Antiarrhythmics Flashcards
Describe phases 0-4 of the action potential in cardiac cells
Phase 0- Rapid depolarization Phase 1- Partial repolarization Phase 2- Plateau Phase 3- Repolarization Phase 4- Pacemaker potential
4 mechanisms of arrhythmias
Altered automaticity
Delayed after-depolarization
Re-entry
Conduction block
Factors leading to arrhythmias
Hypoxemia Electrolyte imbalances Acid-base imbalances Myocardial ischemia Altered SNS activity Bradycardia Medications Ventricular hypertrophy
When to treat?
Cannot treat by correcting the underlying cause
Hemodynamic function is compromised
Disturbance predisposes pt to more serious arrhythmia or comorbidity
Non-pharm treatments
Acute-
Vagal maneuvers
Cardioversion
Prophylaxis-
Radio ablation
Implantable defibrillator
Pacing (external, temp, permanent)
Classification of antiarrhythmic drugs
Class I: Sodium channel blockers Class II: Beta blockers Class III: Potassium channel blockers Class IV: Calcium channel blockers Class V: Unclassified drugs
Class I drugs affect which phase of the action potential?
Phase 0, they block sodium channels. This decreases action potential propagation and slows rate of conduction
Class I drugs
IA (won’t see these anymore)
Quinidine
Procainamide
IB
Lidocaine
Lidocaine blocks which type of Na channels? What is it used for?
Fast channels
Useful in VT, V-fib, PVCs especially those associated with ischemia
Lidocaine is ______% protein bound. How is it metabolized?
50
Hepatic metabolism. Has an active metabolite. Metabolism impaired by cimetidine, propranolol, CHF, MI, liver failure, GA. Induced by barbs, phenytoin, rifampin.
Lidocaine adverse effects
Same as LA toxicity
Class IC agent
Flecainide
Class II agents work on what phase? What effects do they have?
Phase 4. Beta-blockers depress spontaneous phase 4 depolarization.
Lowers myocardial O2 needs
Slows conduction through AV node, elongates PR interval
Decreased automaticity
What are class II agents used for?
SVT, atrial and ventricular arrhythmias
Suppress and treat dysrhythmias during MI and reperfusion
Also useful for digoxin toxicity induced dysrhythmias and SVT
Class II agents
Propranolol
Metoprolol
Esmolol
Labetalol (off-label)
Propranolol metabolism and side effects
Highly protein bound, hepatic metabolism with weak metabolite
Bradycardia, hypotension, myocardial depression, fatigue, bronchospasm
Use with caution in reactive airway disease and hypovolemia
Propranolol dose/kinetics
1mg/min IV (total 3-6mg)
2-5 min onset, peak 10-15 min, 3-4 hour duration
Metoprolol dose/kinetics
B1 selective
5mg IV over 5 min, max 15mg, onset 2.5 min, duration 3-4 hours
Metabolized by the liver
Can be used in mild CHF
Esmolol dose/kinetics
B1 selective
0.5 mg/kg IV bolus over 1 min, 50-300 mcg/kg/min, duration <15 mins
Little effect on BP at smaller doses
Esmolol is useful in
Preventing recurrence of tachyarrhythmias, both supraventricular and ventricular caused by SNS stimulation
Esmolol is metabolized
Rapidly by plasma esterases, not the same for sux
Class III agents work on which phase?
Phase 1 and 2, by blocking K channels depolarization is prolonged, increasing action potential duration
Reduces the time during the cycle that cells are excitable, making the triggering of a pro-arrhythmic event less likely
Class III agents are useful in
Supraventricular and ventricular arrhythmias
Prophylaxis in CV surgery in pts with high incidence of a-fib
Preventative therapy in pts who have survived sudden cardiac death who are not candidates for ICD
Control of a-fib
Class III agents
Amiodarone
How does amiodarone work? What is it useful for?
Blocks K/Na/Ca channels, has alpha/beta antagonist activity (thus also class I, II, and IV activity)
Treatment/prophylaxis in SVT, VT/VF. A-fib
First line drug in VT/VF resistant to defibrillation
Amiodarone dosing/kinetics
Bolus of 150-300mg IV over 2-5 minutes, then 1mg/hr for 6 hrs, then 0.5mg/hr for 18 hrs
Looooooong half-life (29 days), hepatic metabolism, active metabolites
Highly protein bound, large volume of distribution, excreted in bile
Amiodarone side effects
Pulmonary toxicity Photosensitive rashes Grey/blue skin Thyroid problems Corneal deposits CNS/GI disturbances Torsades de pointes Heart block Hypotension Nightmares (25%) Abnormal LFT (20%) Reduces clearance of digoxin and warfarin
Class IV agents work on which phase?
Phase 2, by blocking Ca channels conduction through the AV node is decreased and Phase 2 is shortened
Contractility is also decreased by these agents
Class IV agents are useful in
SVT and ventricular rate control in a-fib/flutter
Prevent recurrence of SVT
Not used in ventricular arrhythmias
Class IV agents
Verapamil
Diltiazem
Verapamil dosing/kinetics
2.5-10mg IV over 1-3 minutes
Highly protein bound, half-life 6-8hrs
Hepatic metabolism, excreted in urine/bile
Do not use with beta-blocker, can cause complete heart block
Verapamil side effects
Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade
Verapamil cautions
Myocardial depression and hypotension with inhalational agents
Increased risk of LA toxicity
Hyperkalemia with dantrolene
Decreased digoxin clearance
Diltiazem dosing/kinetics
5-20mg IV (0.25-0.35 mg/kg) over 2 min, 10 mg/hr infusion
Half-life 4-6hrs
Highly protein bound, hepatic metabolism, excreted in urine
Diltiazem side effects
Myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs NM blockade
Class V agents
Adenosine, digoxin, phenytoin, atropine
Adenosine MOA
Slows AV node conduction
Used for acute treatment
Termination of SVT/diagnosis of VT (does nothing for VT)
Adenosine dosing/kinetics
6mg IV rapid bolus, 6-12mg repeat dose after 3 min
Half-life <10 secs
Eliminated by plasma and vascular endothelial cell enzymes
Adenosine side effects
Excessive AV/SA node inhibition, facial flushing, headache, dyspnea, chest discomfort, nausea, bronchospasm
Contraindicated in asthma, heart block
Digoxin MOA
Increases vagal activity, decreasing SA node activity and prolongs conduction through AV node
Decreases HR, preload and afterload
Slows AV conduction by increasing AV node refractory period
Positive inotrope
Used for a-fif/flutter (controls V rate), especially with heart failure
Digoxin dosing/kinetics
0.5-1mg in divided doses over 12-24hrs
Onset 30-60 minutes
Narrow therapeutic index
Weak protein binding
90% excreted by kidneys, reduce dose in renal failure and the elderly
Digoxin adverse effects
Arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation- worsened by hypokalemia/magnesemia
Toxicity treatment- Phenytoin for V arrhythmias Pacing Atropine Digoxin immune fab
Phenytoin MOA
Resembles lidocaine in its effects
Used for arrhythmias brought on by digoxin toxicity
Can also be used in VTs and Torsades
Phenytoin dosing/kinetics
1.5 mg/kg IV every 5 min up to 10-15 mg/kg
Therapeutic levels 10-18 mcg/ml
Metabolized by the liver, excreted in urine
E1/2 time of 24 hours
Phenytoin adverse effects
CNS depression, inhibits insulin secretion, bone marrow depression, nausea
Atropine MOA/dosing/kinetics
Muscarinic antagonist
Treats unstable bradyarrhythmias (asystole/PEA)
0.4-1.0mg IV, repeat as needed
Onset <1min, duration 30-60min
Metabolized by liver
Atropine cautions
Doses less then 0.4mg can produce a paradoxical response
Crosses BBB, produces CNS effects
