Vaughan Williams Classification
Class I drugs: Predominantly block the fast sodium channel. They, in turn, are divided into three subgroups.
Class IA. Drugs that reduce V m w (rate of rise of action potential upstroke [phase 01) and prolong action potential duration: quinidine, procainamide,disopyrarnide.
Class IB. Drugs that do not reduce V max and that shorten action potential duration: mexiletine, phenytoin, and lidocaine.
Classic IC : Drug that reduce V max, primarily slow conduction, and can prolong refractoriness minimally: flecainide, propafenone, and moricizine.
Class II drugs: Drugs that block beta-adrenergic receptors and include propranolol, timolol, metoprolol, and thers.
Class III drugs: Drugs that predominantly block potassium channels and prolong repolarization. They include sotalol, amiodarone, bretylium.
Class IV drugs: Drugs that predominantly block the slow calcium channel and include verapamil, diltiazem.
Class I drugs: Predominantly block the fast sodium channel. They, in turn, are divided into three subgroups.
Class IA. Drugs that reduce V m w (rate of rise of action potential upstroke [phase 01) and prolong action potential duration: quinidine, procainamide,disopyrarnide.
Class IB. Drugs that do not reduce V max and that shorten action potential duration: mexiletine, phenytoin, and lidocaine.
Classic IC : Drug that reduce V max, primarily slow conduction, and can prolong refractoriness minimally: flecainide, propafenone, and moricizine.
Class II drugs: Drugs that block beta-adrenergic receptors and include propranolol, timolol, metoprolol, and thers.
Class III drugs: Drugs that predominantly block potassium channels and prolong repolarization. They include sotalol, amiodarone, bretylium.
Class IV drugs: Drugs that predominantly block the slow calcium channel and include verapamil, diltiazem.
Unclassijied: Adenosine, digoxin, magnesium.
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| Antiarrhythmic Drugs: Effects on Cardiac Action Potential |
Use-dependence: Some drugs exert greater inhibitory effects on the upstroke of the action potential at more rapid rates of stimulation and after longer periods of,stimulation, a characteristic called use-dependence. With increased time spent in diastole (slower rate), a greater proportion of receptors become drug f e e , and the drug exerts less effect. Class IB agents demonstrate use dependent block of fast sodium channel.
Reverse Use-dependence: Some drugs exert greater effects at slow rates than at fast rates, a property known as reverse use-depe~zdence. This is particularly true for drugs that lengthen repolarization. The QT interval becomes prolonged more at slow than fast rates.
Arrhythmia Suppression - Mechanisms
All arrhythmias occur due to changes in cellular action potential. AADs exert their effect by altering ion channels and re-changing the shape of action potential. Cardiac arrhythmias are caused by either abnormal automaticity,triggered activity or re-enby. Most antiarrhythmic agents in therapeutic doses depress the automatic firing rate of spontaneously discharging ectopic sites while minimally affecting the,discharge rate of the normal sinus node. Slow-channel blockers like verapamil, beta-blockers like propranolol, and some antimhythmic agents like amiodarone also depress spontaneous discharge of the normal sinus node, whereas drugs that exert vagolytic effects, such as disopyramide or quinidine, can increase the sinus discharge rate. Drugs can also suppress early orAnti-Arrhythndc Drugs, Pacemak-delayed afterdepolarizations and eliminate triggered arrhythmias due to these are, Defibrillators mechanisms. Re-entry depends on presence of unidirectional block and ciitical interrelationship between refractoriness and conduction velocity. AADs that depress conduction can transform the unidirectional block to bidirectional block and thus terminate re-entry or prevent it from occurring by creating an area of complete block in the reentrant pathway.
Drug Metabolites
Drug metabolites may alter the effects of the parent compound by exerting similar actions, competing with the parent compound, or mediating drug toxicity.Quinidine has at least four active metabolites but none with a potency exceeding the parent dug. About 50 per cent of procainamide is metabolized to NAPA.Only the parent drug blocks cardiac sodium channels and slows impulse propagation in the His-Purkinje system. NAPA prolongs repolarization and is a less effective antiarrhythrnic drug but competes with procainamide for renotubular secretory sites and can increase the parent drug's elirninatioil half-life. Lidocaine's metabolite can compete with lidocaine for sodium channels and partially reverse block produced by lidocaine.
Pharmacogenetics
Genetically determined metabolic pathways account for many of the differences in patient's responses to some drugs. The genetically deteilnined activity of hepatic N-acetyltransferase regulates the development of antinuclear antibodies and development of the lupus syndrome in response to procainarnide. Slow acetylator phenotypes appear more prone to develop lupus than do rapid acetylators.
Quinidine in low doses can inhibit hepatic P450 enzyme and thereby alter concentrations of the drugs and metabolites given in combination that are affected by the enzyme, such as propafenone or flecainide. Cimetidiile and ranitidine also affect drug metabolism, probably by inhibiting hepatic P450-metabolizing enzymes. Drugs such as rifampin, phenobarbital, and phenytoiil induce synthesis of larger amounts of cytochrome P450, leading to lower concentrations of parent drugs that are extensively metabolized, whereas erythromycin and grapefruit juice inhibit enzyme activity, leading to accumulation of the parent coinpound. Cisapride, 'an agent to improve gasttic motility, by itself does not cause QT prolongation but when given with an inhibitor of cytochrome P450 (such as erythromycin), can lead to QT prolongation and torsades de pointes.
Side Effects
Proarrhythmia: Drug-induced or drug-aggravated cardiac arrhythmias constitute a major clinical problem. Proarrhythmia can be manifested as an increase in frequency of a pre-existing arrhythmia, sustaining of a previously onsu sustained arrhythmia (even making it incessant), or development of arrhythmias the patient has not previously experienced, Electrophysiological mechanisms relate to prolongation of repolarization, development of early afterdepolarizations to cause torsades de pointes, and alterations in re-entry pathways to initiate or sustain ventricular tachyarrhythrnias. Proarrhythmic events occur in 5 to 10 per cent of patients. The more commonly known proarrhythmic events occur within several days of beginning drug therapy or changing dosage and are represented by such developments as incessant ventricular tachycardia (VT), long QT syndrome, and torsades de pointes.
Torsades de pointes (twisting around a point) is a distinctive type of polymorphic VT associated with QT prolongation (Fig,2.2). Class IA and Class 111 drugs prolong action potential duration, increasing QT interval, cause pause-dependent early after-depolarizations leading to VT. Digitoxicity is associated with enhanced delayed after-depolarizations leading to polymorphic VT that is not pause dependent. Bradyarrhythrnias are a form of proarrhythmia occurring due to excessive suppression of sinoatrial and atrioventricular nodes ( beta-blockers,calcium channel blockers, digoxin toxicity) or block in distal His-Purkinje system (Class IA, TC, Class 111 drugs). Treatment of the condition is by stopping the offending drug and instituting temporary pacing. AADs can worsen hemodynamics by depressing ventricular function or by causing hypotension. In CAST study, compared to controls, flecainide caused four times more mortality in post-myocardial infarct patients with reduced left ventricular function and complex vei~tricular ectopy.
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| Torsades de Pointes |
Class IA Drugs
Act by blocking rapid sodium channel. They are moderately effective in treating most types of ats11ythmias.They also cause significant side effects-on end organs as well as proan-liythmia.
Class IB Drugsers, Defibrillators
These drugs are moderately useful in treating ventricular anhythmias. In contrast ;O other Class I drugs, these agents have a low incidence of side effects.
Class IC Drugs
These drugs are very effective in treating both atrial and ventricular tachycudias and gene ally cause only 111ilc1 end-organ toxicity. CAST study revealed the ' significant proxrhyth~l~ic potential of tllcse drugs in patients with ventriculs~r dysfunction.
Class I1 Drugs: Beta-Blocking Agents
These agents act by blunting the arlhythrnogenic actions of catecholamines. They significantly reduce the incidence of sudden cardiac arrest by preventing cardiac tachyarrhythmias.Siilce adrcncrgic stirnulation is most profownd normally in the sinoatrial and atrioventricular nodes, these 'slructurcs are most affected by beta-blockers. This results in slowing of heart rate and conduction delay across rat~ioventriculor node.These agents have a profound effect on ischemic myocardiurn and have been shown to reduce risk of ventricular l'ibrillatjon cluring ischemia.Coillrno~l
Adverse Effects of P-blockers
As a direct consequence of adrenergic blockade, these agents can cause brady cardia, myocardial depression, bronchoconst~iction, claudication, Raynaud's phenomenon, fatigue, mental depression. In diabetes mellitus, these dlugs can with P, selectivity avoid bronchospasin,mask symptoms of hypoglycemia. DI-U~S claudication, Raynaud's phenomenon. Diugs with low lipid solubility help in preventing CNS side effects.
Class I11 Drugs
These drugs prolong the duration of cardiac action potential by bloclung potassium channels and increase refractory periods of conduction tissues.Amiodarone: Displays activity of all four classes of antiarrhyth~nic agents, with major effect of homogeneous prolongation of the action potential.
Indications: It is a broad spectrum antiatrhythmic dmg. It is effective for any type of tachyarrhythmia.It is moderately effective in converting atrial flutter and ahid fibrillation to sinus rhythm. It is effective for paroxysmal supraventricular tachycardias (SVT) including accessory pathway mediated tachycardia and AV nodal re-entrant tachycardia. It is one of the most effective agents developed for treatment of VT and ventricular fibrillation. Patients who have an internal cardioverter-defibiillator (ICD) receive fewer shocks if they are treated with amiodarone compared with other conventional drugs.
Adverse Effects: Has high incidence of side effects ranging from minor to life- threatening. Mild gastsointestinal (GI) side effects are comlnon (25 per cent) with high dose loading phase but uncommon with maintenance dose.Pulmo~lary toxicity is the most serious adverse reaction, mechanism may beI related to hypersensitivity. Acute anliodarone induced pneumonitis (2-5 per cent incidence) and chronic interstitial fibrosis can occur. At maintenance doses less than 300 mg/d, pullnonary toxicity is uncommon. Although asymptomatic elevations of liver enzymes are found in most patients, the drug is not stopped unless values exceed two or three times normal in a patient with initially abnormal values. Neurological dysfunction, photosensitivity (perhaps minimized by sunscreens), bluish slun discoloration and hyperthyroidism (1 to 2 per cent) or hypothyroidism (2 Lo 4 per cent) can occur.
Drug Interactions: When given concoinitantly with amiodarone, the doses of warfarin, digoxin, and other antiarrhythmic drugs should be reduced by one third to one half.
Bretylium 'Pbsylate
This drug is approved for parenteral use only in patients with life-threatening vei~tiicular tachyarrhythmias. Bretylium is selectively concentrated in sympathetic ganglia and their postganglionic adrenergic nei-ve terminals. After initially causing norepinephrine release, bretylium prevents norepinephrine release by depressing sympathetic nervc terminal excitability resulting in chemical sympathectomy-like state. After an inilial increase in blood pressure,the drug can cause significant hypotension by blocking the elferent linlb o r the baroreceptor reflex. Brelylium has been effective in trealing patients with drug-resistant recurrent ventricular tnchyar-rhylhinias and in treating viclims of out-of-hospital VF.
Adverse Effects:
Hypotension, most prominently orthostatic but also supine, appears to be the most significant side effect and can be prevented with tricyclic drugs such as protriplyline.
Sotalol
Both d- and I-isomers liave similx effects on prolonging repola~ization,whereas the I-isomer is responsible for virtually all the beta-blocking activity.Effective in tieating ventiicular tachyarrhythmias, sotalol is also useful to prevent recurrence of a wide variety of SVTs, including atrial flutter and fibrillation, atrial tachycardia, AV node re-entry, and AV re-entry. Sotalol has been shown to be superior to liclocaine for acute termination of sustained VT and is useful in patients with arrhythmogenic light ventricular dysplasia. It may decrease the frequency of ICD discharges and reduce the defibrillation threshold.
Class IV Drugs: Calcium channel Blocking Agents Many calcium-channel blocking agents are available, but only two drugs-verapamil and diltiazem- are approved for treatment of cardiac tachyarrhythmias.Clinical Pharmacology of Verapamil and Diltiazem After an oral dose, more than 90 per cent of verapamil is absorbed but bioavailability is reduced to 20 per cent to 35 per cent by first-pass hepatic metabolism. About 90 per.cent of the drug is protein bound.Elimination half-life is 5- 12 hours.
Diltiazem is also well absorbed after oral administration and is 40 per cent bioavailable after first-pass metabolism. It is 70 per cent to 80 per cent protein bound. It ik metabolized in liver and elimination half life is 3.5 hours.Both the drugs are available for intravenous administration, used in treatment of emergent SVTs.
Dosage
Usual oral dose of verapamil is 240-360 mgfday given every eight hours.Diltiazcm is given eveiy 6-8 hours to a daily dose of 120-360mg. Vaiious long-acting preparations are available for veraparnil and diltiazem. The most commonly used IV dose of verapamil is 10 mg infused over I to 2 minutes while cardiac rhythm and blood pressure are monitored. The initial effect may be maintained by a continuous infusion of the drug at a rate of 0.005 mgfkgfmin.Diltiazem is given intraveilously at a dose of 0.25 mgkg as a bolus over 2 minutes, followed if necessary by infusion at 10mg/hr.
Electrophysiologic Effects
These drugs block the slow calcium-channel and reduce the plateau height of the action potential. Veraparnil and diltiazem suppress electrical activity in the normal sinus and AV nodes in concentrations that do not suppress action potentials of fast-channel-dependent cells. Verapamil does not exert a significant direct effect on atrial or ventricular refractoriness or on anterograde or retrog ade properties of accessoiy pathways. However, reflex sympathetic stimulation may increase the ventricular response over the accessory pathway during atrial fibrillation in patients with the Wolff-Parkinson-White (WPW) syndrome. Even though verapamil terminates a left septa1 fascicular VT, hemodynarnic collapse can occur if intravenous verapamil is given to patients with the more common forms of VT.
Adverse Effects
Verapamil has negative inotropic effect and can precipitate congestive heart failure in patients with impaired ventricular function.Both dmgs can cause constipation, nausea, bradya~rhythn~ias (seen with pre-existent sinoatrial or
atrioventricular nodal disease), hypotension.
Unclassified Drugs
Digoxin, adenosine and magnesium are often used for treating cardiac arrhythmias; as these agents do not fit into Vaughan-Williams classification, they are discussed separately.
Digoxin
Digoxin preparations have been available for clinical use since 1700s. Digoxin is well absorbed orally, is excreted by kidneys and has an elimination half-life of 1.7 days. It increase parasympathetic tone and has greatest effect on sinoatrial (SA) and atrioventricular (AV) nodes. Apart from antimhythrnic effect, it increases intracellular calcium during myocardial contraction, increasing contractility.
Anti-Arrhythmic Drugs, Pacemakers
Digoxill is well tolerated but toxicity can be a seiious clinical problem withers, Defibrillators gastroiiitesti~lal (nausea, volniting, anorexia, diarrhea, cramps), neurological disturbances (visual, delirium) and significant airhyth~nias which are potentially life-tl~reatening. Digoxin toxicity is enhanced by low potassium levels. For ventricular arrhythmias occurring due to high digoxin levels,cardioversion is better -avoided; correcting hypokalemia, administering phenytoin or lidocaine and when available using digoxin-specific antibodies is efiective.
Adenosine
It is a naturally occurring ilucleoside that has a prol'ound but very short-lastin;depressive effect Dn SA node and AV node,*8pproved for acute trcatment of SVT.Adenosine is removed from the vascular space by vascular endothelium and the formed blood elements which result in vcry rapid clearance of adenosine from the circ~ilation. Elinlination half-lifc is 1 to 6 seconds. .
Dosage: To terininntc tachycardia, a bolus of adenosine is rapidly injected intravenously into a central vein (if possible) at doses of 6 to 12 mg. Pediatric dosing should be 0.1 to 0.3 mglkg. Transient sinus slowing or AV node block results.
Transient side ci'fects occur in almost 40 per cent of palicnts with SVT given adenosi~ie and arc most commonly flushing, dyspnea, and chest pressure. These synlptoms are ileeling, lasting less than one minute, and are well tolerated.Ventiicular ectopics, ttansicnl sinus bradycardia, sinus arrest, and AV block are common when an SVT abruptly terminates. Atrial fibrillation(AF) is occasionally observed (1 2 per cent) and is problc~natic in patients with WPW syndro~ile when the accessory pathway conducts anlegradely rapidly.
Magnesium
The most well estal~lishecl use oS pnrcnteral magnesiunl as an antiarrhythmic agent is in Iherapy of Lorsades de pointes. The precise mechanism by which it ameliorates ru-rhyth~nias is uilclear but it has an impoilant iniluence on sodium- potassiumn pump in Lhe cell membrane and changes the action potential. Apart from being drug of first choice for emergency treatment of torsades, it also has a place in treating a1~11ythmias duc to digoxin toxicity, multifocal atrial tachycardia and in preventing arhylhmias after cardiac surgery.
Dosuge: 8-16111Eq (I-2g) of magnesium sulphate can be infused rapidly over several. minutes.
toxicity: Is exacerbated in renal failure. Manifestations include ECG chonges (increased PR interval rund QRS duration), loss of deep tendon reflexes and respiratory ptifalysis.
As a direct consequence of adrenergic blockade, these agents can cause brady cardia, myocardial depression, bronchoconst~iction, claudication, Raynaud's phenomenon, fatigue, mental depression. In diabetes mellitus, these dlugs can with P, selectivity avoid bronchospasin,mask symptoms of hypoglycemia. DI-U~S claudication, Raynaud's phenomenon. Diugs with low lipid solubility help in preventing CNS side effects.
Class I11 Drugs
These drugs prolong the duration of cardiac action potential by bloclung potassium channels and increase refractory periods of conduction tissues.Amiodarone: Displays activity of all four classes of antiarrhyth~nic agents, with major effect of homogeneous prolongation of the action potential.
Indications: It is a broad spectrum antiatrhythmic dmg. It is effective for any type of tachyarrhythmia.It is moderately effective in converting atrial flutter and ahid fibrillation to sinus rhythm. It is effective for paroxysmal supraventricular tachycardias (SVT) including accessory pathway mediated tachycardia and AV nodal re-entrant tachycardia. It is one of the most effective agents developed for treatment of VT and ventricular fibrillation. Patients who have an internal cardioverter-defibiillator (ICD) receive fewer shocks if they are treated with amiodarone compared with other conventional drugs.
Adverse Effects: Has high incidence of side effects ranging from minor to life- threatening. Mild gastsointestinal (GI) side effects are comlnon (25 per cent) with high dose loading phase but uncommon with maintenance dose.Pulmo~lary toxicity is the most serious adverse reaction, mechanism may beI related to hypersensitivity. Acute anliodarone induced pneumonitis (2-5 per cent incidence) and chronic interstitial fibrosis can occur. At maintenance doses less than 300 mg/d, pullnonary toxicity is uncommon. Although asymptomatic elevations of liver enzymes are found in most patients, the drug is not stopped unless values exceed two or three times normal in a patient with initially abnormal values. Neurological dysfunction, photosensitivity (perhaps minimized by sunscreens), bluish slun discoloration and hyperthyroidism (1 to 2 per cent) or hypothyroidism (2 Lo 4 per cent) can occur.
Drug Interactions: When given concoinitantly with amiodarone, the doses of warfarin, digoxin, and other antiarrhythmic drugs should be reduced by one third to one half.
Bretylium 'Pbsylate
This drug is approved for parenteral use only in patients with life-threatening vei~tiicular tachyarrhythmias. Bretylium is selectively concentrated in sympathetic ganglia and their postganglionic adrenergic nei-ve terminals. After initially causing norepinephrine release, bretylium prevents norepinephrine release by depressing sympathetic nervc terminal excitability resulting in chemical sympathectomy-like state. After an inilial increase in blood pressure,the drug can cause significant hypotension by blocking the elferent linlb o r the baroreceptor reflex. Brelylium has been effective in trealing patients with drug-resistant recurrent ventricular tnchyar-rhylhinias and in treating viclims of out-of-hospital VF.
Adverse Effects:
Hypotension, most prominently orthostatic but also supine, appears to be the most significant side effect and can be prevented with tricyclic drugs such as protriplyline.
Sotalol
Both d- and I-isomers liave similx effects on prolonging repola~ization,whereas the I-isomer is responsible for virtually all the beta-blocking activity.Effective in tieating ventiicular tachyarrhythmias, sotalol is also useful to prevent recurrence of a wide variety of SVTs, including atrial flutter and fibrillation, atrial tachycardia, AV node re-entry, and AV re-entry. Sotalol has been shown to be superior to liclocaine for acute termination of sustained VT and is useful in patients with arrhythmogenic light ventricular dysplasia. It may decrease the frequency of ICD discharges and reduce the defibrillation threshold.
Class IV Drugs: Calcium channel Blocking Agents Many calcium-channel blocking agents are available, but only two drugs-verapamil and diltiazem- are approved for treatment of cardiac tachyarrhythmias.Clinical Pharmacology of Verapamil and Diltiazem After an oral dose, more than 90 per cent of verapamil is absorbed but bioavailability is reduced to 20 per cent to 35 per cent by first-pass hepatic metabolism. About 90 per.cent of the drug is protein bound.Elimination half-life is 5- 12 hours.
Diltiazem is also well absorbed after oral administration and is 40 per cent bioavailable after first-pass metabolism. It is 70 per cent to 80 per cent protein bound. It ik metabolized in liver and elimination half life is 3.5 hours.Both the drugs are available for intravenous administration, used in treatment of emergent SVTs.
Dosage
Usual oral dose of verapamil is 240-360 mgfday given every eight hours.Diltiazcm is given eveiy 6-8 hours to a daily dose of 120-360mg. Vaiious long-acting preparations are available for veraparnil and diltiazem. The most commonly used IV dose of verapamil is 10 mg infused over I to 2 minutes while cardiac rhythm and blood pressure are monitored. The initial effect may be maintained by a continuous infusion of the drug at a rate of 0.005 mgfkgfmin.Diltiazem is given intraveilously at a dose of 0.25 mgkg as a bolus over 2 minutes, followed if necessary by infusion at 10mg/hr.
Electrophysiologic Effects
These drugs block the slow calcium-channel and reduce the plateau height of the action potential. Veraparnil and diltiazem suppress electrical activity in the normal sinus and AV nodes in concentrations that do not suppress action potentials of fast-channel-dependent cells. Verapamil does not exert a significant direct effect on atrial or ventricular refractoriness or on anterograde or retrog ade properties of accessoiy pathways. However, reflex sympathetic stimulation may increase the ventricular response over the accessory pathway during atrial fibrillation in patients with the Wolff-Parkinson-White (WPW) syndrome. Even though verapamil terminates a left septa1 fascicular VT, hemodynarnic collapse can occur if intravenous verapamil is given to patients with the more common forms of VT.
Adverse Effects
Verapamil has negative inotropic effect and can precipitate congestive heart failure in patients with impaired ventricular function.Both dmgs can cause constipation, nausea, bradya~rhythn~ias (seen with pre-existent sinoatrial or
atrioventricular nodal disease), hypotension.
Unclassified Drugs
Digoxin, adenosine and magnesium are often used for treating cardiac arrhythmias; as these agents do not fit into Vaughan-Williams classification, they are discussed separately.
Digoxin
Digoxin preparations have been available for clinical use since 1700s. Digoxin is well absorbed orally, is excreted by kidneys and has an elimination half-life of 1.7 days. It increase parasympathetic tone and has greatest effect on sinoatrial (SA) and atrioventricular (AV) nodes. Apart from antimhythrnic effect, it increases intracellular calcium during myocardial contraction, increasing contractility.
Anti-Arrhythmic Drugs, Pacemakers
Digoxill is well tolerated but toxicity can be a seiious clinical problem withers, Defibrillators gastroiiitesti~lal (nausea, volniting, anorexia, diarrhea, cramps), neurological disturbances (visual, delirium) and significant airhyth~nias which are potentially life-tl~reatening. Digoxin toxicity is enhanced by low potassium levels. For ventricular arrhythmias occurring due to high digoxin levels,cardioversion is better -avoided; correcting hypokalemia, administering phenytoin or lidocaine and when available using digoxin-specific antibodies is efiective.
Adenosine
It is a naturally occurring ilucleoside that has a prol'ound but very short-lastin;depressive effect Dn SA node and AV node,*8pproved for acute trcatment of SVT.Adenosine is removed from the vascular space by vascular endothelium and the formed blood elements which result in vcry rapid clearance of adenosine from the circ~ilation. Elinlination half-lifc is 1 to 6 seconds. .
Dosage: To terininntc tachycardia, a bolus of adenosine is rapidly injected intravenously into a central vein (if possible) at doses of 6 to 12 mg. Pediatric dosing should be 0.1 to 0.3 mglkg. Transient sinus slowing or AV node block results.
Transient side ci'fects occur in almost 40 per cent of palicnts with SVT given adenosi~ie and arc most commonly flushing, dyspnea, and chest pressure. These synlptoms are ileeling, lasting less than one minute, and are well tolerated.Ventiicular ectopics, ttansicnl sinus bradycardia, sinus arrest, and AV block are common when an SVT abruptly terminates. Atrial fibrillation(AF) is occasionally observed (1 2 per cent) and is problc~natic in patients with WPW syndro~ile when the accessory pathway conducts anlegradely rapidly.
Magnesium
The most well estal~lishecl use oS pnrcnteral magnesiunl as an antiarrhythmic agent is in Iherapy of Lorsades de pointes. The precise mechanism by which it ameliorates ru-rhyth~nias is uilclear but it has an impoilant iniluence on sodium- potassiumn pump in Lhe cell membrane and changes the action potential. Apart from being drug of first choice for emergency treatment of torsades, it also has a place in treating a1~11ythmias duc to digoxin toxicity, multifocal atrial tachycardia and in preventing arhylhmias after cardiac surgery.
Dosuge: 8-16111Eq (I-2g) of magnesium sulphate can be infused rapidly over several. minutes.
toxicity: Is exacerbated in renal failure. Manifestations include ECG chonges (increased PR interval rund QRS duration), loss of deep tendon reflexes and respiratory ptifalysis.
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