Pharm Antiarrhythmic

Front 1

causes of arrhythmia

Back 1

coronary ischemia.

tissue hypoxia.

electrolyte disturbances.

Over stimulation of SNS.

General anesthetics.

Any other condition or drug that may affect cardiac transmembrane potentials and lead to abnormal impulse formation or conduction.

Front 2

Digitalis glycosides can cause what?

Back 2

cause after depolarizations by increasing Calcium influx into cardiac cells; also impair AV node conduction and can cause AV block.

Front 3

“torsade de pointes” caused by what drugs

Back 3

Caused by certain antiarrhythmic drugs, psychotropic drugs, antibiotics and other miscellaneous drugs like cisapride.

Front 4

Back 4

yea

Front 5

after polarization caused by what drugs

Back 5

digitalis.

Front 6

abnormal impulse formation After depolarizations occur when and definition

Back 6

abnormal impulses resulting from spontaneous generation of action potentials during or immediately after phase 3 repolarization "ob#

Front 7

Abnormal impulse CONDUCTION example

Back 7

reentry process

Front 8

Sympathomimetics can cause arrhythmias how?

Back 8

increase automaticity of SA node, AV node or His-Purkinje fibers

Front 9

Non-pharmacological therapy for arrhythmias

Back 9

cardiac ablation.

implantable defibrillator.

Front 10

fluoroquinolones are known to cause what in the heart?

Back 10

arrhythmias. Especially with longer term use.

Front 11

type 1 / class 1 MOA?

Back 11

a. bind to Na channels when they are open and inactivated, dissociate from the channel during the resting state. More pronounced effect on cardiac tissue that is rapidly firing.

Front 12

type 1 / class 1 are called what?

Back 12

Na channel blockers

Front 13

types 1b within type 1 or class 1 antiarrhythmic drugs?

know for your own benefit

Back 13

greater affinity for inactivated state and slow recovery. More pronounced effect on ischemic tissue.

Depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization

Front 14

types 1a within type 1 or class 1 antiarrhythmic drugs?know for your own benefit

Back 14

. greater affinity for open state with slow recovery.

Depress phase 0, prolonging repolarization

Front 15

types 1c within type 1 or class 1 antiarrhythmic drugs?know for your own benefit

Back 15

greater affinity for open state and very slow recovery. Greater effect on ventricular conduction .

Markedly depress phase 0, minimal effect on repolarization.

Front 16

Type II/Class II are what kind of drugs

Back 16

b-adrenergic receptor blockers a. Decrease slope of phase 4.

Front 17

Type IA drugs MOA?

Back 17

block Na+ channel and K+ channel. Suppress abnormal automaticity but do not significantly affect SA node automaticity and heart rate. All have some antimuscarinic (atropine-like) activity and may inhibit PNS effects on SA node and AV node. Depress phase 0, prolonging repolarization.

Front 18

quinidine is an example of? typle/class?

Back 18

type 1A

Front 19

ADR's of quinidine which are type 1A's?

Back 19

hypotension, GI effects (diarrhea 30-40%), thrombocytopenia, cinchonism (ASA toxicity -tinnitus, blurred vision, dizziness) headache, confusion, torsades de pointes.

cinchonism

cinchonism

Front 20

DDI's of quinidine which are type 1A's?

Back 20

i. –CYP450 substrate and inhibitor. Several interactions.

Front 21

procainamide is made from what?

Back 21

lidocaine

Front 22

how is procainamide made active in the body?

Back 22

Absorbedfrom gut and converted to active metabolite N-acetylprocainamide(NAPA)

Front 23

i. Indications-of procainamide?

Back 23

Tx most types of supraventricular and ventricular arrhythmias. Produces less hypotension than quinidine IV – so more often used IV for TX of acute ventricular arrhythmias.

Front 24

ADR's of procainamide

Back 24

hypotension, GI effects, CNS effects,hematologic (thrombocytopenia), anticholinergic effects, liver toxicity,

lupus-like syndrome. (50%)

lupus-like syndrome. (50%)

Front 25

DDI of procainamide

Back 25

i. CYP2D6 substrate

Front 26

Disopyramide is what class / type

Back 26

type 1A/Class 1A

Front 27

Disopyramide indications

Back 27

ventricular arrhythmias

Front 28

Disopyramide ADR's

Back 28

hypotension,anticholinergic effects(blurred vision, urinary retention), CHF, CNS effects including hallucinations.

Front 29

Type IB drugs MOA?

Back 29

Electrophysiological properties make them particularly suitable for ventricular arrhythmias. Strong affinity for Na channels in depolarized ischemic tissue, but lack of effect on Na channels in normal cardiac tissue. Depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization

Front 30

why does lidocaine work in the ventricles???

Back 30

lidocaine does work in ischemia, which is why it works well in the ventricles.

Front 31

lidocaine indications

Back 31

i. Ventricular tachycardia and other acute ventricular arrhythmias. Not useful for supraventricular arrhythmias.

Also a local anesthetic.

Front 32

lidocaine first pass effect stuff I should know

Back 32

i. Extensive first pass hepatic inactivation after PO, therefore must be given IV.

Front 33

lidocaine ADRs

Back 33

CVS (bradycardia, hypotension, heart block), CNS(drowsiness, paresthesias, disorientation, muscle twitching- may lead to seizures). May also cause psychosis and respiratory depression

Front 34

Type IC drugs MOA

Back 34

block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization.

Front 35

flecamide indications

Back 35

i. Treatment of supraventricular arrhythmias and documented life threatening ventricular arrhythmias.

Front 36

flecamide ADR's

Back 36

reentry ventricular tachycardia, CHF, GI, CNS,blurred vision

Front 37

flecamide DDI's

Back 37

CYP450 substrate, CYP2DR inhibitor

Front 38

Propafenone MOA

Back 38

– block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization .

Similar effects as flecainide except less effects on QT interval. Also has some beta blocking activity.l

Front 39

flecamide MOA

Back 39

– block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization

Front 40

Propafenone indications

Back 40

i. Treatment of supraventricular arrhythmias and documented life threatening ventricular arrhythmias

Front 41

Propafenone ADR's

Back 41

– reentry ventricular tachycardia. -same as flecainide but also hematological.

Front 42

Propafenone DDi's

Back 42

CYP450 substrate, CYP1A2, 2D6 inhibitor

Front 43

TYPE II/CLASS II DRUGS MOA

Back 43

1. inhibitsSNS activation of cardiac automaticity and conduction. Slow heart rate,decrease AV node conduction velocity and increase AV node refractory period

Front 44

TYPE II/CLASS II DRUGS Indications?

Back 44

1. Used for prevention and treatment of supraventricular arrhythmias and for their ability to reduce ventricular ectopic depolarizations and sudden death in pts with myocardial infarction

Front 45

Esmolol indications?

how?

how long?

Who gets it?

Back 45

acute SVT tx.

rapidly metabolized, short half life.

Only hospital patients get it IV. No PO form.

Front 46

Metoprolol and Propranolol tx what?

Back 46

a. Both available PO or INJ for treatment and suppression of supraventricular and ventricular arrhythmias

Front 47

Metoprolol indications?

Back 47

i. given IV in early phase of MI followed by PO – protects the heart against the damage caused by ischemia and free radicals that may be formed during reperfusion of coronary arteries when fibrinolytics are used.

Front 48

Acebutolol can be used in preg when

Back 48

B/D in 2nd & 3rd trimester

Front 49

Amiodarone MOA

Back 49

block K+ channels and prolong the ventricular action potential depolarization and refractory period.

i. Type III, but also blocks Na channels, Ca channels and b-adrenergic receptors. Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods.q=iO

Front 50

Amiodarone properties

Back 50

i. organic iodine compound similar to thyroid hormones. Unusual kinetics, very long half-life (40 days).

Front 51

amiodarone indications

Back 51

POfor supraventricular and ventricular arrhythmias incl AF, atrial flutter, SVT and life threatening ventricular tachycardia. IV for acute life-threatening VF or sustained VT.

Front 52

amiodarone ADR's

Back 52

Several.GI effects, CV effects (hypotension, AV block, arrhythmias incl torsades (less torsades than other Class III agents), visual disturbances, thyroid dysfunction,pulmonary fibrosis and pneumonitis, blue-gray skin discoloration

Front 53

amiodarone DDI

Back 53

CYP450 substrate and inhibitor of almost all isoenzymes. Several DDI which increase levels of other important drugs like digoxin, phenytoin, warfarin skin

Front 54

Dronedarone properties

Back 54

i. –structurally similar to amiodarone but with shorter half-life, less lipophilicity and no iodine group so les risk of thyroid, pulmonary and neurological side effects

Front 55

Dronedarone MOA

Back 55

block K+ channels and prolong the ventricular action potential depolarization and refractory period. i. Type III, but also blocks Na channels, Ca channels and b-adrenergic receptors. Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods.

Front 56

Dronedarone indications

Back 56

– to reduce risk of CV hospitalization inpatients with Afib or A-flutter with certain CV risk factors

Front 57

Dronedarone ADR's

Back 57

Like amiodarone but w/ less thyroid, pulmonary and neurological (visual) ADRs

Front 58

Dronedarone DDI's

Back 58

several CYP450 DDIs esp w digoxin, CCBs and warfarin. Watch warfarin carefully.

Front 59

Ibutilide MOA

Back 59

-Different MOA than other Type III drugs. Promotes influx of Na+ through slow inward Na channels which counteracts the outward K+ current thereby prolonging repolarization.

oral chemical cardioversion.

Front 60

Sotalol MOA?

Back 60

i. non-selective beta-blocker with ability to block K+ current during ventricular action potential.

Front 61

Dofetilide indications and MOA

Back 61

chemical cardioversion and blockK+ channels.

prolong the ventricular action potential depolarization andrefractory period

Front 62

Bretylium MOA

Back 62

prolongs ventricular action potential in normal tissue more than ischemic tissue

Front 63

TYPE IV DRUGS are what?

Back 63

CCB's non DHP

Front 64

CCB's MOA

Back 64

1. decrease AV node conduction velocity and increase AV node refractory period (blocks Ca+from entering slow channels during depolarization)

Front 65

CCB's indications

Back 65

IV for acute PSVT, PO for AF (avoid if coexisting HF).

Front 66

non DHP- CCB's examples

Back 66

verapamil and diltiazem

Front 67

Adenosine MOA

Back 67

activates specific G protein-coupled adenosine receptors resulting in hyperpolarization and slowing of AV node conduction velocity.

Front 68

adenosine indications

Back 68

SVT or PSVT

Front 69

adenosine ADR's

Back 69

a. flushing,dizziness, bradycardia, syncope

Front 70

digoxin MOA

Back 70

a. increases vagal tone, slows AV node conduction velocity and increases AV node refractory period

Front 71

digoxin gives you an arrhythmia how do you tx it?

Back 71

lidocaine

Front 72

indications for quinidine

Back 72

i. TX most types of supraventricular and ventricular arrhythmias

Front 73

ADR's of quinidine

Back 73

cinchonism, hypotension,GI effects (diarrhea 30-40%), thrombocytopenia, cinchonism (ASA toxicity - tinnitus, blurred vision,dizziness) headache, confusion, torsades de pointes.

Front 74

Mexiletine metabolism

Back 74

do not undergo first pass effect therefore used PO

Front 75

Mexiletine indications

Back 75

long term basis for suppression of ventricular arrhythmias

Front 76

ADR's of mexilentine

Back 76

GI and CNS effects, agranulocytosis with tocainide

Front 77

Moricizine unusuualy properties

Back 77

phenothiazine analogue.

Front 78

Moricizine indications

Back 78

documented life-threatening ventriculararrhythmias. (Long term use may be associated with increased mortality rate inpts with history of MI)

Front 79

abnormal conduction example? and what causes them?

Back 79

reentry arrythmias.

re-excitation caused by same impulse that already went through that part.

Front 80

sotalol indications

Back 80

ventricular arrhythmias, a fib (avoid in Heart failure)

Front 81

sotalol ADR's

Back 81

dosedependent torsades de pointes, hypotension, bradycardia, bronchospasm

Front 82

dofetilide ADR's

Back 82

dose dependant torsades de pointes, CNS effects.

Front 83

bretylium indications and ADR's

Back 83

indications VF.

ADR's GI effects, orthostatic hypotension, CNS effects

Front 84

digoxin indications

Back 84

AF, PSVT.

Front 85

digoxin ADR's

Back 85

GI, CNS, arryhthmias (you can tx arrhythmias with lidocaine)

Front 86

MagnesiumSulfate MOA?

Back 86

slowsrate of SA node impulse formation and prolongs conduction time

Front 87

MagnesiumSulfate indications

Back 87

VT , VF, and torsades de pointes

Front 88

MagnesiumSulfate ADR's?

Back 88

diarrhea, CNS depression, flushing

Front 89

how to manage A fib?

Back 89

first control rate with BB's, CCB's or digoxin.

Rhythm control you can do electrical cardioversion, cardiac ablation, pharmacological conversion.

with cardioversion make sure to anticoag for 3 weeks prior to cardioversion.

Perform a TEE to check for thrombi.

Front 90

risk factors for A fib induced stroke on the chad2 scale and how many points each has?

Back 90

CHF= 1

HTN= 1

Age >75 = 1

DM= 1

Previous stroke =2

Front 91

stroke rate for chad 2 scores?

0

1

2

3

4

5

6

Back 91

0= 1.9

2= 2.8

3= 4

4=8.5

5=12.5

6=18.2

Front 92

Chad2 score tx from points.

0

1

2 or more

Back 92

0 aspirin 81-325 mg daily.

1 aspirin 81-325 mg daily or warfarin with INR 2-3 based on patient preference.

2 or more is warfarin INR 2-3 unless they need to avoid warfarin.

Front 93

Lupus like syndrome

Back 93

Procainamide

Front 94

Cinochism

Back 94

Quinidine.

Front 95

Anticholinergic effects

Back 95

Disopyramide

Front 96

Psychosis

Back 96

Lidocaine

Front 97

Blue/green skin.

Back 97

Amiodarone

Front 98

Arrhythmia

Back 98

Digoxin

Front 99

Pulmonary fibrosis

Back 99

Amiodarone

Front 100

Dose dependant torsades de pointes

Back 100

Dofetilide

Front 101

Thyroid dysfunction

Back 101

Amiodarone

Front 102

Hematologic effects

Back 102

Propafenone

Front 103

Diarrhea in 30 to 40% of patients

Back 103

Quinidine

Front 104

Agranulocytosis

Back 104

Mexilitine

Front 105

Phenothiazine analogue

Back 105

Moricizine