Anti-arryhthmatics

Question 1

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

Answer 1

T. only sympathetics

Question 2

What are arrhythmias caused by in a general sense?

Answer 2

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

Question 3

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

Answer 3

T.

Question 4

What things could cause latent pacemakers to fire more rapidly?

Answer 4

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

Question 5

Describe arrhythmias caused by abnormal triggered automaticity.

Answer 5

abnormal impulse generation following a normal action potential

Question 6

What are some arryhthmias caused abnormal ‘triggered’ automaticity?

Answer 6

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

Question 7

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

Answer 7

long QT related arrhythmias i.e. Tornado de pointes

Question 8

What causes delayed after-depolarization?

Answer 8

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

Question 9

Treatment for delayed after-depolarization caused by digoxin overload?

Answer 9

Digibind

Question 10

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

Answer 10

2 and 3 repolarization

Question 11

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

Answer 11

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

Question 12

What is re-entry?

Answer 12

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

Question 13

What conditions are needed for re-entry to occur?

Answer 13

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

Question 14

What is re-entry typically caused by?

Answer 14

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

Question 15

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

Answer 15

T. greater than 140 bpm

Question 16

Where in the heart can re-entrant arrhythmias occur?

Answer 16

any location- atria, AV node, ventricle

Question 17

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

Answer 17

• a fib (disorganized) or

- a flutter (organized)

Question 18

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

Answer 18

paroxysmal supraventricular tachycardia (PSVT)

Question 19

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

Answer 19

• ventricular tachycardia (organized)

- ventricular fibrillation (disorganized)

Question 20

What is the preferred treatment for sustained ventricular tachycardia?

Answer 20

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

Question 21

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

Answer 21

A class I anti-arrhythmic (Na+ channel blocker) such as procainamide or lidocaine

A class III (K+ channel blocker) such as sotolol or amiodarone

Question 22

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

Answer 22

by slowing conduction through the circuit and by increasing effective refractory period

also slow automaticity

Question 23

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

Answer 23

by prolonging depolarization and increasing the effective refractory period (ERP) by extending phase 3

phase 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

Question 24

What are the class II anti-arrhythmics?

Answer 24

BBs- metoprolol and atenolol

Question 25

What are the class IV anti-arrhythmics?

Answer 25

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

Question 26

What are some other anti-arrhythmics?

Answer 26

adenosine receptor agonists- adenosine vagal activators- digoxin, carotid massage vagal blocker- atropine

Question 27

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

Answer 27

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

Question 28

What are the class IA anti-arrhythmics?

Answer 28

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

Question 29

What are the class IB anti-arrhythmics?

Answer 29

Lidocaine

Question 30

What are the class IC anti-arrhythmics?

Answer 30

Flecamide

Question 31

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

Answer 31

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 survival Slows AV node conduction by blocking positive influence of catecholamines particularly blocks exercise-induced increase in ventricular rate in atrial fibrillation.

Question 32

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

Answer 32

T.

Question 33

What are the main effects of Class IV AAs?

Answer 33

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

Question 34

What are some adverse effects of Class IV AAs?

Answer 34

- SA, AV block - impaired myocardial contractility - hypotension

Question 35

Class IV AAs are contraindicated in which patients?

Answer 35

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

Question 36

What arrhythmia is digoxin used for?

Answer 36

atrial fibrillation via enhanced vagal efferents to the AV node

Question 37

What are the effects of digoxin in a fib?

Answer 37

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

Question 38

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

Answer 38

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

Question 39

What is adenosine used for?

Answer 39

Used to terminate acute PSVT by blocking AV node- 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

Question 40

How is adenosine given?

Answer 40

administered rapidly IV. T/2 10 seconds!

Question 41

Side effects of adenosine?

Answer 41

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