic activation
b. Toxicity caused by digitalis
Adverse effects:
Sedation, depression, cardiac failure, nausea, vomiting, bronchconstriction, diarrhea, rashes, fever, impaired metabolism (Due to reduced glycogenolysis and glucagon secretion caused by β-blockade)
Class II Antiarrhythmic Drugs
Class II drugs are β-adrenergic receptor antagonists.
Action:
These agents have the ability of decreasing Phase 4 depolarization thus suppresses the automaticity, causing a prolonged AV conduction and decreased cardiac rate and contractility.
Therapeutic uses:
Class II drugs are used in the treatment of tachycardia due to promoted activity of sympathetic system.
They are also useful in the treatment of atrial flutter and fibrillation.
They are used in AV nodal re-entrant tachycardia.
Action:
These agents have the ability of decreasing Phase 4 depolarization thus suppresses the automaticity, causing a prolonged AV conduction and decreased cardiac rate and contractility.
Therapeutic uses:
Class II drugs are used in the treatment of tachycardia due to promoted activity of sympathetic system.
They are also useful in the treatment of atrial flutter and fibrillation.
They are used in AV nodal re-entrant tachycardia.
Propafenone
Same as that of flecainide. It has the ability of allowing conduction in all the tissues of heart.
Subscribe to:
Posts (Atom)
-
Q: What do you know about ergot alkaloids? Ans: These include alkaloids which we get from the ergot fungus Claviceps purpurea or derived ...
-
(For detailed study of Pharmaceutical Incompatibility Click here) Multiple Choice Questions (MCQs) from Pharmaceutical Incompatibility in ...
-
Multiple Choice Questions (MCQs) of Powders and Granules from Pharmaceutics 1. _______ powders consist of more than one ingredients. a. Si...
