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38 Cards in this Set
- Front
- Back
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Which tissue in the heart is a “slow conducting” tissue and thus would be the most influenced by a class IV antiarrhythmic drug which is more than 90% effective to arrest a supraventricular tachycardia caused by re-entry in this tissue?
a. Atrial muscle b. The right Bundle of His c. The atrioventricular (AV) node d. Left or right ventricular muscle (myocardium) e. A Purkinje fiber (2006exam3) |
c. The atrioventricular (AV) node
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match each drug with a description (each may be used only once)
drugs: (a)amiodarone, (b)tocainide, (c)flecainide, (d)propranolol, (e)disopyramide 1. A class Ic drug which blocks sodium (Na+) channels in a not “use-dependent” manner and thus has little effect on the effective refractory period (ERP). 2. A class III drug which may delay repolarization of cardiac tissue: It can have a high volume of distribution. 3. A drug which blocks Na+ channels in a “use-dependent manner and thus slows conduction velocity through ventricular muscle; It has a stronger effect on ventricular tissue than other drugs of its class 4. A class Ib drug which enhances the iK1 current, particularly in “damaged” ventricular muscle 5. A class II drug which would likely slow the heart rate and/or decrease AV node conduction; It might be efficacious against a cardiac dysrhythmia caused by an ectopic pacemaker involving an abnormal Ca++ current (2006exam3) |
1.A class Ic drug which blocks sodium (Na+) channels in a not “use-dependent” manner and thus has little effect on the effective refractory period (ERP): (c)flecainide
2.A class III drug which may delay repolarization of cardiac tissue: It can have a high volume of distribution: (a)amiodarone 3. A drug which blocks Na+ channels in a “use-dependent manner and thus slows conduction velocity through ventricular muscle; It has a stronger effect on ventricular tissue than other drugs of its class: (e)disopyramide 4. A class Ib drug which enhances the iK1 current, particularly in “damaged” ventricular muscle: (b)tocainide 5.A class II drug which would likely slow the heart rate and/or decrease AV node conduction; It might be efficacious against a cardiac dysrhythmia caused by an ectopic pacemaker involving an abnormal Ca++ current: (d)propranolol |
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This class III antiarrhythmic drug is more likely to cause torsade de pointes (TdP) in women compared to men.
a. Quinidine b. Adenosine c. d,l-Sotalol d. Esmolol e. Diltiazem (2006exam3) |
c. d,l-Sotalol
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Torsade de points, a dangerous polymorphic ventricular tachycardia cardiac dysrhythmia, is associated with (not a consequence of TdP):
a. no P wave in the electrocardiogram (EKG). b. a prolonged QT interval in the electrocardiogram. c. an inverted T wave in the electrocardiogram. d. the use of a class II antiarrhythmic drug. e. no QRS complex in the electrocardiogram. (2006exam3) |
b. a prolonged QT interval in the electrocardiogram.
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This class Ia antiarrhythmic drug is slowly metabolized by the liver in about 25% of patients to the cardioactive metabolite NAPA; It is more likely to produce adverse effects in these patients (like a reaction which mimics systemic lupus erythematosus).
a. Ibutilide b. Procainamide c. Lidocaine d. Bretylium e. Verapamil (2006exam3) |
b. Procainamide
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This drug is considered an orally effective lidocaine which is a class Ib antiarrhythmic drug which restores the resting membrane potential of “damaged” cardiac tissue to a more normal level.
a. Propafenone b. Disopyramide c. Acebutolol d. Tocainide e. Moricizine (2006exam3) |
d. Tocainide
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This class Ic antiarrhythmic drug has a “strong” effect to reduce the conduction velocity (CV) of cardiac tissue, but because it is structurally similar to propranolol it needs to be used with caution in those with coexisting COPD.
a. Procainamide b. Mexilitine c. Propafenone d. Disopyramide e. d,l-Sotalol (2006exam3) |
c. Propafenone
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Correctly match the antiarrhythmic drug with each short description. Use each choice only once.
drugs: Quinidine, Adenosine, Amiodarone, Diltiazem, Mexilitine a. This drug cannot be used to treat a ventricular tachycardia associated with an accessory conduction pathway between the atria and the ventricles (Kent Bundle). b. This drug has a very short half life (iv use) and hyperpolarizes AV nodal cells. c. Can cause cinchonism, a reversible CNS-related adverse reaction. d. Of the five choices, this drug would have the greatest likelihood of producing torsade de pointes e. This class I (other) drug has mixed class Ia and Ib properties. (2006exam3) |
diltiazem: a. This drug cannot be used to treat a ventricular tachycardia associated with an accessory conduction pathway between the atria and the ventricles (Kent Bundle).
adenosine: b. This drug has a very short half life (iv use) and hyperpolarizes AV nodal cells. quinidine: c. Can cause cinchonism, a reversible CNS-related adverse reaction. amiodarone: d. Of the five choices, this drug would have the greatest likelihood of producing torsade de pointes mexilitine: e. This class I (other) drug has mixed class Ia and Ib properties. |
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This class IC antidysrhythmic drug strongly blocks Na+ channels in a not “use-dependent” manner to decrease the conduction velocity of “fast” cardiac tissues; Does not delay Na+ channel reactivation and thus has little or no effect on the effective refractory period (ERP).
a. Procainamide b. Flecainide c. Propranolol d. Tocainide e. Amiodarone (2004exam3) |
b. Flecainide
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This class IB antidysrhythmic drug blocks Na+ channels (not use dependent) and enhances the iK1 potassium current; May “work” better in abnormal cardiac tissue.
a. Disopyramide b. Propafenone c. Ibutilide d. Lidocaine e. Diltiazem (2004exam3) |
d. Lidocaine
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Correctly match the drug with each short description. Each may be used only once
drugs: Amiodarone, procainamide, Propafenone, verapamil, Disopyramide a. Class III antidysrhythmic drug which antagonizes the iX1 potassium current; Prolongs the action potential duration and the ERP; May cause reversible corneal deposits. b. Class Ic antidysrhythmic drug; Structurally similar to propranolol; Proarrhythmic properties; Some people (~10%) have slow liver metabolism c. Used i.v. to treat supraventricular tachycardia cause by re-entry in the AV node (>90% effective); Not effective for the Wolff-Parkinson-White Syndrome; May suppress ectopic pacemakers caused by abnormal Ca++ entry into cardiac cells. d. Class IA antidysrhythmic drug; Strong anticholinergic effects; Effect on ventricular tissue more pronounced than other drugs of same class. e. Class IA antidysrhythmic drug; Some people are slow hepatic metabolizers of the drug; May cause a reversible systemic lupus erythematosus-like reaction, especially at higher doses and during chronic use (2004exam3) |
amiodarone: a. Class III antidysrhythmic drug which antagonizes the iX1 potassium current; Prolongs the action potential duration and the ERP; May cause reversible corneal deposits.
propafenone: b. Class Ic antidysrhythmic drug; Structurally similar to propranolol; Proarrhythmic properties; Some people (~10%) have slow liver metabolism verapamil: c. Used i.v. to treat supraventricular tachycardia cause by re-entry in the AV node (>90% effective); Not effective for the Wolff-Parkinson-White Syndrome; May suppress ectopic pacemakers caused by abnormal Ca++ entry into cardiac cells. disopyramide: d. Class IA antidysrhythmic drug; Strong anticholinergic effects; Effect on ventricular tissue more pronounced than other drugs of same class. procainamide: e. Class IA antidysrhythmic drug; Some people are slow hepatic metabolizers of the drug; May cause a reversible systemic lupus erythematosus-like reaction, especially at higher doses and during chronic use |
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Correctly select the incorrect statement about the use of the Vaughan-Williams classification of antidysrhythmic drugs.
a. It is not always apparent which of multiple effects are responsible for suppression of cardiac dysrhythmias. b. The classification is based on drug effects in abnormal cardiac tissue that may generate a cardiac dysrhythmia. c. The classification is useful as a conversational shorthand for keeping track of the mechanism of action of antidysrhythmic drugs d. The metabolites of many drugs may contribute to antidysrhythmic drug effects. e. Drugs within a class are not necessarily clinically similar (2004exam3) |
b. The classification is based on drug effects in abnormal cardiac tissue that may generate a cardiac dysrhythmia.
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Select the most important mechanism by which a class IA antidysrhythmic drug like quinidine can convert a cardiac dysrhythmia caused by a re-entry mechanism in a branch of the Purkinje system (involves a unidirectional block) to a normal sinus rhythm.
a. Decreased ERP b. A cholinergic effect (increased vagal activity) c. Decreased action potential conduction velocity (i.e., decreased phase 0) d. Enhancement of a K+ channel e. Antagonism of cardiac beta1 receptors. (2004exam3) |
c. Decreased action potential conduction velocity (i.e., decreased phase 0)
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A class II antidysrhythmic drug which can treat supraventricular tachycardia caused by re-entry in the AV node (~70% effective) and can slow the heart rate and decrease AV node conduction velocity.
a. Procainamide b. Flecainide c. Propranolol d. Tocainide e. Amiodarone (2004exam3) |
c. Propranolol
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This antidysrhythmic drug (Class V?) is an endogenous compound with a very short half life and is effective i.v. to treat AV node cardiac dysrhythmias.
a. Norepinephrine b. Esmolol c. Magnesium chloride d. Adenosine e. Atropine (2004exam3) |
d. Adenosine
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This drugs puts a person at risk for the potentially serious cardiac arrhythmia Torsades de Pointes (TdP) because it may prolong the QT interval of the ECG:
a. adenosine b: lidocaine c. tocainide d. amiodarone e. verapamil (2005exam3) |
d. amiodarone
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Match each drug with its mechanism of action (use each only once).
Drugs: lidocaine, amiodarone, quinidine, flecainide, propranolol a. blocks Na+ channels in a "use-dependent" manner; prolongs the effective refractive period (ERP) because the drug delays reactivation of NA+ channels. b. Blocks Na+ channels; not "use-dependent"; enhances the iK1 current; restores the resting membrane potential back to a more normal level. c. blocks the iK1 K+ current responsible for most of phase 3 repolarization; prolongs the cardiac muscle action potential. d. blocks Na+ channels; not "use-dependent"; little or no influence on the ERP e. slows heart rate; decreases AV node CV; may be efficacious to treat cardiac arrhythmias caused by an ectopic pacemaker involving abnormal intracellular Ca2+ (2005exam3) |
quinidine: a. blocks Na+ channels in a "use-dependent" manner; prolongs the effective refractive period (ERP) because the drug delays reactivation of Na+ channels.
lidocaine: b. Blocks Na+ channels; not "use-dependent"; enhances the iK1 current; restores the resting membrane potential back to a more normal level. amiodarone: c. blocks the iK1 K+ current responsible for most of phase 3 repolarization; prolongs the cardiac muscle action potential. flecainide: d. blocks Na+ channels; not "use-dependent"; little or no influence on the ERP propranolol: e. slows heart rate; decreases AV node CV; may be efficacious to treat cardiac arrhythmias caused by an ectopic pacemaker involving abnormal intracellular Ca2+ |
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This class III drug used to treat cardiac arrhythmias is a racemic mixture of the D and L isomers, and women are at a greater risk for TdP compared to men:
a. propafenone b. moricizine c. flecainide d. sotalol e. disopyramide (2005exam3) |
d. sotalol
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This class Ia drug is often used to treat atrial arrhythmias, but may cause reversible CNS side effects such as cinchonism:
a. ibutilide b. diltiazen c. quinidine d. tocainide e. amiodarone (2005exam3) |
c. quinidine
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This class Ia drug is slowly metabolized to an active metabolite by about 25% of people taking the drug:
a. lidocaine b. procainamide c. sotalol d. disopyramide e. mexilitine (2005exam3) |
b. procainamide
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Which of the following is a potential problem or drawback of the Vaughan-Williams classification of antiarrhythmic drugs?
a. drugs within the same class may not always be clinically similar b. many drugs, especially the newer antiarrhythmic drugs, have multiple effects c. the metabolites of many drugs may contribute to antiarrhythmic effects d. The classification is based largely on drug action in normal cardiac tissue e. all of the above are potential drawbacks. (2005exam3) |
e. all of the above are potential drawbacks.
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Correctly select the antiarrhythmic drug which has multiple pharmacodynamic effects belonging to more than one of the classes of the Vaughan-Williams classification:
a. tocainide b. flecainide c. disopyramide d. mexilitine e. verapamil (2005exam3) |
d. mexilitine
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Digoxin is often preferred over digitoxin for the treatment of mild to moderate heart failure because:
a. digoxin has a different mechanism of action (different pharmacodynamics) compared to digitoxin b. digoxin has a shorter half-life of elimination compared to digitoxin c. digitoxin is no longer available d. digoxin leads to fewer non-cardiac and cardiac adverse reactions than digitoxin (2005exam3) |
b. digoxin has a shorter half-life of elimination compared to digitoxin
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When digoxin is efficacious to treat heart failure, systemic vascular resistance decreases because:
a. digoxin directly causes arteriolar dilation. b. sympathetic reflexes decrease because of better tissue perfusion. c. digoxin directly decreases heart rate d. a and b e. b and c (2004exam3) |
b. sympathetic reflexes decrease because of better tissue perfusion.
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Match each drug with a short description.
Drugs: (a)tocainide, (b)propafenone, (c)quinidine, (d)diltiazem, (e)bretylium 1. Blocks cardiac Na+ channels in 'use-dependent' manner; class Ia drug; can cause the very dangerous Torsades de Pointes (TdP) dysrhythmia. 2. Blocks cardiac Na+ channels; enhances a cardiac K+ current; class Ib drug 3. Class Ic and II drug; used with caution in those with COPD or heart failure 4. Class III drug; used IV only in those patients with severe, life-threatening ventricular arrhythmias 5. Blocks Ca2+ channels; class IV drug (2003exam3) |
1. Blocks cardiac Na+ channels in 'use-dependent' manner; class Ia drug; can cause the very dangerous Torsades de Pointes (TdP) dysrhythmia: (c)quinidine
2. Blocks cardiac Na+ channels; enhances a cardiac K+ current; class Ib drug: (a)tocainide 3. Class Ic and II drug; used with caution in those with COPD or heart failure: (b)propafenone 4. Class III drug; used IV only in those patients with severe, life-threatening ventricular arrhythmias: (e)bretylium 5. Blocks Ca2+ channels; class IV drug: (d)diltiazem |
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Class Ia drug; about 25% of patients are slow metabolizers of the drug to an active metabolite and thus are more prone to a systemic lupus erythematosus-like reaction:
a. amiodarone b. moricizine c. lidocaine d. procainamide e. disopyramide (2003exam3) |
d. procainamide
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A class Ia drug like disopyramide can terminate a re-entry arrhythmia in the Purkinje system by:
a. enhancing a cardiac K+ current b. converting a unidirectional block to a bidirectional block c. blocking cardiac Ca2+ channels d. decreasing systemic blood pressure e. blocking Na+ channels by a non 'use-dependent' mechanism (2003exam3) |
b. converting a unidirectional block to a bidirectional block
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This drug has prominent class III effects to block K+ channels and is a good antiarrhythmic except it can cause reversible corneal deposits or potentially fatal pulmonary toxicity:
a. amiodarone b. moricizine c. lidocaine d. ibutilide e. disopyramide (2003exam3) |
a. amiodarone
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Which drug is the most effective to terminate supraventricular tachycardia caused by re-entry in the AV node because it acts directly on Ca2+ channels:
a. ibutilide b. propranolol c. tocainide d. encainide e. verapamil (2003exam3) |
e. verapamil
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Based on the Vaughan-Williams classification of antiarrhythmic drugs, correctly match each drug with one description:
a. lidocaine b. amiodarone c. quinidine d. verapamil e. flecainide 1. class III: blocks K+ channels (and influences Na+ currents); increases refractoriness (ERP) and the QT interval. 2. Class Ia; blocks Na+ channels ("use-dependent"); slows phase 0 depolarization; decreases conduction velocity and delays phase 3 repolarization. 3. class Ib; blocks Na+ channels (not "use-dependent") and enhances a K+ channel. 4. Class Ic; blocks Na+ channels (not "use-dependent"); slows phase 0 depolarization; decreases conduction velocity with little effect on phase 3 repolarization. 5. Class IV drug: blocks Ca++ channels; slows heart rate and decreases AV node conduction velocity. (2002 exam 3) |
1. class III: blocks K+ channels (and influences Na+ currents); increases refractoriness (ERP) and the QT interval: (b) amiodarone
2. Class Ia; blocks Na+ channels ("use-dependent"); slows phase 0 depolarization; decreases conduction velocity and delays phase 3 repolarization: (c)quinidine 3. class Ib; blocks Na+ channels (not "use-dependent") and enhances a K+ channel: (a)lidocaine 4. Class Ic; blocks Na+ channels (not "use-dependent"); slows phase 0 depolarization; decreases conduction velocity with little effect on phase 3 repolarization: (e)flecainide 5. Class IV drug: blocks Ca++ channels; slows heart rate and decreases AV node conduction velocity: (d)verapamil |
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This class Ia drug is pharmacodynamically like quinidine, but most people rapidly metabolize the drug to the active metabolite NAPA; can cause a systemic lupus erythematosus-like reaction with higher doses and/or prolonged use, especially in slow metabolizers:
a. procainamide b. disopyramide c. tocainide d. flecainide e. sotalol (2002 exam 3) |
a. procainamide
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Used only in a hospital setting for serious ventricular cardiac arrhythmias; intravenous use only because of extensive first-pass metabolism when taken orally; enhances a K+ current; a class Ib drug:
a. lidocarin b. dysopyramide c. esmolol d. flecainide e. sotalol (2002 exam 3) |
a. lidocaine
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An endogenous compound; used IV to treat cardiac arrhythmias involving the AV node; very short half life of elimination measured in seconds:
a. lidocaine b. disopyramide c. esmolol d. diltiazem e. adenosine (2002 exam 3) |
e. adenosine
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Class Ia drug; compared to other class Ia drugs, has a more pronounced ventricular effect; has stronger anticholinergic (atropine-like) properties, and has stronger effects on cardiac contractility and on blood pressure:
a. procainamide b. disopyramide c. quinidine d. flecainide e. sotalol (2002 exam 3) |
b. disopyramide
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A class III drug; has some class Ia, class II and class IV properties; effective for severe ventricular cardiac arrhythmias, especially those associated with ischemia; causes corneal deposits, photosensitivity and pulmonary toxicity; can have a very high volume of distribution with prolonged use:
a. amiodarone b. disopyramide c. mexilitine d. moricizine e. ibutalide (2002 exam 3) |
a. amiodarone
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Class Ib drug; effective to treat cardiac arrhythmia caused by accelerated Purkinje fiber automaticity, and suppresses ectopic pacemaker activity caused by abnormal Ca2+ currents; restores RMP to more normal levels:
a. lidocaine b. disopyramide c. esmolol d. diltiazem e. quinidine (2002 exam 3) |
a. lidocaine
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Class Ia drug; blocks Na+ channels in a "use-dependent" manner; slowly disassociates from receptor in Na+ channel; delays reactivation of Na+ channels to the resting state and thus increases the effective refractory period (ERP):
a. amiodarone b. disopyramide c. tocainide d. bretylium e. ibutalide (2002 exam 3) |
b. disopyramide
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This class Ia drug is effective to stop a cardiac arrhythmia caused by a reentry mechanism in Purkinje fibers because it might convert a unidirectional block to a bidirectional block:
a. lidocaine b. amiodarone c. quinidine d. verapamil e. propranolol (2002 exam 3) |
c. quinidine
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