Antidysrhythmics

Front 1

Slows the conduction of cardiac impulses in both normal and depolarized fibers; depolarized fibers are more sensitive.

Back 1

Quinidine

Front 2

List the two Class Ia agents we talked about in class.

Back 2

Quinidine and Procanamide

Front 3

Prolongs the action potential duration & lengthens the QT interval

Back 3

Quinidine

Front 4

Increases the effective refractory period

Back 4

Quinidine

Front 5

Decreases automaticity, particularly in ectopic pacemakers

Back 5

Quinidine

Front 6

Has vagolytic action at the AV node by antagonizing muscarinic action

Back 6

Quinidine

Front 7

If given IV, this drug can cause peripheral vasodilataion and myocardial depression, therefore is not usually administered IV

Back 7

Quinidine

Front 8

Metabolized by hepatic hydroxylation and urinary excretion of drug and metabolites

Back 8

Quinidine

Front 9

Used to treat PSVT, Atrial flutter, & atrial fibrilation

Back 9

Quinidine

Front 10

It may be necessary to pre treat with verapamil or a B-blocker before administering this drug

Back 10

Quinidine due to its vagolytic action

Front 11

Which causes a widening of the QRS and prolongation of the QT interval that can precipitate torsades?

Back 11

Quinidine

Front 12

Hypotension with IV administration can be caused by this drug due to peripheral alpha-adrenergic blockade & myocardial depression.

Back 12

Quinidine

Front 13

Recurrent lightheadedness & fainting episodes associated with onset torsades is called

Back 13

Quinidine syncope

Front 14

A triad of syncope is known as cinhonism. What are the three symptoms of this triad

Back 14

tinnitus, headache, dizziness

Front 15

Oral administration of this drug can cause nausea, vomiting, and diarrhea

Back 15

Quinidine

Front 16

An anesthesia consideration with someone on quinidine is that it can do what to neuromuscular blocking drugs.

Back 16

It can accentuate neuromuscular blockers.

Front 17

This drug reduces Vmax & conduction velocity, prolongues repolarization, & increases effective refractory period

Back 17

Procainamide = similar effects to those of quinidine

Front 18

Decreases automaticity in ectopic pacemakers

Back 18

Procainamide

Front 19

This drug has a weaker vagolytic action at the AV node compared to quinidine

Back 19

Procainamide

Front 20

Can be given PO or IV (IV infusion to maintain therapeutic Cp)

Back 20

Procainamide

Front 21

40-60% of administered is eliminated unchanged in the urine

Back 21

Procainamide

Front 22

This drug is, in part, acetylated in the liver to N-acetyl procainamide which has antidysrhythmic activity and is also eliminated by the kidneys. Therefore dose reduction is needed in patients with renal disease

Back 22

Procainamide

Front 23

This drug is used to treat VF/VT, re-entry SVT not controlled with adenosine and vagal maneuvers, & unknown cause of stable wide-complex tachycardia

Back 23

Procainaminde

Front 24

This drug may cause hypotension and negative inotropic effect, especially with rapid IV infusion.

Back 24

Procainamide

Front 25

This may prolong QT interval and predispode to polymorphic VT.

Back 25

Procainamide

Front 26

Slow acetylators may experience a lupus-like syndrome with chronic therapy of this medication

Back 26

Procainamide

Front 27

Can cause fever and agranulocytosis that is potentially fatal

Back 27

Procainamide

Front 28

This drug can potentiate effects of depolarizing and nondepolarizing muscle relaxants.

Back 28

Procainamide

Front 29

This class antidysrhythmic drugs bind to & blocks Na channels in cardiac tissues. Have intermediate potency

Back 29

Class Ia

Front 30

This class of antidysrhythmics reduce maximum velocity of action potential upstroke.

Back 30

Class Ia

Front 31

This class of antidysrhythmics increase action potential duration.

Back 31

Class Ia

Front 32

This class of antidysrhythmic drugs binds to & blocks Na channels in cardiac tissues and have low potency

Back 32

Class Ib

Front 33

This class of antidysrhythmics have no effect on, or decrease in action potential duration

Back 33

Class Ib

Front 34

This Class Ib drug preferentially supresses conduction in depolarized dysrhythmogenic cardiac cells. It has little effect in normal cardiac cells.

Back 34

Lidocaine

Front 35

This drug may terminate re-entry pathways and decreased automaticity.

Back 35

Lidocaine

Front 36

This drug is not given po because it undergoes an extensive first-pass metabolism

Back 36

Lidocaine

Front 37

Given IV this drug has rapid onset (45-90 sec) and short duration (hepatic metabolism) of action that permits ready titration of IV delivery

Back 37

Lidocaine - this is an advantage over procainamide

Front 38

Liver disease or reduced liver blood flow decreases hepatic clearance and increases t1/2 of this drug.

Back 38

Lidocaine

Front 39

This drug is used for treating pulseless VF/VT (after shock and vasopressor)

Back 39

Lidocaine

Front 40

This drug is used to treat monomorphic or polymorphic VT

Back 40

Lidocaine

Front 41

At therapeutic Cp (</= 5mcg/mL)has no effects on ECG. But with Cp > 5mcg/mL can cause peripheral vasodilation and cardiac depression which leasd to hypotension.

Back 41

Lidocaine

Front 42

CNS toxicity can occur at Cp > 5mcg/mL - seizures possible, especially if hypoxemia, hyperkalemia, or acidosis is present.

Back 42

Lidocaine

Front 43

This drug can cause respiratory or cardiac depression can occur at Cp > 10mcg/mL

Back 43

Lidocaine

Front 44

Mexiletine is the orally active form of which drug?

Back 44

Lidocaine

Front 45

This drug is used for chronic pain for example in diabetic neuropathy. Also infrequently used for the treatment of ventricular dysrhythmias.

Back 45

Mexiletine

Front 46

Mexiletine and phenytoin are in which class of antidysrhythmic drugs?

Back 46

Class Ib

Front 47

This drugs use is limited as an antidysrhythmic and is primarily an anticonvulsant.

Back 47

phenytoin

Front 48

This drug has electrophysiologic actions in the heart similar to lidocaine

Back 48

phenytoin

Front 49

This drugs one heart indication is the treatment of polymorphic VT with long baseline QT interval (torsades)

Back 49

phenytoin

Front 50

This class of antidysrhythmic drugs bind to and block Na channels in cardiac tissue with high potency

Back 50

Class Ic

Front 51

This class of antidysrhythmic has no significant effect on action potential duration

Back 51

Class Ic

Front 52

The CAST trial showed that patients with ventricular dysrhythmias treated with this drug had increasded mortality

Back 52

flecainide

Front 53

Flecainide is in which class of antidysrhythmics?

Back 53

Class Ic

Front 54

What are the Class Ib antidysrhythmic drugs we covered in class?

Back 54

Lidocaine, mexiletine, and phenytoin

Front 55

This class Ic antidysrhythmic can be used to treat PSVT or atrial fibrilation/flutter in patients with otherwise normal cardiac function

Back 55

flecainide

Front 56

What are the class Ic antidysrhythmics we covered in class?

Back 56

flecainide, propafenone, & moricizine

Front 57

This class Ic antidysrhythmic is structurally similar to propranolol and has weak beta activity

Back 57

Propafenone

Front 58

This drug is used to treat PSVT or atrial fib/flutter, but not ventricular dysrhythmias

Back 58

Propafenone

Front 59

This class Ic antidysrhythmic has multiple active metabolites with long half lives

Back 59

moricizine

Front 60

Beta-adrenergic antagonists are a member of which class of antidysrhythmic agents?

Back 60

Class II

Front 61

These agents depress automaticity (phase 4 depolarization) and impulse conduction

Back 61

Beta-adrenergic antagonists
(class II)

Front 62

This class of antidysrhythmic agents act in the AV node to slow conduction, increase effective refractory period, and terminate re-entry

Back 62

Class II

Front 63

These drugs are used to convert to NSR or control of ventricular rate in patients with SVTs (re-entry SVT, atrial fib/flutter)

Back 63

Class II; beta-adrenergic antagonists

Front 64

List 3 Class II antidysrhythmic beta blockers

Back 64

Esmolol, metoprolol, propranalol, atenolol, labetalol

Front 65

This class II antidysrhythmic is useful for the treatment of intraoperative SVT.

Back 65

Esmolol

Front 66

Class II antidysrhythmic agents are...

Back 66

beta-adrenergic antagonists; beta blockers

Front 67

Class III antidysrhythmic agents are.....

Back 67

Drugs that prolong repolarization

Front 68

This drug has primarily Class III action, but also class I, II, and IV

Back 68

Amiodarone

Front 69

What is amiodarone's class III action?

Back 69

Blocks rectifier potassium current & prolonges action potential duration and effective refractory period; slows conduction in the his-perkinje system and in accessory pathways

Front 70

What is amiodarone's class I action?

Back 70

Blocks sodium channels

Front 71

Inhibition of sympathetic activation of beta receptors would be which class of amiodarone's action?

Back 71

Class II

Front 72

What class action of amiodarone has weak Ca channel blockade -- effect tends to slow AV node conduction & heart rate?

Back 72

Class IV

Front 73

This class III antidysrhythmic drug supresses ectopic pacemaker activity and prolonges QT interval with a rare occurrence of torsades.

Back 73

amiodarone

Front 74

This class III agent causes hypotension, bradycardia, pulmonary fibrosis, liver injury, thyroid disturbances, and can worsened dysrhythmias

Back 74

amiodarone

Front 75

This class III antidysrhythmic delays repolarization by inhibiting K efflux and stimulates inward Na leak

Back 75

ibutilide

Front 76

This class III is used for the treatment of SVT, in particular atrial fib/flutter of short duration (<48 hours).

Back 76

ibutilide = converts to NSR

Front 77

Sotalol is a beta blocker with class III antidysrhythmic activity. What does that mean?

Back 77

It prolongs phase III repolarization and depresses automaticity (phase IV repolarization)

Front 78

This drug is given orally because the IV form is not approved for use in the U.S.

Back 78

sotalol

Front 79

This class III agent is used to treat monomorphic VT, rate control in a.fib/flutter, and WPW.

Back 79

sotalol

Front 80

Sotalol may cause nausea, diarrhea, bradycardia, myocardial depression, and torsades. Yes or no

Back 80

No; it causes bradycardia, torsades, and myocardial depression.

Front 81

Class IV agents are...

Back 81

Calcium channel blockers

Front 82

Verapamil and diltiazem are in which class of antidysrhythmics?

Back 82

Class IV

Front 83

Specifically verapamil and diltiazem block L-type Ca channel blockers. T or F?

Back 83

True

Front 84

These two class IV antidysrhythmic agents slow phase 0 depolarization in the SA node and AV node

Back 84

verapamil and diltiazem

Front 85

Verapamil and diltiazem increase anterograde conduction of secondary pathways and should be avoided in what syndrome?

Back 85

WPW

Front 86

Verapamil and diltiazem are used to treat narrow-complex re-entry SVT and control of ventricualr rate in afib and flutter, but will not what to the rhythm.

Back 86

Convert it to NSR (but I have seen it used for this purpose)

Front 87

Calcium channel blockers verapamil and diltiazem are contraindicated in WPW, but what else?

Back 87

Wide complex tachycardia of unknown origin

Front 88

Class IV agents can cause what two adverse reactions?

Back 88

AV block and myocardial depression

Front 89

Class V antidysrhythmic agents we covered in class are...

Back 89

Adenosine, digoxin, and Magnesium sulfate

Front 90

As a drug this Class V agent binds to cell membrane receptors and increases K permiability and decreases Ca influx that leads to hyperpolarization and suppression of Ca-dependant action potentials in the AV node

Back 90

adenosine

Front 91

This class V agent is used to slow conduction and increase refractory period in the AV node and can interrupt re-entry mechanisms

Back 91

adenosine

Front 92

Dose of this drug is: 6mg IV push. May follow with two 12mg IV doses 1 - 2 minutes apart if necessary

Back 92

adenosine

Front 93

This drug is metabolized by erythrocytes & vascular endothelial cells and has a t1/2 of <10 seconds.

Back 93

adenosine

Front 94

Adenosine is a _____ ________that is endogenous in all cells?

Back 94

purine nucleoside

Front 95

This Class V antidysrhythmic can be use to treat most forms of stable narrow-complex SVT and wide-complex regular tachycardia defined to be re-entry SVT with abnormal conduction

Back 95

andenosine

Front 96

This drug causes facial flushing, asystole, dyspnea, chest pain, and bronchospasm.

Back 96

adenosine

Front 97

Digoxin is in what class of antidysrhythmic agents?

Back 97

Class V

Front 98

This class V agent can be used to control ventricular rate in a.fib/flutter and is an alternative treatment for SVT.

Back 98

Digoxin

Front 99

This antidysrhythmic enhances vagal discharge to the heart; slows conduction through the AV node

Back 99

digoxin

Front 100

Digoxin administration with hypokalemia can cause....

Back 100

dysrhythmias

Front 101

this class V antidysrhythmic agent can be used to treat cardiac arrest due to hypomagnesemia or torsades and life threatening dysrhythmias due to digitalis toxicity

Back 101

magnesium sulfate

Front 102

Rate is very rapid >250 bpm. Usually caused by re-entrant loop around an area of atrial tissue

Back 102

Atrial Flutter

Front 103

Caused by multiple circus movements in the atria with a loss of atrial kick

Back 103

Atrial fibrilation

Front 104

Caused by Kent bundle that causes ventricular pre-excitation. Connects the atria to the ventricles

Back 104

Wolf-Parkinson-White Syndrome

Front 105

Caused by James fibers that connect the atria to the distal AV node

Back 105

Long-Ganong-Levine syndrome

Front 106

rhythm caused by ectopic pacemaker cells in the bundle of his

Back 106

Junctional tachycardia

Front 107

Narrow-complex tachycardias have a QRS duration of

Back 107

<120ms

Front 108

Wide-complex tachycardias have a QRS duration of

Back 108

>/=120ms