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STEP Pharm I > Anti-Arryhthmics > Flashcards

Anti-Arryhthmics Flashcards

1
Q

T or F. There is no parasympathetic (vagal) innervation in the heart past the AV node

A

T. only sympathetics

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2
Q

What are arrhythmias caused by in a general sense?

A

abnormal impulse generation (automaticity) or abnormal propagation (re-entry)

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3
Q

T or F. The SA node fires at a more rapid rate than the atrial conducting fibers, AV node or purkinje fibers

A

T.

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4
Q

What things could cause latent pacemakers to fire more rapidly?

A

-B1 stimulation-hypokalemia-fiber stretch-hypoxemia-acidosis-injury

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5
Q

Describe arrhythmias caused by abnormal triggered automaticity.

A

abnormal impulse generation following a normal action potential

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6
Q

What are some arryhthmias caused abnormal ‘triggered’ automaticity?

A

-early after depolarization (EAD) interrupts phase 3 repolarization -delayed after-depolarization (DAD)

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7
Q

Early after depolarization (EAD) interrupts phase 3 re-polarization causes what?

A

long QT related arrhythmias i.e. Tornado de pointes

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8
Q

What causes delayed after-depolarization?

A

result from calcium overload in digoxin toxicity and is exacerbated by catecholamines and hypokalemia

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9
Q

Treatment for delayed after-depolarization caused by digoxin overload?

A

Digibind

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10
Q

Torsades de pointes occurs in the setting of prolongation of phase __ and __ of the action potential (reflected as prolonged QT interval)

A

2 and 3 repolarization

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11
Q

What things can cause early after-depolarization (or delayed phase 3 re-polarization)?

A

-K+ channel blocking anti-arrhythmics (class III) -hypokalemia-low heart rate

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12
Q

What is re-entry?

A

occurs when an impulse repetitively activates the same area of the heart leading to sustained arrhythmias

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13
Q

What conditions are needed for re-entry to occur?

A

-an anatomic or physiologic obstacle (circuit)-unidirectional block-conduction time must exceed effective refractory period in the ‘slow’ circuit

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14
Q

What is re-entry typically caused by?

A

a premature impulse (automaticity) that gives off ‘daughter impulses’ resulting in rapid activation of the ventricle (or atrium)

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15
Q

T or F. Re-entrant arrhythmias are characteristically rapid and sustained

A

T. greater than 140 bpm

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16
Q

Where in the heart can re-entrant arrhythmias occur?

A

any location- atria, AV node, ventricle

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17
Q

A re-entrant arrhythmia in the atria could be what?

A

-a fib (disorganized) or -a flutter (organized)

18
Q

A re-entrant arrhythmia in the AV node could be what?

A

paroxysmal supraventricular tachycardia (PSVT)

19
Q

A re-entrant arrhythmia in the ventricles could be what?

A

-ventricular tachycardia (organized)-ventricular fibrillation (disorganized)

20
Q

What is the preferred treatment for sustained ventricular tachycardia?

A

DC cardioversion followed by drug therapy to prevent recurrence of re-entry

21
Q

What are some options that can used for drug therapy in sustained ventricular tachycardia?

A

A class I anti-arrhythmic (Na+ channel blocker) such as procainamide or lidocaineA class III (K+ channel blocker) such as sotolol or amiodarone

22
Q

How would a class I anti-arrhythmic (sodium channel blocker) such as procainamide or lidocaine interrupt re-entry?

A

by slowing conduction through the circuit and by increasing effective refractory period also slow automaticity

23
Q

How would a class III anti-arrhythmic (sodium channel blocker) such as procainamide or lidocaine interrupt re-entry?

A

by prolonging depolarization and increasing the effective refractory period (ERP) by extending phase 3phase 2 and 3 re-polarization is delayed, extending the action potential and potentially prolonging the QT interval resulting in increased risk of early after-depolarization (EAD) and Torsado de pointes

24
Q

What are the class II anti-arrhythmics?

A

BBs- metoprolol and atenolol

25
Q

What are the class IV anti-arrhythmics?

A

NDHP CCBs- Verapamil and DiltiazemDHPs have little anti-arrhyhtmic effect at clinically used doses

26
Q

What are some other anti-arrhythmics?

A

adenosine receptor agonists- adenosinevagal activators- digoxin, carotid massagevagal blocker- atropine

27
Q

Sodium channel blockers (class I) are divided into three subclasses based on what?

A

dissociation rate (T) from the Na+ channel-class IA: T>1 sec (extends phase 2 the most because at high doses they also block K+ channels- can lead to EAD and sustained arrhythmias like torsades)-class IB: T less than 1sec (may slightly quicken re-polarization)-class IC: T>10 sec

28
Q

What are the class IA anti-arrhythmics?

A

Procainamide, Quinidine, Disopyramide Quinidine and Disopyramide are rarely used because of prominent side effects

29
Q

What are the class IB anti-arrhythmics?

A

Lidocaine

30
Q

What are the class IC anti-arrhythmics?

A

Flecamide

31
Q

What is the electrophysiologic effect of class II anti-arrhythmics?

A

reduce enhanced automaticity related to catecholamines and ischemia reduce atrial and ventricular arrhythmias in patients with CHD (which produces a lot of catecholamines) and improves survivalSlows AV node conduction by blocking positive influence of catecholamines particularly blocks exercise-induced increase in ventricular rate in atrial fibrillation.

32
Q

T or F. Class II anti-arrhythmics are used to treat symptomatic PVC’s (can be due to increased catecholamines or ischemia) in patients with and without structural heart disease

A

T.

33
Q

What are the main effects of Class IV AAs?

A

reduce SA node automaticity and AV node conduction with little effect on electrophysiology of fast conduction tissues (atrial, ventricular conduction system) under normal conditions

34
Q

What are some adverse effects of Class IV AAs?

A

-SA, AV block-impaired myocardial contractility-hypotension

35
Q

Class IV AAs are contraindicated in which patients?

A

-CHF-sinus bradycardia-atrioventricular block (prolonged PR interval)

36
Q

What arrhythmia is digoxin used for?

A

atrial fibrillation via enhanced vagal efferents to the AV node

37
Q

What are the effects of digoxin in a fib?

A

reduces SA node automaticity, AV conduction.Controls ventricular rate in supraventricular arrhythmias. Interrupts re-entry in AV node.

38
Q

Direct effect (arrhythmogenic): increased normal automaticity, delayedafterdepolarizations: APC’s, VPC’s Paroxysmal Atrial Tachycardia with Block,Ventricular Tachycardia. (Na/K ATPase inhibition with calcium overload).

A

Direct effect (arrhythmogenic): increased normal automaticity, delayedafter-depolarizations: APC’s, VPC’s Paroxysmal Atrial Tachycardia with Block,Ventricular Tachycardia. (Na/K ATPase inhibition with calcium overload).

39
Q

What is adenosine used for?

A

Used to terminate acute PSVT by blocking AVnode- patient will enter asystole for about 2-3 seconds as you hit the SA AND AV nodes (adenosine receptor mediated). Acute use only Very good diagnostic for supra ventricular arrhythmias (a fib, a flutter, or PSVT)Hyper polarizes the SA and AV node

40
Q

How is adenosine given?

A

administered rapidly IV. T/2 10 seconds!

41
Q

Side effects of adenosine?

A

Chest tightness common, transient asystole (less than 3 seconds) can occur, flushing, PSVT can recur if other treatment not given.

STEP Pharm I (36 decks)

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