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184 Cards in this Set
- Front
- Back
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What are Class I antiarrhythmics? (name 3)
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Antiarrhythmics that block myocardial Na+ channels: quinidine, lidocaine, flecanide
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What are Class II antiarrhythmics? (name 1)
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Sympatholytic antiarrhythmic agents (β-adrenergic blockers): propranolol
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What are Class III antiarrhythmics? (name 2)
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Antiarrhythmics that block myocardial K+ channels: sotolol (bretylium, amiodorone)
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What are Class IV antiarrhythmics? (name 1)
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Antiarrhythmics that block myocardial Ca2+ channels: verapamil (diltiazem)
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Examples of Miscellaneous Antiarrhythmics? (3)
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digitalis glycosides, adenosine, magnesium
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What are cardiac arrhythmias?
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disorders of rate, rhythm, impulse generation, or conduction of electrical impulses within the heart
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What is phase 0 of the AP cardiac phases?
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In a nonpacemaker cell, an increase in conductance of Na+ ions results in phase 0 depolarization. In pacemaker cell or cells in AV node, an increase in conductance of Ca2+ results in phase 0 depolarization (“slow response” action potentials).
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What is phase 1 of the AP cardiac phases?
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This phase of initial repolarization is due to two factors: the inactivation of the inward Na+ current and the activation of a transient outward current. The transient outward current is thought to involve activation of Cl- and K+ currents.
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What is phase 2 of the AP cardiac phases?
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The plateau results from a voltage-dependent ↓ K+ conductance (the inward rectifier, IK1) and is maintained by the influx of Ca2+ through Ca2+ channels that inactivate slowly at + membrane potentials.
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What is phase 3 of the AP cardiac phases?
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The repolarization phase results from a combination of two factors: inactivation of the plateau Ca2+ current and ↑ magnitude of the Ks+ and Kr+ currents.
Kr (rapid K current) = HERG + KCNE 2 Ks (slow K current) = KCNQT1 (KvLQT) + KCNE 1 (min K) |
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What is phase 4 of the AP cardiac phases?
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Characterized by return of the membrane potential to the resting potential of the cell. In a pacemaker cell, however, there is a slow diastolic depolarization, often called phase 4 depolarization or simply the pacemaker potential. [A declining K+ current in the presence of a background leakage current of Na+ may account for diastolic depolarization. Activation of the Ca2+ and a nonselective inward current may also play a role]
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What are the A/V rates and rhythm in sinus tachycardia?
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atria rate = 100-200
ventricular rate = 100-200 rhythm = regular |
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What are the A/V rates and rhythm in sinus bradycardia?
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atria rate = 40-60
ventricular rate = 40-60 rhythm = regular |
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What are the A/V rates and rhythm in atrial flutter?
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atria rate = 240-350
ventricular rate = 80-150 rhythm = regular |
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What are the A/V rates and rhythm in atrial fribrillation?
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atria rate = 300-600
ventricular rate = 140-175 rhythm = very irregular |
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What are the AV rates and rhythm in paroxysmal atrial tachycardia?
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atria rate = 150-250
ventricular rate = 150-250 rhythm = regular |
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What are the AV rates and rhythm in AV nodal tachycardia?
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atria rate = 100-180
ventricular rate = 100-180 rhythm = regular |
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What are the AV rates and rhythm in ventricular tachycardia?
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atria rate = variable
ventricular rate = 100-250 rhythm = regular/irreg |
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What are the AV rates and rhythm in ventricular fibrillation?
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atria rate = variable
ventricular rate = >300 rhythm = no pulse/irregular |
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What do most arrhythmias result from?
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disorders of impulse formation, impulse conduction, or a combination of both
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What factors can precipitate a cardiac arrhythmia? (4)
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1. ischemia with resulting pH and electrolyte abnormalities
2. excessive myocardial fiber stretch 3. excessive discharge/sensitivity to autonomic transmitters 4. exposure to foreign chemicals or toxic substances |
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Do all arrhythmias involve a change in pacemaker site?
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No - some (like sinus tachy/brady) don't. Those that do involve development of an ectopic pacemaker.
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What percent of MI patients have get arrhythmias?
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80-90%
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What percent of general anesthesia patients have get arrhythmias?
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20-50%
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What percent of digitalis patients have get arrhythmias?
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10-20%
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What factors may lead to the development of an ectopic pacemaker? (3)
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1. Latent pacemaker emergence
2. Current of injury 3. Early/delayed After-depolarizations development (torsades de pointes or toxic effects of class III antiarrythmics v. toxic digitalis/norepi respectively) |
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What is Early After-depolarizations?
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Excessive AP prolong with initiation of depolarization during the plateau
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What is delayed After-depolarizations?
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Initiation of depolarization following AP, associated with Ca overload
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How are impulse conduction disorders grouped?
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Either involving reentry (slowed conduction with development of circus movement) or not (differing degrees of AV block)
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What factors favor a development of reentry circuits in impulse conduction disorders?
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Long reentry pathway
Slow conduction Short effective refractory period |
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What is Torsade de pointes?
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Rotation of QRS axis on the ECG around isoelectric baseline which is initiated by a short sequence of ventricular beats with marked QT prolongation
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How is Torsade de pointes treated?
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Therapy aimed at correcting electrolyte abnormalities, eliminate triggered upstrokes (magnesium), shorten AP duration (increase heart rate w/ isoproterenol or pacing).
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What is Brugada Syndrome?
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ventricular fibrillation associated w/ ST segment elevation (SCN5A LF)
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What is Progressive Cardiac Conduction Disorder?
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impaired His-Purkinje conduction, right or left bundle block leading to AV block (SCN5A LF)
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What is Familial Atrial Fibrillation?
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KCNQ1 GF mutation reduces AP duration and effective refractory period in atrial cells
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What antiarrhythmics can cause "acquired long QT" in normal patients?
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quinidine or sotolol
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What drugs put congenital long QT patients at risk for a serious ventricular arrhythmia?
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some antiarrhythmic agents, antihistamines and antibiotics that block myocardial K+ channels
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What's the mechanism of action for antiarrhythmics that work on Na/Ca channels?
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1. block myocardial Na+ or Ca2+ channels
2. by prolonging the time for these channels to recover from activation. |
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What's the mechanism of action for antiarrhythmics that work on K+?
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modulate the magnitude and time course of K+ currents responsible for action potential repolarization and maintenance of the diastolic membrane potential
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What effects do antiarrhythmics have on a normal heart?
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Minimal - most antiarrhythmic agents seem to selectively depress areas exhibiting abnormal pacemaker activity or conduction, while having minimal effects on normal healthy tissue
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What happens to normal hearts at toxic concentrations of antiarrhythmics?
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Toxic can depress automaticity and conduction velocity and even be arrhythmogenic
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What conditions are known to precipitate arrhythmias?
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Conditions such as hypoxia, metabolic poisoning, ischemia, or elevated extracellular K+ (depol myocardial cells)
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What's one possible mechanism for the selectivity of antiarrhythmic agents (polarization mechanism)?
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they could cause a greater degree of depression in cells that are depolarized, compared to normally polarized cells.
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What does it mean that most antiarrhythmic agents block channels in a state-dependent manner?
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They bind with a higher affinity to activated or inactivated channels than to resting channels. Cells that become depolarized will have more channels in the inactivated state and will bind antiarrhythmic compounds with a higher affinity.
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What's one possible mechanism for the selectivity of antiarrhythmic agents (frequency mechanism)?
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Antiarrhythmics may also exhibit some selectivity for cells that are firing at abnormally fast rates - might be due to the prolongation of the recovery of inactivated channels. This is believed to account for the phenomenon of "frequency-dependent block"
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Name 3 drugs that are Class IA antiarrhythmics.
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Quinidine
Procainamide Disopyramide |
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Name 4 drugs that are Class IB antiarrhythmics.
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Lidocaine
Phenytoin Tocainide Mexiletine |
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Name 3 drugs that are Class IC antiarrhythmics.
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Flecainide
Propafenone Moricizine |
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Name 8 drugs that are Class II antiarrhythmics.
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Propranolol
Metoprolol Nadolol Atenolol Acebutolol Pindolol Sotalol Timolol |
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Name 5 drugs that are Class III antiarrhythmics.
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Bretylium
Amiodarone Sotalol Dofetalide Ibutilide |
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Name 3 drugs that are Class IV antiarrhythmics.
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Verapamil
Diltiazem Bepridil |
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What are Class I antiarrhythmics?
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blockers of fast Na+ channel
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What are Class II antiarrhythmics?
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Beta blockers
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What are Class III antiarrhythmics?
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blockers of K+ channel
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What are Class IV antiarrhythmics?
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blockers of Ca2+ channel
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What are Class IA antiarrhythmics?
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moderate block of sodium channels; dissociate from channel w/ intermediate kinetics
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What are Class IB antiarrhythmics?
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weak block; dissociate from channel with very rapid kinetics
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What are Class IC antiarrhythmics?
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pronounced block; dissociate from channel with slow kinetics
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How do drugs with fast dissociation kinetics affect sodium channels based on frequency?
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produce little blocks in cells with normal rates or with moderate membrane depolarization (lidocaine, class 1B)
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How do drugs with moderate dissociation kinetics affect sodium channels based on frequency?
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Produce blocks in cells with normal rates and normal resting membrane potentials but blocks are greatly accentuated at faster rates and depolarized potentials (quinidine, class 1A).
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How do drugs with slow dissociation kinetics affect sodium channels based on frequency?
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produce very pronounced block which is accentuated by fast rates and depolarization-very little frequncy dependence since they often do not dissociate (flecainide, class 1C).
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What is quinidine?
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broad spectrum orally active antiarrhythmic agent - class IA prototype
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Quinidine's mechanism of action?
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reduce Vmax of cardiac action potentials in a frequency dependent manner by its ability to preferentially block activated Na+ channels ("local anesthetic properties" = reduction in membrane responsiveness)
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What is quinidine's effects on pacemaker activity?
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slows pacemaker activity by depressing the rate of phase 4 depolarization in SA nodal cells and especially in ectopic pacemakers
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What is quinidine's effects on repolarization and effective refractory period?
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repolarization is prolonged and the effective refractory period lengthened in the atrium, ventricle, and His-Purkinje system
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What is a special effect quinidine has a low doses?
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potent anticholinergic properties in areas of the heart that are richly innervated, namely, the SA and AV nodes
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Due to the indirect effects of low dose quinidine, what can occur after initial administration?
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There may be a small SA nodal tachycardia and an increase in AV nodal conduction velocity (decrease in PR interval) as a result of the indirect, anticholinergic effects of the drug.
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What are the direct effects of quinidine?
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A decrease in heart rate and a slowing of AV nodal conduction velocity (increase in PR interval)
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What is Procainamide?
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A class IA antiarrhythmic that has much less anticholinergic effect; therefore the effects on heart rate and AV nodal conduction velocity are more direct-characterized by a decrease in HR and a prolongation of the PR interval
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What is Disopyramide?
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A class IA antiarrhythmic that has similar if not more potent anticholinergic properties than quinidine
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What drug is often coadministered in quinidine or disopyramide treatment of atrial flutter or fibrillation? Why?
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a digitalis glycoside will very often be coadministered to minimize the anticholinergic properties
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What effect does quinidine have on sodium current? What is it's recovery?
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blocks activated channels
Recovery = moderately slow (tau 5 sec) |
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What effect does quinidine have on Ca and K current?
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Decreases both (increases APD)
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What effect does quinidine have on the ANS?
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Indirect anticholinergic and alpha blocker
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What effect does quinidine have on HR and ECG?
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Decreases HR and increases QRS and QT with variable PR effects.
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What is the dose and route for quinidine?
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200-500 mg q6hr
Oral in 200 or 300 mg tablets of IV 80 mg/mL |
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What's the half-life and theraputic amount in body for quinidine?
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6hrs (hepatic and renal)
2-5 micrograms/mL |
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Primary adverse effects of quinidine?
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Nausea, vomitting, and thrombocytopenia. It's a potent vasodilator with toxic effects that may be precipitated by increased digoxin
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Contraindications for quinidine?
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Heart failure
Hypotension |
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What is lidocaine?
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Prototype class IB antiarrythmic.
Local anesthetic that blocks activated and inactivated Na+ channels |
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Which cells does lidocaine effect the most? What is the effect?
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Reduces Vmax in ventricular cells (especially depolarized cells).
Has minimal effects on normal cells but significantly depresses damaged or depolarized cells. |
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What effects does lidocaine have on pacemaking activities?
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• little effect on automaticity of the SA node; lidocaine does suppress automaticity of both ectopic ventricular pacemakers and Purkinje fibers
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What's the primary use of lidocaine (with regards to arrhythmias)?
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Effective in the treatment of ventricular arrhythmias, espec those assoc with acute MI (little efficacy for supraventricular arrhythmias)
Drug of choice for the treatment of digitalis-induced arrhythmias, of either atrial or ventricular origin |
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Why isn't lidocaine given orally?
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Inactive when administered orally because of the large first pass liver metabolism.
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What are Mexiletine and tocainide?
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chemically related derivatives of lidocaine that are orally active (resistant to the first-pass hepatic metabolism)
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What is Phenytoin?
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An anticonvulsant and Class IB antiarrhythmic with greater depression of membrane responsiveness
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What is the effect of lidocaine on sodium current? What's the recovery?
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Blocks inactivated and activated channels
Recovery: very fast (tau 0.2 sec) |
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What is the effect of lidocaine on K current?
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Increases (Decreases APD)
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What is the effect of lidocaine on ECG readings?
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Decreased QT
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What's the dose and route for lidocaine?
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150mg + 1-4 mg/min IV
IV or IM |
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What's the half life and therapuetic dose for lidocaine?
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2 hrs (hepatic)
2-6 micrograms/mL |
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What are the adverse effects of lidocaine?
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seizures, tremors, convulsions
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What is Flecainide?
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Prototype of Class IC antiarrhythmics.
potent blocker of myocardial Na+ and K+ channels |
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Mechanism of action for Flecainide?
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Depresses membrane responsiveness = slows conduction velocity.
Effective in supressing PVCs but can be very arrhythmogenic. |
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What's the major clinical use of Flecainide?
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Supraventricular arrhythmias
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What is the effect of Flecainide on Na current and what's the recovery?
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blocks activated channels
Recovery: very slow (tau 15 sec) |
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What is the effect of Flecainide on Ca and K current?
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Decreases both
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What's the effect of Flecainide on inotropy and ECG?
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Inotropy = very negative
ECG = increased PR, significantly increased QRS |
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Dose and route for Flecainide?
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100-200 mg q 12 hrs
Oral |
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Half life and therapuetic dose for Flecainide?
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14 hrs (hepatic and renal)
0.2-1 micrograms/mL |
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Adverse effects of Flecainide?
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CNS and GI effects, plus it can cause arrhythmias
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Contraindications for flecainide?
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AV conduction disturbances
heart failure beta blockers calcium antagonists |
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What is Propafenone?
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A Class IC antiarrhythmic that has significant sympatholytic activity and has been reported to also block Ca2+ channels.
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What is the effect of Propafenone on SA nodes?
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may depress SA nodal automaticity and lead to SA node sinus node block.
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When is Propafenone used?
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Used to suppress ventricular tachycardias and ectopic ventricular rhythms, but should be used with the same reservations as flecainide.
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What is Moricizine?
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A Class IC antiarrhythmic - phenothiazine derivative that is a relatively potent sodium channel blocker that does not prolong action potential duration
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When is Moricizine used?
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used for treatment of ventricular arrhythmias
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What's interesting about the half-life of Moricizine?
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It's long because it has multiple metabolites, some of what are active.
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What is Propranolol?
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Class II antiarrhythmic
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What are the two major effects of Propranolol that make it an antiarrhythmic?
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1. blockade of myocardial β1 receptors, preventing the actions of endogenous catecholamines
2. direct membrane effects-block at higher concentrations myocardial Na+ channels and depress membrane responsiveness ("quinidine-like effect") |
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What are the effects of Propranolol at the nodes?
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Slows SA nodal and ectopic pacemaker automaticity and slows AV nodal conduction
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Is Propranolol more effective in the atria or ventricles?
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Small prolongation of the AP duration and refractoriness that is greater in the atrium than in ventricular tissue
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Clinical uses of Propranolol?
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supraventricular arrhythmias
Recurrent MI prophylaxis |
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What are the effects of propranolol on Na, Ca, and K currents?
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Blocks Na channels at high concentrations
Decreases Ca and K |
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What are the effects of propranolol on the ANS?
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beta blocker
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What are the effects of propranolol on inotropy and ECG?
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negative
Increased PP, PR, and QRS with decreased QT |
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What's the dose and route of propranolol?
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100-200mg q12hr
oral |
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Half life and therapuetic dose of propranolol?
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4-6 hrs (hepatic)
40-100 micrograms/mL |
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Adverse effects of propranolol?
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Precipitates failure, AV conduction block, sedation depression
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When is propranolol contraindicated?
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AV conduction disturbances
Heart failure |
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What are some other class II antiarrhythmics?
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metoprolol, acebutolol, esmolol, sotolol
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What's different about metoprolol and acebutolol compared to propranolol?
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Greater selectivity for beta1
Differences in cardiac membrane channel effects and intrinsic sympathmimetic activity |
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When's esmolol used?
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emergency control of ventricular rate in pts with atrial flutter or fibrillation (duration of action = 10 min IV)
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What is Sotolol?
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Prototype class III antiarrhythmic. Potent beta blocker that also prolongs action potential duration and refractoriness
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What is the effect of Sotolol on the heart?
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Prolong repolarization and refractoriness uniformly and increase the QT interval. They may slow SA nodal automaticity
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When is Sotolol used clinically?
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treatment of supraventricular arrhythmias and life-threatening ventricular arrhythmias (refractory to other drugs)
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When may the effects of Sotolol be compromised?
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By ischemia or fast HR
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When may the effects of Sotolol be exacerbated?
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long cycle lengths or hypokalemia. Some have proarrhythmic properties which result in ventricular tachycardias resembling Torsades de pointe.
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What is the effect of Sotolol on K current?
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Decreases
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What is the effect of Sotolol on the ANS?
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beta blocker
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What is the effect of Sotolol on inotropy?
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negative
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What is the effect of Sotolol on ECG patterns?
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Significantly increases PP, PR and QT
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Dose and route for Sotolol?
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80-320 mg q12hr
oral |
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Half life for Sotolol?
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7hrs (renal - excreted unchanged)
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Adverse effects of Sotolol?
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Torsade de pointes
precipitates hypotension heart failure, bradycardia (monitor with ECG at first) |
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Contraindications of Sotolol?
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patients taking other drugs that prolong QT
Kidney failure |
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What are Ibutilide and dofetalide?
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Class III antiarrhythmics - may selectively block myocardial Kr+ channels involved in initiating action potential repolarization
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Clinical use of Ibutilide and dofetalide?
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IV ibutilide is effective in restoring normal sinus rhythm in patients with atrial flutter and fibrillation
oral dofetalide is often used to maintain normal sinus rhythm after conversion. |
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What is Amiodarone?
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Class III antiarrhythmic that prolongs action potentials by blocking several types of K channels
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What's similar between Amiodarone and lidocaine?
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preferentially blocks inactivated myocardial Na+ channels - therefore is more effective in depressing conduction in cells that are depolarized or have a longer action potential duration
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What is Bretylium?
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Class III antiarrhythmic that has indirect and direct effects on the heart; it is concentrated in adrenergic nerve terminals and interferes with the release of catecholamines
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What is the major effect of Bretylium?
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prolongation of action potential duration and refractoriness in atrium, ventricle, and the His-Purkinje system
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When is Bretylium used clinically?
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used to treat ventricular fibrillation when lidocaine and cardioversion have failed.
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What is Verapamil?
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Class IV Antiarrhythmic that blocks both activated and inactivated calcium channels
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Major effect of Verapamil in the heart?
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decrease SA nodal rate, prolong AV nodal refractoriness and prolong the PR interval
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What inidrect effects does Verapamil have why?
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Peripheral vasodilation (due to block of vascular smooth muscle calcium channels) = an indirect reflex increase in SA node rate
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When is Verapamil used clinically?
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supraventricular arrhythmias (convert atrial tachycardia to normal sinus rhythm)
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What does the cardiotoxic effects of Verapamil relate to?
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it's negative inotropic properties and cardiac depressant effects
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When is Verapamil contraindicated?
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Sick sinus syndrome
AV conduction disturbances CHF Hepatic dysfunction |
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When should one administer Verapamil with caution?
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when it's administered with other drugs like beta blockers or digitalis glycosides that also slow AV nodal conduction
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What are the effects of Verapamil on Na and Ca current?
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Decreases both (Na only in depolarized cells)
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What are the effects of Verapamil on the ANS?
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Reflexive increase in autonomic tone
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What are the effects of Verapamil on inotropy?
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negative
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What are the effects of Verapamil on ECG readings?
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increase PP and significant increase in PR
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Dose and route for Verapamil?
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5-10 mg bolus with 5-10 mg q4-6hrs
Oral or IV/IM |
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Half life for Verapamil?
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5 hrs (hepatic/renal)
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Adverse effects of Verapamil?
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hypotension
cardiodepression |
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What are Diltiazem and bepridil? Uses?
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Ca channel blocking drugs that are useful Class III antiarrhythmics.
Used in management of supraventricular arrhythmias, including controlling of rate in atrial fibrillation |
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What is Digitalis?
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Miscellaneous Antiarrhythmic - (glycoside) due to it's indirect "vagal enhancing" properties
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How does digitalis effect the heart?
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inhibit myocardial Ca2+ currents and enhance K+ currents resulting in an increase in AV nodal refractoriness
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Main clinical uses of digitalis?
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heart failure (due to +inotropic effects)
terminating AV nodal reentrant arrhythmias and controlling ventricular rate in atrial fibrillation. |
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What's important about the therapuetic index of digitalis? Why?
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It's low due to the possibility of life threatening arrhythmias from intracellular calcium overload and induction of delayed after-depolarizations
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What's the effect of digitalis on the ECG?
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increased PR and alteration of ST
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What is Adenosine?
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Miscellaneous Antiarrhythmic - a naturally occurring nucleoside that interacts with G-protein coupled receptors to activate myocardial K+ currents and antagonizes the stimulatory effects of norepinephrine on myocardial Ca2+ currents
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What are the antiarrhythmic effects of Adenosine?
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similar to those of Ca2+ channel blockers: slowing of SA nodal rate, increases in AV nodal refractoriness and slowing of AV nodal conduction velocity
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When is adenosine used clinically?
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Given as a bolus to tx supraventricular tachycardias
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Half life of adenosine?
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Very short (seconds) due to carrier medicated cellular uptake
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Adverse effects of adenosine?
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hypotension, bronchospasm or transient asystole (minimized due to short half life)
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When's magnesium used as an antiarrhythmic?
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1-2 g MgSO4 IV to prevent recurrent episodes of Torsades de pointes and digitalis-induced ventricular arrhythmias.
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When's potassium used as an antiarrhythmic?
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Restore normal body gradients
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What's the effect of hypokalemia?
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potentates the development of delayed after-depolarizations and ectopic pacemaker activity, especially in the presence of digitalis
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What's the effect of hyperkalemia?
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slows conduction and suppresses ectopic activity
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What's the drug of choice for rate control in the case of Afib/flutter?
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Verapamil, ditiazem, beta blockers, or digoxin
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What's the drug of choice for cardioversion in the case of Afib/flutter?
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DC Cardioversion
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What's the drug of choice for chronic tx in the case of Afib/flutter?
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Verapamil, ditiazem, beta blockers, or digoxin (rate control)
Amiodorone, sotolol, flecainide, propafenone, dofitilide (maintenance of sinus rhythm) |
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What's the drug of choice for acute management of supraventricular tachycardias?
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IV adenosine, verapamil, ditiazem
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What's the drug of choice for long-term suppression of supraventricular tachycardias?
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Verapamil, ditiazem, beta blockers, digoxin, flecainide, amiodorone, sotolol, propafenone
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What's the drug of choice for PVCs?
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None if pt is asymptomatic
Beta blockers |
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What's the drug of choice for sustained vent tachycard?
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amiodorone (alts: procainamide or lidocaine)
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What's the drug of choice for vent fibrillation?
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amiodorone (alts: procainamide or lidocaine)
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What's the drug of choice for glycoside-induced vent tachyarrhythmias?
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digoxin-immune Fab (antibody fragments). Self limiting if you stop digitalis
Alternatives: lidocain or phenytoin |
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What's the drug of choice for drug induced torsades de pointes?
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IV magnesium
Alternatives: cardiac pacing or isoproterenol |
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What's an important consideration before initiating antiarrhythmic therapy?
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All affect normal cardiac ion channels are are therefore extremely toxic
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What are alternatives to antiarrhythmics?
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RF ablation for reentry arrhythmias
Implantable cardioverter-defibrillator (ICD). |
