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Antiarrhythmics

Class I antiarrhythmics include sodium channel blockers that are classified as Class Ia, Ib, or Ic based on their binding properties and effects. Class Ia drugs like procainamide have intermediate binding and prolong the action potential. Class Ib drugs like lignocaine have fast binding and decrease action potential duration. Class Ic drugs like flecainide have slow, strong binding and do not change action potential duration. Class II drugs are beta blockers that decrease sympathetic stimulation. Class III drugs are potassium channel blockers that prolong the refractory period like amiodarone and sotalol. They carry a risk of QT prolongation. Amiodarone has multiple mechanisms of action and a long half

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ANTIARRHYTHMICS Dr Andrew Crofton ED Registrar
VAUGHAN-WILLIAMSClass Action Examples Class Ia Sodium channel blockers (intermediate association/dissociation – moderate blockade) Disopyramide, quinidine, procainamide Class Ib Sodium channel blockers (fast – weak blockade) Lignocaine, phenytoin Class Ic Sodium channel blockers (slow – strong blockade) Flecainide, propafenone Class II Beta-blockers Metoprolol, esmolol, labetalol, propranolol Class III Potassium-channel blockers Amiodarone, ibutilide, sotalol, vernakalant Class IV Calcium-channel blockers Diltiazem, verapamil Unclassified Atropine, digoxin, adenosine, isoproterenol, magnesium
CLASS I All reduce the slope of Phase 0 Class Ia – Prolonged action potential duration Class Ib – Decreased action potential duration Class Ic – No change in action potential duration
CLASS IA – INTERMEDIATE NA CHANNEL BLOCK Block open sodium channels and have slow dissociation causing increased refractory period Quinidine and disopyramide are rarely used Procainamide
CLASS IA - PROCAINAMIDE  Pharmacodynamics  Increases refractory period, decreases automaticity and conduction, prolongs cardiac action potentials  Pharmacokinetics  NAPA (active metabolite) blocks potassium channels leading to QT prolongation  Hepatic metabolite then renally excreted  2.5-4.7hr half-life; NAPA 6-8hrs half-life  Onset 5-10 min and duration 1-2 hours  Dosing  20-50mg/min IV until arrhythmia suppressed, hypotension or QRS >50% longer than original followed by 1-4mg/min  OR  100mg IV every 5 min until above
CLASS IB (FAST - WEAK BLOCKADE) High affinity for open and inactive sodium channels with very rapid dissociation Increases threshold for excitability to reduce automaticity Rapid dissociation means they are less effective for myocardial tissues with rapid conduction e.g. atrial tissue Ratio of effective refractory period to action potential is increased Good efficacy in ischaemic myocardium
CLASS IB - LIGNOCAINE Pharmacodynamics  Preferentially acts on ischaemic tissues to decrease conduction  Negligable effect on cardiac action potential  Minimal effect on QT or refractory period either Pharmacokinetics  Hepatically metabolised and renally excreted  7-30min half-life (initial) and terminal half-life 1.5-2 hours  Onset 45-90s and duration 10-20 min
CLASS IB - LIGNOCAINE Dosing in ventricular arrhythmia  Loading dose 1mg/kg IV over 2 minutes  Maintenance 4mg/min for 1 hour; 2mg/min for 1 hour then 1mg/min for 22 hours Dosing in VF  1-1.5mg/kg IV loading then 0.5-0.75mg/kg every 5-10min Indications  Second-line to amiodarone in ventricular arrhythmias Adverse effects  CNS numbness speech impairment, somnolence, dizziness and seizures
CLASS IC – STRONG SLOW DISSOCIATION Generally indicated for SVT Marked prolongation of QRS without QT prolongation Only act on open sodium channels High proarrhythmic potential that is amplified by myocardial tissue disease, increased sympathetic tone and higher heart rates Associated with increased mortality when used in cardiovascular disease or MI
PROPAFENONE Also beta-blocker Selective for rapid conducting tissues e.g. atrial tissue Indicated for recent-onset AF (<7 days) Single oral dose 450mg (<70kg) or 600mg (>70kg) Adverse effects  Hypotension, bradycardia, bronchospasm, Aflutter with 1:1 conduction and ventricular proarrhythmia  Avoid in CAD or structural heart disease, asthma, hepatic dysfunction or CCF
FLECAINIDE Reduces excitability primarily in His-Purkinje and ventricular myocardium Indicated for conversion of new-onset AF (<7 days) One-time oral dose of 200mg (<70kg) or 300mg (>70kg) Adverse effects  Hypotension, Aflut with 1:1 and ventricular proarrhythmia  Avoid in CCF, CAD, structural heart disease or hypokalaemia
CLASS II: BETA-BLOCKERS Indications: HTN, SVT, ventricular arrhythmias, recurrent AF (rate control) and thyrotoxicosis Non-cardioselective (beta-1 and 2): Propranolol Cardioselective (beta-1): Esmolol, metoprolol  Better for those with asthma, COAD, IDDM  Dose-dependent cardioselective means lost at high doses Vasodilatory, non-selective: Labetalol
PROPRANOLOL Non-selective beta-1 and beta-2 antagonist Pharmacokinetics  Onset oral 1-2 hours; IV <1 min  Hepatically metabolised  3-6 hour half-life  Dosing  Tachyarrhythmia: 1-3mg slow IV push, repeated very 2-5 min up to 5mg total Adverse effects include bradycardia, heart block, hypotension, acute heart failure and bronchospasm
ESMOLOL Short-acting, selective beta-1 antagonist which prevents excessive adrenergic stimulation of the myocardium, causing increased sinus cycle length, prolongation of sinoatrial recovery time and decreased AV nodal conduction Onset 2-10min Duration of action 10-30 min Metabolised in blood by RBC esterases Half-life 9 min Dosing  SVT – 500mcg/kg bolus over 1 min then infusion 50mcg/kg/min titrated to therapeutic effect in 50mcg/kg/min increments every 4 minutes Adverse effects  Hypotension (most common), bradycardia, heart block  Nausea, bronchospasm, pulmonary oedema
METOPROLOL Selective beta-1 antagonist Decreases CO, reduced sympathetic outflow and suppresses renin activity to treat hypertension Onset of action 1-2 hrs PO and 20 min IV Hepatically metabolised Half-life 3-4 hours Dosing  1.25-5mg IV every 5 minutes up to total 15mg Adverse effects  Bradycardia, heart block, hypotension and bronchospasm
LABETALOL Combined selective alpha-1 and non-selective beta blocker Beta-blocker: Alpha-block 3:1 in oral and 7:1 in parenteral formulation Used primarily for antihypertensive effect Onset 20min - 2hr orally or 2-5min IV Duration 8-12hr oral or 2-18 hr IV Hepatically metabolised Half-life 6-8 hr oral and 5.5hr IV Dosing  20mg IV push over 2 min; then 40-80mg at 10 min intervals up to 300mg  2mg/min infusion titrated to response (total 300mg cumulative dose) Adverse effects  Orthostatic hypotension, nausea, dizziness, fatigue, heart failure, hyperkalaemia, hepatotoxicity and bronchospasm
CLASS III – POTASSIUM-CHANNEL BLOCKERS Inhibit inward potassium currents leading to significantly lengthened refractory period Myocardial tissue in a refractory state is less prone to reentrant tachycardia Prolong the QT and carry risk of Torsades
AMIODARONE Used in acute management and chronic suppression of SVT and ventricular arrhythmias MOA:  Alpha, beta, calcium channel, potassium channel blockade  Blocks inactivated sodium channels to prolong the refractory period which in turn decreases the HR and may cause sinus bradycardia  Non-competitive alpha and beta-blockade decreases sinoatrial node function leading to reduced heart rate, prolonged PR interval  Blocks inward K+ channel rectifier to slow AV nodal conduction and prolong the PR interval  Blocks myocardial calcium channels to modify automaticity of Purkinje fibres Effects on ECG  Slowed heart rate and possibly sinus bradycardia  Prolonged PR, QRS and QT intervals
AMIODARONE Highly lipophilic and extensively distributed into tissues Large oral or IV loading doses are required to fill this tissue reservoir or serum levels drop precipitously Terminal-phase elimination dominates after tissue stores become saturated leading to half-life of <55 days and duration of action of 50 days Hepatically metabolised and biliary excretion
AMIODARONE Indications  Acute rate control or cardioversion and maintenance of sinus rhythm  Acute management and chronic suppression of ventricular arrhythmias Dosing  Pulseless VT/VF: 300mg IV rapid bolus with single repeat 150mg if required  Stable VT or polymorphic VT with normal QT OR Cardioversion of AF or rate control in pre-excitation tachycarrhythmias  150mg IV in 100mL 5% dextrose over 10 min, followed by 1mg/min for 6 hours, then 0.5mg/min for next 18 hours  Alternatively LITFL states  5mg/kg bolus in 250mL 5% dextrose over 60 min then 15mg/kg/day infusion
AMIODARONE Adverse reactions to IV dosing  Bradycardia, hypotension and phlebitis  Infusion rates should not exceed 30mg/min and total daily doses not exceed 2.2g  Amiodarone precipitates in saline  Dose adjustments only required for severe hepatic dysfunction Adverse reactions  Cardiovascular – Sinus bradycardia (5% with oral), Torsades (<1%), thrombophlebitis, AV nodal block, hypotension (16% with IV) [may be due to infusion rate or IV solution emulsifier polysorbate 80]  CNS – Gait and movement disorders, paraesthesias, peripheral neuropathy or dizziness  GI - Nausea, vomiting, anorexia, constipation (10-33%)  Hepatic – Raised LFT (in 15-50%), monitor at baseline and 6 monthly  Pulmonary – 2-7% incidence. Often reversible pulmonary fibrosis, eosinophilia, interstitial pneumonia, allergic alveolitis. Monitor baseline PFT’s and repeat CXR annually  Thyroid - Hypothyroidism (4-22%), hyperthyroidism (3-10%) monitor 3-6 monthly  Ocular corneal deposits
AMIODARONE Interactions  Need dose reductions for digoxin, warfarin, procainamide, quinidine, simvastatin, lovastatin
DRONEDARONE Non-iodinated, less lipophilic derivative of amiodarone Primarily Class III but has all four mechanisms like amiodarone Lower rates of pulmonary and thyroid toxicity
SOTALOL Unique non-selective beta-blocker with electrophysiological characteristics of Class III agents Prolongs repolarisation and refractoriness without affecting conduction Onset of action 1-2 hours for oral and 5-10 hrs after IV Duration of action 8-16 hours Half-life 12 hours and increases in renal impairment No metabolites and is excreted unchanged in urine Effective agent for supression of unstable ventricular arrhythmias refractory to other agents
SOTALOL Can suppress SVT and AF but not indicated for cardioversion of AF Normal PO dose is 80mg BD In monomorphic VT can give 1.5mg/kg IV over 5 min Contraindicated if QTc >450ms and infusion ceased if QTc lengthens to >500ms (must be calculated q2- 4hrly) Adverse effects include bradycardia, hypotension 4.3% rate of new or worsened arrhythmia and 2.4% rate of Torsades
IBUTILIDE Prolongs refractory period in atrial and ventricular tissues Inhibits slow inward funny sodium current (rather than outward potassium currents) Blockade of delayed rectifier potassium current may also contribute Onset of action 90 min Metabolised in liver with 2-12 hour half-life Indicated for rapid cardioversion of AF or flutter Can be used in AF with accessory pathway Loading dose 1mg IV or 0.01mg/kg over 10 minutes and repeated every 10 mnutes Adverse effects include hypotension, hypertension, bradycardia, sinus arrest, syncope, QTc prolongation, congestive heart failure and torsades
VERNAKALANT Inhibits sodium and potassium channels Atria more susceptible to refractory period prolongation Used for rapid cardioversion of AF
CLASS IV: CALCIUM-CHANNEL BLOCKERS Inihibit L-type calcium cahnnels, resulting in slowed AV nodal conduction and increased refractory period of nodal tissue In myocardium effects the action potential plateau and modulate strength of muscle contraction Non-dihydropyridine CCB’s have more cardioselectivity and are generally used for SVT and rate control in AF
DILTIAZEM Slows AV nodal conduction, increases AV nodal refractory period, decreases automaticity and prolongs the PR interval Oral onset 15-60min Duration 1-3 hours More commonly used for rate control vs. cardioversion for rapid AF CI: Wide-complex tachyarrhythmia as may be due to WPW with aberrancy, sick sinus, 2nd/3rd degree block, severe hypotension, cardiogenic shock, use with IV beta-blockers and ventricular tachycardia IV bolus 0.25mg/kg over 2 min and infusion 5-15mg/hr then transition to oral therapy Adverse: Bradyarrhythmia, asystole, fatigue, headache, hypotension, AV block, peripheral oedema, syncope and dizziness
VERAPAMIL Non-dihydropyridine More frequently used for SVT management than diltiazem as more potent AV blockade Longer half-life and duration of action than diltiazem Hepatically metabolised with active metabolites 70% renally excreted 3-7hr half-life
VERAPAMIL Onset 1-5min after IV and 10-20min duration SVT conversion rate to sinus of around 90% (similar to adenosine) Same CI as diltiazem 2.5-5mg IV over 2 minutes Similar adverse effect profile
DIGOXIN Cardiac glycoside with positive inotropic, negative chronotropic and negative dromotropic effects due to inhibition of Na-K ATPase and direct vagal effect Narrow therapeutic index (0.5-2ng/mL) Numerous drug interactions Indications  Rate control in AF (specifically in those with CCF)  Symptom reduction in CCF unrelieved by diuretics and ACEi  Contraindicated in ventricular arrhyhthmias but should also be avoided WPW due to risk of VF, acute MI, beri-beri, electrolyte imbalances, sinus node disease, AV block and renal impairment  Conflicing results on mortality
DIGOXIN For AF 250mcg IV loading every 2 hours up to 1.5mg total with reduced dosing in elderly or renal impairment Adverse effects  GI, gynaecomastia, skin rash, eosinophilia, thrombocytopaenia  Can cause sinus bradycardia, AV and sinoatrial block and ventricular arrhythmias Symptoms of toxicity  Mental status changes, visual disturbance, delirium and seizures  Typically PAT with block but can cause any arrhythmia except for fast AF Hepatic metabolism with 50-70% renal excretion mostly as unchanged drug 38 hour half-life Onset 5-60min, peak 1-6 hours and duration 3-4 days
ATROPINE Rapid onset of action, 2-3 hour half-life Hepatically metabolised Dose 600mcg IV every 3-5 minutes (max 3mg) No longer indicated for asystole or PEA Use with caution in coronary heart disease, acute MI, CCF, tachycardia and hypertension as may worsen clinical state through initiating tachyarrhythmia Doses <0.5mg and slow injection have been associated with paradoxical bradycardia Adverse effects include tachyarrhythmia, constipation, blurred vision and photophobia
ADENOSINE Endogenous nucleoside that binds adenosine receptors and inhibits adenylate cyclase, resulting in decreased flow of calcium ions into the AV node Decreases sinoatrial node depolarisation by activation of acetylcholine-sensitive potassium currents Results in hyperpolarisation and automaticity in cardiac nodal tissue Used for treatment of SVT with or without reentry pathways Ineffective for AF, flutter or ventricular tachycardias but can be diagnostic in this setting Half-life <10s
ADENOSINE Dosing schedule  6/12/12 mg Reduce initial dose to 3mg if on dipyramidole or carbamazepine due to upregulation of adenosine receptors, heart transplant patients or central line administration Effects antagonised by caffeine, theophylline and may require higher doses Adverse effects  Transient asystole (<5s), chest pressure, headache, flushing, nausea  Bronchospasm and AF can occur but incidence is rare
MAGNESIUM SULPHATE Inhibits calcium currents that cause pathologic early after- depolarisations and cardiac dyssynchrony Slows sinoatrial node activity, prolongs myocardial conduction time, stabilises excitable membranes and is a cofactor in ion movement Rapid onset of action and indicated in Torsades, polymorphic VT associated with prolonged QT and cardiac arrest where VF or pulseless VT is associated with Torsades If have pulse, 1-2g (5-10mmol) IV diluted and administered as rapid bolus Rapid IV administration leads to vasodilation, flushing and hypotension
ISOPRENALINE/ISOPROTERENOL Beta-1 and beta-2 agonist Increased chronotropic and inotropic activities Vasodilatory Immediate onset, half-life 2.5-5min and duration 10-15min Indications: Refractory bradyarrhythmias, AV nodal block and refractory torsades (overdrive pacing) Contraindicated in angina, pre-existing ventricular arrhythmias, tachyarrhythmias or digoxin toxicity Initiate with bolus 20mcg then infusion at 2mcg/min and titrate every 5- 10min up to 10mcg/min Adverse effects – Hypotension, premature ventricular beats, tachyarrhythmias, ventricular arrhythmia, dyspnoea and pulmonary oedema
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Antiarrhythmics

  • 1.
    ANTIARRHYTHMICS Dr AndrewCrofton ED Registrar
  • 2.
    VAUGHAN-WILLIAMSClass Action Examples ClassIa Sodium channel blockers (intermediate association/dissociation – moderate blockade) Disopyramide, quinidine, procainamide Class Ib Sodium channel blockers (fast – weak blockade) Lignocaine, phenytoin Class Ic Sodium channel blockers (slow – strong blockade) Flecainide, propafenone Class II Beta-blockers Metoprolol, esmolol, labetalol, propranolol Class III Potassium-channel blockers Amiodarone, ibutilide, sotalol, vernakalant Class IV Calcium-channel blockers Diltiazem, verapamil Unclassified Atropine, digoxin, adenosine, isoproterenol, magnesium
  • 3.
    CLASS I All reducethe slope of Phase 0 Class Ia – Prolonged action potential duration Class Ib – Decreased action potential duration Class Ic – No change in action potential duration
  • 4.
    CLASS IA –INTERMEDIATE NA CHANNEL BLOCK Block open sodium channels and have slow dissociation causing increased refractory period Quinidine and disopyramide are rarely used Procainamide
  • 5.
    CLASS IA -PROCAINAMIDE  Pharmacodynamics  Increases refractory period, decreases automaticity and conduction, prolongs cardiac action potentials  Pharmacokinetics  NAPA (active metabolite) blocks potassium channels leading to QT prolongation  Hepatic metabolite then renally excreted  2.5-4.7hr half-life; NAPA 6-8hrs half-life  Onset 5-10 min and duration 1-2 hours  Dosing  20-50mg/min IV until arrhythmia suppressed, hypotension or QRS >50% longer than original followed by 1-4mg/min  OR  100mg IV every 5 min until above
  • 6.
    CLASS IB (FAST- WEAK BLOCKADE) High affinity for open and inactive sodium channels with very rapid dissociation Increases threshold for excitability to reduce automaticity Rapid dissociation means they are less effective for myocardial tissues with rapid conduction e.g. atrial tissue Ratio of effective refractory period to action potential is increased Good efficacy in ischaemic myocardium
  • 7.
    CLASS IB -LIGNOCAINE Pharmacodynamics  Preferentially acts on ischaemic tissues to decrease conduction  Negligable effect on cardiac action potential  Minimal effect on QT or refractory period either Pharmacokinetics  Hepatically metabolised and renally excreted  7-30min half-life (initial) and terminal half-life 1.5-2 hours  Onset 45-90s and duration 10-20 min
  • 8.
    CLASS IB -LIGNOCAINE Dosing in ventricular arrhythmia  Loading dose 1mg/kg IV over 2 minutes  Maintenance 4mg/min for 1 hour; 2mg/min for 1 hour then 1mg/min for 22 hours Dosing in VF  1-1.5mg/kg IV loading then 0.5-0.75mg/kg every 5-10min Indications  Second-line to amiodarone in ventricular arrhythmias Adverse effects  CNS numbness speech impairment, somnolence, dizziness and seizures
  • 9.
    CLASS IC –STRONG SLOW DISSOCIATION Generally indicated for SVT Marked prolongation of QRS without QT prolongation Only act on open sodium channels High proarrhythmic potential that is amplified by myocardial tissue disease, increased sympathetic tone and higher heart rates Associated with increased mortality when used in cardiovascular disease or MI
  • 10.
    PROPAFENONE Also beta-blocker Selective forrapid conducting tissues e.g. atrial tissue Indicated for recent-onset AF (<7 days) Single oral dose 450mg (<70kg) or 600mg (>70kg) Adverse effects  Hypotension, bradycardia, bronchospasm, Aflutter with 1:1 conduction and ventricular proarrhythmia  Avoid in CAD or structural heart disease, asthma, hepatic dysfunction or CCF
  • 11.
    FLECAINIDE Reduces excitability primarilyin His-Purkinje and ventricular myocardium Indicated for conversion of new-onset AF (<7 days) One-time oral dose of 200mg (<70kg) or 300mg (>70kg) Adverse effects  Hypotension, Aflut with 1:1 and ventricular proarrhythmia  Avoid in CCF, CAD, structural heart disease or hypokalaemia
  • 12.
    CLASS II: BETA-BLOCKERS Indications:HTN, SVT, ventricular arrhythmias, recurrent AF (rate control) and thyrotoxicosis Non-cardioselective (beta-1 and 2): Propranolol Cardioselective (beta-1): Esmolol, metoprolol  Better for those with asthma, COAD, IDDM  Dose-dependent cardioselective means lost at high doses Vasodilatory, non-selective: Labetalol
  • 13.
    PROPRANOLOL Non-selective beta-1 andbeta-2 antagonist Pharmacokinetics  Onset oral 1-2 hours; IV <1 min  Hepatically metabolised  3-6 hour half-life  Dosing  Tachyarrhythmia: 1-3mg slow IV push, repeated very 2-5 min up to 5mg total Adverse effects include bradycardia, heart block, hypotension, acute heart failure and bronchospasm
  • 14.
    ESMOLOL Short-acting, selective beta-1antagonist which prevents excessive adrenergic stimulation of the myocardium, causing increased sinus cycle length, prolongation of sinoatrial recovery time and decreased AV nodal conduction Onset 2-10min Duration of action 10-30 min Metabolised in blood by RBC esterases Half-life 9 min Dosing  SVT – 500mcg/kg bolus over 1 min then infusion 50mcg/kg/min titrated to therapeutic effect in 50mcg/kg/min increments every 4 minutes Adverse effects  Hypotension (most common), bradycardia, heart block  Nausea, bronchospasm, pulmonary oedema
  • 15.
    METOPROLOL Selective beta-1 antagonist DecreasesCO, reduced sympathetic outflow and suppresses renin activity to treat hypertension Onset of action 1-2 hrs PO and 20 min IV Hepatically metabolised Half-life 3-4 hours Dosing  1.25-5mg IV every 5 minutes up to total 15mg Adverse effects  Bradycardia, heart block, hypotension and bronchospasm
  • 16.
    LABETALOL Combined selective alpha-1and non-selective beta blocker Beta-blocker: Alpha-block 3:1 in oral and 7:1 in parenteral formulation Used primarily for antihypertensive effect Onset 20min - 2hr orally or 2-5min IV Duration 8-12hr oral or 2-18 hr IV Hepatically metabolised Half-life 6-8 hr oral and 5.5hr IV Dosing  20mg IV push over 2 min; then 40-80mg at 10 min intervals up to 300mg  2mg/min infusion titrated to response (total 300mg cumulative dose) Adverse effects  Orthostatic hypotension, nausea, dizziness, fatigue, heart failure, hyperkalaemia, hepatotoxicity and bronchospasm
  • 17.
    CLASS III –POTASSIUM-CHANNEL BLOCKERS Inhibit inward potassium currents leading to significantly lengthened refractory period Myocardial tissue in a refractory state is less prone to reentrant tachycardia Prolong the QT and carry risk of Torsades
  • 18.
    AMIODARONE Used in acutemanagement and chronic suppression of SVT and ventricular arrhythmias MOA:  Alpha, beta, calcium channel, potassium channel blockade  Blocks inactivated sodium channels to prolong the refractory period which in turn decreases the HR and may cause sinus bradycardia  Non-competitive alpha and beta-blockade decreases sinoatrial node function leading to reduced heart rate, prolonged PR interval  Blocks inward K+ channel rectifier to slow AV nodal conduction and prolong the PR interval  Blocks myocardial calcium channels to modify automaticity of Purkinje fibres Effects on ECG  Slowed heart rate and possibly sinus bradycardia  Prolonged PR, QRS and QT intervals
  • 19.
    AMIODARONE Highly lipophilic andextensively distributed into tissues Large oral or IV loading doses are required to fill this tissue reservoir or serum levels drop precipitously Terminal-phase elimination dominates after tissue stores become saturated leading to half-life of <55 days and duration of action of 50 days Hepatically metabolised and biliary excretion
  • 20.
    AMIODARONE Indications  Acute ratecontrol or cardioversion and maintenance of sinus rhythm  Acute management and chronic suppression of ventricular arrhythmias Dosing  Pulseless VT/VF: 300mg IV rapid bolus with single repeat 150mg if required  Stable VT or polymorphic VT with normal QT OR Cardioversion of AF or rate control in pre-excitation tachycarrhythmias  150mg IV in 100mL 5% dextrose over 10 min, followed by 1mg/min for 6 hours, then 0.5mg/min for next 18 hours  Alternatively LITFL states  5mg/kg bolus in 250mL 5% dextrose over 60 min then 15mg/kg/day infusion
  • 21.
    AMIODARONE Adverse reactions toIV dosing  Bradycardia, hypotension and phlebitis  Infusion rates should not exceed 30mg/min and total daily doses not exceed 2.2g  Amiodarone precipitates in saline  Dose adjustments only required for severe hepatic dysfunction Adverse reactions  Cardiovascular – Sinus bradycardia (5% with oral), Torsades (<1%), thrombophlebitis, AV nodal block, hypotension (16% with IV) [may be due to infusion rate or IV solution emulsifier polysorbate 80]  CNS – Gait and movement disorders, paraesthesias, peripheral neuropathy or dizziness  GI - Nausea, vomiting, anorexia, constipation (10-33%)  Hepatic – Raised LFT (in 15-50%), monitor at baseline and 6 monthly  Pulmonary – 2-7% incidence. Often reversible pulmonary fibrosis, eosinophilia, interstitial pneumonia, allergic alveolitis. Monitor baseline PFT’s and repeat CXR annually  Thyroid - Hypothyroidism (4-22%), hyperthyroidism (3-10%) monitor 3-6 monthly  Ocular corneal deposits
  • 22.
    AMIODARONE Interactions  Need dosereductions for digoxin, warfarin, procainamide, quinidine, simvastatin, lovastatin
  • 23.
    DRONEDARONE Non-iodinated, less lipophilicderivative of amiodarone Primarily Class III but has all four mechanisms like amiodarone Lower rates of pulmonary and thyroid toxicity
  • 24.
    SOTALOL Unique non-selective beta-blockerwith electrophysiological characteristics of Class III agents Prolongs repolarisation and refractoriness without affecting conduction Onset of action 1-2 hours for oral and 5-10 hrs after IV Duration of action 8-16 hours Half-life 12 hours and increases in renal impairment No metabolites and is excreted unchanged in urine Effective agent for supression of unstable ventricular arrhythmias refractory to other agents
  • 25.
    SOTALOL Can suppress SVTand AF but not indicated for cardioversion of AF Normal PO dose is 80mg BD In monomorphic VT can give 1.5mg/kg IV over 5 min Contraindicated if QTc >450ms and infusion ceased if QTc lengthens to >500ms (must be calculated q2- 4hrly) Adverse effects include bradycardia, hypotension 4.3% rate of new or worsened arrhythmia and 2.4% rate of Torsades
  • 26.
    IBUTILIDE Prolongs refractory periodin atrial and ventricular tissues Inhibits slow inward funny sodium current (rather than outward potassium currents) Blockade of delayed rectifier potassium current may also contribute Onset of action 90 min Metabolised in liver with 2-12 hour half-life Indicated for rapid cardioversion of AF or flutter Can be used in AF with accessory pathway Loading dose 1mg IV or 0.01mg/kg over 10 minutes and repeated every 10 mnutes Adverse effects include hypotension, hypertension, bradycardia, sinus arrest, syncope, QTc prolongation, congestive heart failure and torsades
  • 27.
    VERNAKALANT Inhibits sodium andpotassium channels Atria more susceptible to refractory period prolongation Used for rapid cardioversion of AF
  • 28.
    CLASS IV: CALCIUM-CHANNEL BLOCKERS InihibitL-type calcium cahnnels, resulting in slowed AV nodal conduction and increased refractory period of nodal tissue In myocardium effects the action potential plateau and modulate strength of muscle contraction Non-dihydropyridine CCB’s have more cardioselectivity and are generally used for SVT and rate control in AF
  • 29.
    DILTIAZEM Slows AV nodalconduction, increases AV nodal refractory period, decreases automaticity and prolongs the PR interval Oral onset 15-60min Duration 1-3 hours More commonly used for rate control vs. cardioversion for rapid AF CI: Wide-complex tachyarrhythmia as may be due to WPW with aberrancy, sick sinus, 2nd/3rd degree block, severe hypotension, cardiogenic shock, use with IV beta-blockers and ventricular tachycardia IV bolus 0.25mg/kg over 2 min and infusion 5-15mg/hr then transition to oral therapy Adverse: Bradyarrhythmia, asystole, fatigue, headache, hypotension, AV block, peripheral oedema, syncope and dizziness
  • 30.
    VERAPAMIL Non-dihydropyridine More frequently usedfor SVT management than diltiazem as more potent AV blockade Longer half-life and duration of action than diltiazem Hepatically metabolised with active metabolites 70% renally excreted 3-7hr half-life
  • 31.
    VERAPAMIL Onset 1-5min afterIV and 10-20min duration SVT conversion rate to sinus of around 90% (similar to adenosine) Same CI as diltiazem 2.5-5mg IV over 2 minutes Similar adverse effect profile
  • 32.
    DIGOXIN Cardiac glycoside withpositive inotropic, negative chronotropic and negative dromotropic effects due to inhibition of Na-K ATPase and direct vagal effect Narrow therapeutic index (0.5-2ng/mL) Numerous drug interactions Indications  Rate control in AF (specifically in those with CCF)  Symptom reduction in CCF unrelieved by diuretics and ACEi  Contraindicated in ventricular arrhyhthmias but should also be avoided WPW due to risk of VF, acute MI, beri-beri, electrolyte imbalances, sinus node disease, AV block and renal impairment  Conflicing results on mortality
  • 33.
    DIGOXIN For AF 250mcgIV loading every 2 hours up to 1.5mg total with reduced dosing in elderly or renal impairment Adverse effects  GI, gynaecomastia, skin rash, eosinophilia, thrombocytopaenia  Can cause sinus bradycardia, AV and sinoatrial block and ventricular arrhythmias Symptoms of toxicity  Mental status changes, visual disturbance, delirium and seizures  Typically PAT with block but can cause any arrhythmia except for fast AF Hepatic metabolism with 50-70% renal excretion mostly as unchanged drug 38 hour half-life Onset 5-60min, peak 1-6 hours and duration 3-4 days
  • 34.
    ATROPINE Rapid onset ofaction, 2-3 hour half-life Hepatically metabolised Dose 600mcg IV every 3-5 minutes (max 3mg) No longer indicated for asystole or PEA Use with caution in coronary heart disease, acute MI, CCF, tachycardia and hypertension as may worsen clinical state through initiating tachyarrhythmia Doses <0.5mg and slow injection have been associated with paradoxical bradycardia Adverse effects include tachyarrhythmia, constipation, blurred vision and photophobia
  • 35.
    ADENOSINE Endogenous nucleoside thatbinds adenosine receptors and inhibits adenylate cyclase, resulting in decreased flow of calcium ions into the AV node Decreases sinoatrial node depolarisation by activation of acetylcholine-sensitive potassium currents Results in hyperpolarisation and automaticity in cardiac nodal tissue Used for treatment of SVT with or without reentry pathways Ineffective for AF, flutter or ventricular tachycardias but can be diagnostic in this setting Half-life <10s
  • 36.
    ADENOSINE Dosing schedule  6/12/12mg Reduce initial dose to 3mg if on dipyramidole or carbamazepine due to upregulation of adenosine receptors, heart transplant patients or central line administration Effects antagonised by caffeine, theophylline and may require higher doses Adverse effects  Transient asystole (<5s), chest pressure, headache, flushing, nausea  Bronchospasm and AF can occur but incidence is rare
  • 37.
    MAGNESIUM SULPHATE Inhibits calciumcurrents that cause pathologic early after- depolarisations and cardiac dyssynchrony Slows sinoatrial node activity, prolongs myocardial conduction time, stabilises excitable membranes and is a cofactor in ion movement Rapid onset of action and indicated in Torsades, polymorphic VT associated with prolonged QT and cardiac arrest where VF or pulseless VT is associated with Torsades If have pulse, 1-2g (5-10mmol) IV diluted and administered as rapid bolus Rapid IV administration leads to vasodilation, flushing and hypotension
  • 38.
    ISOPRENALINE/ISOPROTERENOL Beta-1 and beta-2agonist Increased chronotropic and inotropic activities Vasodilatory Immediate onset, half-life 2.5-5min and duration 10-15min Indications: Refractory bradyarrhythmias, AV nodal block and refractory torsades (overdrive pacing) Contraindicated in angina, pre-existing ventricular arrhythmias, tachyarrhythmias or digoxin toxicity Initiate with bolus 20mcg then infusion at 2mcg/min and titrate every 5- 10min up to 10mcg/min Adverse effects – Hypotension, premature ventricular beats, tachyarrhythmias, ventricular arrhythmia, dyspnoea and pulmonary oedema
  • 39.
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