Arrhythmia Flashcards
Aim of therapy
To reduce ectopic pacemaker activity
To modify conduction or refractoriness in reentrant circuits to disable the circular movement
Antiarrhythmic agents generally alter:
Diastolic potential in pacemaker cells and/or resting membrane potential in ventricular cells (phase 4)
Phase 4 depolarization
Threshold potential
Action potential duration
Effect on Automaticity:
- Can slow spontaneous discharge by:
Depressing diastolic depolarization
Otherwise known as phase 4
Shifting threshold voltage to zero
Hyperpolarizing resting membrane potential - Affects ectopic sites more than sinus node
Effect on Reentry:
- Improves or depresses conduction
Eliminate unidirectional block
Facilitate conduction so returning wavefront reenters when cells still refractory
Depress conduction to transform unidirection to bidirectional block - Prolong refractoriness relative to action potential duration
Vaughan Williams Classification of Antiarrhythmic Drugs Class I
block sodium channels
works mostly on Phase 0, but also works on the latter parts
T/F: Vaughan Williams Classification of Antiarrhythmic Drugs Class Ia example: Lidocaine
F:
Ia (quinidine, procainamide, disopyramide)
Ib (lidocaine)
Ic (flecainide)
Vaughan Williams Classification of Antiarrhythmic Drugs Class II
β-adrenoreceptor antagonists
works on Phase 4, keeps slope less steep (flattens the slope)
Atenolol, sotalol
Vaughan Williams Classification of Antiarrhythmic Drugs Class III
prolong action potential and prolong refractory period
Works on Phase 0 to 3
Amiodarone, sotalol
Drugs which prolong ERP (effective refractory period) by prolonging action potentials
Vaughan Williams Classification of Antiarrhythmic Drugs Class IV
Calcium channel antagonists
Works on Phase 2
verapamil
T/F: Lidocaine Low toxicity high effectiveness in arrhythmias associated with MI
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Lidocaine toxicity
Toxicity: one of the least cardiotoxic drugs
May precipitate hypotension by depressing myocardial contractility in large doses in patients with heart failure
Neurologic: parethesias, convulsions, dizziness
T/F Flecainide is a potent Na and K channel blocker
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Very effective in suppressing premature ventricular contractions and premature atrial contractions
Class Ic: Flecainide
T/F Class Ic May exacerbate arrhythmias in patients with ventricular arrhythmias + patients with previous MI and ventricular ectopy
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Flecainide route, half-life, metabolism
oral, 20 hours, hepatic and renal metabolism
main use is for patients with paroxysmal AF and those without structural heart diease
Class Ic: Flecainide
Prototype of Class II
propranolol, esmolol
MOA of class II
indirectly reduce the phase 4 slope by blocking positive chronotropic action of norepinephrine
therapeutic use of class II
suppression of ventricular ectopic depolarizations
Amiodarone cardiac effect
Broad spectrum of cardiac actions, high efficacy
Markedly prolongs APD (QT interval)
Significantly blocks inactivated Na channels
Has weak β-adrenergic and calcium channel blocking actions
Indications of amiodarone
Preventing recurrent VT
Adjuvant therapy in patients with ICD
Maintaining sinus rhythm in atrial fibrillation patients with structural heart disease
Amiodarone cardiac toxicity
Symptomatic bradycardia and heart block in patients with preexisting sinus or AV node disease
Prolongs QT interval
Amiodarone toxicity
Pulmonary fibrosis (dose-related)
Hypothyroidism or hyperthyroidism
Amiodarone has iodine in it, so you have to check the patient’s thyroid function every so often.
Abnormal liver function tests and hepatitis
Skin deposits, photodermatitis
T/F: Sotalol is not cardioselective
T both class II and class III effects
Sotalol route, half-life, excretion
oral, 12 hours, renal excretion
Sotalol toxicity
further depression of LV function
Sotalol use
life-threatening ventricular arrhythmias maintaining sinus rhythm in AF
Class IV prototype
Verapamil
Effects of verapamil
Block both activated and inactivated L-type Ca channels
Prolongs AV nodal conduction time and ERP
Slows the SA node
Peripheral vasodilation
Verapamil indication
Termination of SVT (if adenosine not available)
Control heart rate in AF
Verapamil toxicity
Dangerous in patients with VT misdiagnosed as SVT, may cause hypotension and VF
Negative inotropic effects
Can induce AV block
Adenosine half life
<10 seconds
Adenosine cardiac effect
Marked hyperpolarization
Suppression of Ca-dependent AP
Directly inhibits AV nodal conduction
DOC for prompt conversion of SVT to sinus
Adenosine
Magnesium MOA
not well known
use of magnesium
Digitalis-induced arrhythmias if low Mg
Torsade de pointes even if Mg normal (1g/IV)
Main indication of digoxin
Slow the ventricular rate in chronic AF (not very effective in acute setting)
MOA of digoxin
Slowing the sinus node discharge rate
Prolonging AV nodal refractoriness
Toxicity of digoxin
Headache, nausea/vomiting, diarrheas and arrhythmias
Pharmacologic Treatment of Arrhythmias
Eliminate the cause if possible Make a firm diagnosis Determine baseline condition Evaluate need for therapy Weigh benefits vs risks of therapy
T/F Antiarrythmics can be proarrhythmics.
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