Cv2_Maloney_Antiarrhythmics

Front 1

What will slow conduction velocity in ventricular myocytes?

Back 1

Block Fast Na+ Channels
(Phase 0)

Front 2

What will slow conduction velocity in nodal tissue?

Back 2

Block Ca++ Channels
(Phase 0)

**Phase 0 on nodal tissue is controlled by Ca++ influx***

Front 3

Phase 0 = ________

Back 3

Conduction velocity

Front 4

What will prolong the ERP in fast response tissue such as a ventricular myocyte?

Back 4

Block K+ Channels
(Phase 2-3)

**Won't repolarize as fast and will prolong ERP**

Front 5

What will break the reentrant circuit in the ventricles?

Back 5

Block K+ Channels

Block Na+ Channels

Front 6

What ECG pattern will you see with Atrial Flutter?

Back 6

Sawtooth Pattern

Absence of P waves
(no coordinated atrial contraction)

Front 7

A pt. has A-fib with a ventricular rate of 120 bpm. What will rate control do in this patient?

Back 7

Rate Control will slow the AV node and decrease ventricular rate

(A-fib still there, but manageable)

Front 8

What drug(s) would you use in an A-fib patient being treated with a RATE CONTROL protocol?

Back 8

β- BLOCKERS

Non-DHP CCBs

Digoxin

Front 9

What is cardioversion?

Back 9

Going from arrythmia to NSR

Front 10

What is defibrillation?

Back 10

Using electric shock to go from fibrillation to NSR

Front 11

A patient presents A-fib and a ventricular rate of 120 bpm. You want to use a RYTHM CONTROL protocol to treat which will ______________

Back 11

Stop reentry ----> NSR

Front 12

What types of drugs can be used to stop reentry using RYTHM CONTROL in a patient with A-Fib?

Back 12

Na+ Channel Blockers

K+ Channel Blockers

Front 13

Blocking what channels will stop reentry to convert A-fib to NSR?

Back 13

Na+ (influx)--> Phase 0

K+ (efflux)---> Phase 3

Front 14

How can you eliminate AV nodal reentry?

Back 14

Prevent the premature atrial impulse

Break the reentrant circuit in the AV node

Front 15

In AV Nodal reentry, the slow conduction pathway has a _______ recovery time.

Back 15

Short

Front 16

In AV Nodal reentry, the FAST conduction pathway has a _______ recovery time.

Back 16

long recovery time

Front 17

What would you use to block the slow conduction pathway in AV nodal reentry?

Back 17

AV Nodal Blocker
-CCB
-Beta Blocker

Front 18

What would you use to block the fast conduction pathway in AV nodal reentry?

Back 18

Na+ Blocker

K+ Blocker

**Remember, the fast conduction pathway is ventricular myocyte tissue**

Front 19

A critically timed premature atrial impulse can trigger AV reentrant tachycardia in a person with ________

Back 19

WPW

Front 20

In atrial arrythmias, how will the QRS appear?

Back 20

Narrow (which is normal)

Front 21

How can you prevent an orthodromic AVRT (WPW)? (3)

Back 21

Slow conduction/ prolong ERP in accessory pathway

Slow AV node

Stop premature atrial impulses

Front 22

Should you block the AV node in a patient with WPW and A-fib/Flutter?

Back 22

NO!

The accessory pathway would still allow too many impulses through

Front 23

What will help with A-Fib/Flutter plus WPW?

Back 23

Na+ Blocker

K+ blocker

(These block accessory pathway)

Front 24

What is the biggest problem with all antiarrythmic drugs?

Back 24

All antiarrythmic drugs are PROARRYTHMIC!!

Front 25

Will Na+ channel blockers effct nodal tissue, atrial/ventricular myocytes or both?

Back 25

Only Atrial/Ventricular Myocytes

Front 26

Na+ Channel Blockers are Class ___ antiarrythmics

Back 26

Class 1

Front 27

How do different Class 1 antiarrhythmics differ from each other?

Back 27

Rate of recovery

Class 1A---> intermediate
Class 1B---> very fast
Class 1C---> very slow

Front 28

What Class is lidocaine in?

Back 28

Na+ Channel Blocker

Class 1B---> very fast recovery

Front 29

What class is Flecainide in?

Back 29

Na+ Channel Blocker

Class 1C---> very slow recovery

Front 30

What would the Phase 0 slope look like in normal tissue treated with Flecainide?

Back 30

Slope is reduced (less steep)

Conduction Slowed

Class 1C---> very slow recovery

Front 31

What does ischemic tissue do to the normal recovery time of tissue treated with Lidocaine?

Back 31

It takes longer for lidocaine to come off Na+ channel. Some lidocain is left on the Na+ Channel

INCREASE IN STEADY STATE BLOCK

Front 32

What is Steady State Block?

Back 32

The # of channels blocked during Phase 4 or at the start of Phase 0

Front 33

What does an increase in steady state block do to Phase 0?

Back 33

Prolongs it (less steep)

**B/C some of the Na+ channels are blocked. Less Na+ can bind, SLOWING conduction velocity**

Front 34

Do Na+ Channel blockers work better or worse in depolarized/damaged tissue and FASTER HRs?

Back 34

WORK BETTER!

**Increase Steady State Block**

Front 35

What happens if you have HIGH Steady State Block of fast Na+ channels in normal tissue?

Back 35

Here, you would cause an arrythmia (too slow!!)

Front 36

Would Class 1B or 1C drugs have a higher chance of precipitating a cardiac arrythmia from Na+ channel blockade?

Back 36

Class 1C

**They are slower to leave and will mess up the rate even more***

Front 37

Na+ Channel Blockers (Class 1A)

Back 37

Quinidine

Procainamide

Disopyramide

Front 38

"Quin/Procain/-amide"

Back 38

Na+ Channel Blockers (Class 1A)

Front 39

This drug blocks Na+ channels with an intermediate recovery time and also blocks K+ channels

Back 39

Quinidine

Front 40

Decreasing Phase 0 upstroke velocity and Prolonging repolarization does what to Reentry?

Back 40

Decreases reentry

Front 41

What ion is blocked in order to prolong repolarization?

Back 41

K+ efflux

Front 42

Prolonging repolarization _______ ERP

Back 42

increases

Front 43

How do Class IA drugs decrease the firing of ectopic foci?

Back 43

Decrease Phase 4 slope

Increase Threshold

Front 44

How does Quinidine terminate/prevent A-fib or V-tach?

Back 44

Decrease conduction velocity (Phase 0)

Prolong ERP

Front 45

How does quinidine treat (WPW)

Back 45

**Accessory Pathway**
-Decrease Conduction Velocity
-Prolong ERP

**Ectopic Focus**
-Decrease Phase 4 slope

Front 46

Is quinidine useful in all types of arrythmias?

Back 46

Yes

Front 47

Why might you see an intial increase in ventricular rate when treating atrial flutter or fibrillation when using Quinidine?

Back 47

Initially, quinidine inhibits VAGAL EFFECT on the heart

**Antimuscarinic effect INCREASES AV conduction***

Front 48

What can you do to prevent an initial increase in ventricular rate when quinidine is used for cardioversion in AF?

Back 48

Give AV NODAL BLOCKER prior to quinidine therapy

Front 49

What is an adverse effect from Quinidine's K+ Channel blockade?

Back 49

Torsades de pointes

Front 50

What would happen to the QT interval if you prolong the AP duration?

Back 50

Prolonged QT ---> Torsades

Front 51

What can toxic concentrations of Quinidine cause?

Back 51

Arrythmias or Asystole

(depressed cardiac electrical activity)

Front 52

What receptors can quinidine block when administered by IV?

Back 52

Block ALPHA receptors --> hypotension

AVOID IV USE OF QUINIDINE

Front 53

Cinchonism is caused by toxic doses of ________ and causes ______ toxicity..

Back 53

Quinidine, CNS Toxicity

**Tinnitus, hearing loss, headache, blurred vision, confusion, ect...**

Front 54

What is the mechanism for allergic reactions with Quinidine use?

Back 54

Ab's to quinidine-platelet complex cause platelets to lyse

Front 55

You have a patient who is taking Digoxin. Should you start them on Quinidine?

Back 55

NO

Quinidine ↑ serum Digoxin

Front 56

This Class 1A antiarrythmic can be used IV

Back 56

Procainamide

Front 57

What are some of the side effects of Procainamide?

Back 57

Lupus-like syndrome (no long term)

Ganglionic blocker (administer slowly)

Front 58

Why should Procainamide not be used long term?

Back 58

Lupus-like syndrome with longterm use

Front 59

Why should procainamide be administered slowly

Back 59

It can cause an SNS ganglionic block that will DECREASE BP

Front 60

Can Disopyramide be used in a pt. with HF?

Back 60

NO, it has a - ionotropic effect

Front 61

Which has a higher antimuscarinic effect? Quinidine or Disopyramide?

Back 61

Disopyramide

Front 62

Does procainamide block ALPHA receptors?

Back 62

No

Front 63

Which has a higher antimuscarinic activity? Quinidine or Procainamide?

Back 63

Quinidine

Front 64

Which drug has side effects that mimic Atropine?

Back 64

Disopyramide --> antimuscarinic effect

(Urine retention, drymouth, blurred vision, constipation, worse glaucoma)

Front 65

"Lido/Mex"

Back 65

Na+ Channel Blockers Class 1B

Lidocaine

Mexiletine

Front 66

What are the 2 Na+ Channel Blocker (Class 1B) covered in class?

Back 66

Lidocaine

Mexiletine

Front 67

Lidocaine has its greatest effect in ________ and/or _____________ tissue

Back 67

depolarized and/or rapidly driven tissue

Front 68

Do Class 1C Na+ Blockers also block K+ Channels?

Back 68

No

Front 69

How do Class 1C Na+ Blockers effect the Action Potential Duration?

Back 69

They shorten it

Nothing is opposing K+ efflux!

Front 70

What does Lidocaine do to Phase 4 depolarization?

Back 70

prolongs it--> takes more time to reach threshold

Front 71

Lidocaine works mainly in the _______

Back 71

Ventricles

Only effective for Ventricular Arrythmias!

Front 72

How does Lidocaine help treat V-Tach?

Back 72

Decreases conduction velocity (reentrant arrythmia)

Decreases ectopic focus
(foci arrythmia)

Front 73

How does Lidocaine compare to Quinadine?

Back 73

Higher chance of proarrythmic effect with Quinadine

Front 74

Can Lidocaine be used orally?

Back 74

NO

Extensive 1st pass metabolism

Front 75

How is Lidocaine administered?

Back 75

IV

Front 76

Is lidocaine for long term use?

Back 76

NO

Front 77

The CNS side effects from lidocaine use are due to its ___________

Back 77

Local anesthetic effect

Parathesia, slurred speech, convulsions, hearing disturbances

Front 78

Which drug is more proarrythmic, Quinadine or Lidocaine?

Back 78

Quinidine

Front 79

Can Mexiletine be used orally?

Back 79

Yes

Lidocaine analog that is orally effective

Front 80

Mexiletine is what class of antiarrythmic?

Back 80

Class 1B (Na+ Channel Blocker)

Front 81

What are the Na+ Channel Blockers (Class 1C)

Back 81

Flecainide

Propafenone

Front 82

"Fleca/Propa"

Back 82

Na+ Channel Blockers (Class 1C)

Front 83

Flecainide has a _______ recovery blockade

Back 83

LONG

Front 84

Will Flecainide cause Torsades?

Back 84

No, it doesn't block K+ efflux

Front 85

Is the proarrythmic affect greater with quinidine, flecainmide or lidocaine?

Back 85

Proarrythmic Effect

flecainide > quinidine > lidocaine

Flecainide has the greatest proarrythmic effect!

Front 86

This drug is called the "Pill in the pocket" for A-Fib.

Back 86

Flecainide

Front 87

Should flecainide be used in patients with structural heart disease?

Back 87

NO

Flecainide has a greater proarrythmic effect in pt's with structural heart dz

Front 88

What are some contraindications for flecainide use?

Back 88

Hx of:
-MI
-HF
-AV Block or BBB

Front 89

Other than Na+ channels, what else does Propafenone block?

Back 89

BETA receptors

Front 90

What type of effect do β BLOCKERS have on the SA node?

Back 90

Negative chronotropic effect

(Slows SA node down)

Front 91

What do β BLOCKERS do to the AV node?

Back 91

Decrease Conduction velocity

Increase ERP (Increase refractoriness)

Front 92

β BLOCKERS prevent arrythmias caused by excess ________

Back 92

catecholamines

Front 93

Increase in circulating ____ is correlated with the develpoment of arrythmias

Back 93

catecholamines

β BLOCKERS stop catecholamines

Front 94

What Class of antiarrythmics are β BLOCKERS?

Back 94

Class II

Front 95

Would you rather use β BLOCKERS or Quinidine to treat atrial flutter/fibrillation?

Back 95

β BLOCKERS

Quinidine has too many toxicity issues

Front 96

What drug is best to treat arrythmias triggered by physical or emotional stress?

Back 96

β BLOCKERS

Front 97

If a patient has Long QT syndrome caused by mutations of the HERG (gene), what should you use to treat it?

Back 97

β BLOCKERS

HERG mutations produce abnormal Na+ and K+ channels so you want to Block β1 to treat

Front 98

K+ Channel Blockers are what Class of anitarryhthmics?

Back 98

Class III

Front 99

What class of antiarrythmics are K+ Blockers?

Back 99

Class III

Front 100

K+ Channel Blockers (Class III)?

Back 100

Amniodarone
Dronedarone

Sotalol

Ibutilide
Dofetilide

Front 101

Which drug blocks:
-K+ Channels

-Inactivated Na+ Channels

-Weak Ca++ Channel Blocker

-α & β receptors

Back 101

Amniodarone

Front 102

Amniodarone's Ca++ Channel Blocking ability does what to CORONARY and peripheral vasculature?

Back 102

VASODILATE

Front 103

Match Amniodarone's End Results with the ion it's blocking

-Inhibits abnormal automaticity

-Increases atrial. AV node, and ventricular ERP

-Decreases AV conduction and conduction in atria and Ventricles

-Sinus bradycardia

Back 103

-Inhibits abnormal automaticity **Na+**

-Increases atrial. AV node, and ventricular ERP
**K+**

-Decreases AV conduction and conduction in atria and Ventricles **Ca++**

-Sinus bradycardia
**Na+**

Front 104

What is the half life of Amniodarone?

Back 104

13-103 days

You can have side effects for A LONG TIME

Front 105

What levels do you want to check for nine months after stopping Amniodarone?

Back 105

Plasma Levels

Front 106

How will amniodarone prevent reentry?

Back 106

Slow conduction (Na+ blockade)

Prolong ERP in reentrant pathway
(K+ blockade)

Front 107

What are 2 advantages of using Amniodarone?

Back 107

Very Low proarrythmic effect

No negative ionotropic effect
(Can use in HF)

Front 108

Can you use amniodarone to treat an arrhythmia in a patient with HF?

Back 108

Yes!

No negative ionotropic effect

Front 109

What is the drug of choice for treating arrythmias in patients with HF?

Back 109

Amniodarone

Front 110

You have given a drug to treat an arrythmia and the following week, a patient come sin with bluish-gray coloration of her skin in areas that have been exposed to sun. What drug did you give her?

Back 110

Amniodarone

Front 111

Which drug causes either hyperthyroidism of hypothyroidism?

Back 111

Amniodarone

-Structural analog of TH

-Contains large amounts of iodine

-Cytotoxic effect on thyroid follicle cells

Front 112

You have started a patient on Amniodarone to stop/prevent an atrial flutter. 2 weeks later, the patient complains of a persistent cough. What are you thinking?

Back 112

Adverse Effect of Amniodarone

Pneumonitis ---> Pulmonary Fibrosis
-can be rapidly progressive and fatal

COUGH IS USUALLY 1ST SYMPTOM

Front 113

You started a patient on amniodarone and they complain of trouble walking, numbness in their fingers and muscle weakness. What are you thinking?

Back 113

Adverse Effect of Amniodarone

*Peripheral Neuropathy*

Front 114

Amniodarone prolongs the QT interval. Is this likely to cause Torsades?

Back 114

No, there is a very low incidence of torsades with Amniodarone

Front 115

Due to this drug's potential of serious side effects, the FDA requires that a Medication Guide be given to all patients.

Back 115

Amniodarone

Front 116

What is the difference between amnidarone and dronedarone?

Back 116

No iodide in dronedarone

Front 117

Have anti-thyroid activities been seen d/t dronedarone use?

Back 117

No

It doesn't contain iodide

Front 118

Compare the half lives of amniodsarone and dronedarone

Back 118

The iodine in amniodarone makes it more lipophilic --> LONG t1/2

Dronedarone (no Iodide) has a half live of 1-2 days

Dronedarone is potentially LESS TOXIC

Front 119

Would you put a patient with NYHA class IV HF on dronedarone?

Back 119

NO

It was proven in clinical trials to KILL these people
Contraindicated in these patients with recent acute decompensation

Front 120

Would you put a person with NYHA Class II HF with recent decompensation in the hospital on dronedarone?

Back 120

NO

Front 121

You have placed a patient on a drug and they present to your office with severe liver failure and are in need a transplant. What drug was it?

Back 121

Dronedarone

Front 122

What channels/receptors does Sotalol (Class III) block?

Back 122

BETA Blocker

K+ Channel blocker

Front 123

What effect would Sotalol have on conduction velocity in fast response tissue?

Back 123

NO EFFECT on conduction velocity

Sotalol does not block Na+ Channels
(Phase 0)

Front 124

How does sotalol stop reentry in the atria or ventricles?

Back 124

Block K+

Prolongs ERP

Front 125

What aspect of Sotalol's MOA could cause side effects such as fatigue, sinus bradycardia and dyspnea?

Back 125

Beta Blockade

Front 126

You have recently upped a patient's dosage of Sotalol. They have to go to the hospital for Torsades. What caused this?

Back 126

K+ blockade

Prolonged repolarization ---> prolong QTi

Front 127

How is Ibutilide administed for conversion of atrial fibrillation and flutter to NSR?

Back 127

IV

Front 128

How is dofetilide administered for conversion of a-fib and flutter to NSR and is used to MAINTAIN NSR?

Back 128

Oral

Front 129

MOA Ibutilide and Dofetilide in treating arrythmias

Back 129

Class III

These two only block K+ Channels

Prolong the ERP

Front 130

Can dofetilide be used in patients with HF?

Back 130

Yes, does not reduce CO

No (-) ionotropic effect

Front 131

Can Ibutilide be used in patients with HF?

Back 131

No, shown to increase polymorphic VT in those with HF or low LVEF

Front 132

Which 2 drugs in Class III have the highest incidence of Torsades?

Back 132

Dofetilide and Ibutilide

Front 133

How can you minimize the chance of getting dofetilide-induced Torsades de pointes?

Back 133

Initiate therapy in Hospital

Dose is calculated based on creatinine clearance and its effect on QTi

Front 134

Are DHP CCBs such as Nifedipine useful against arrythmias

Back 134

No, DHP CCBs don't affect the heart itself

Front 135

What are the Ca+ Blockers used for arrythmias?

Back 135

Verapamil and Diltiazem

Front 136

What class of antiarrythmics are Ca+ Calcium Channel Blockers?

Back 136

Class IV

Front 137

What effect will Verapamil have on AV nodal conduction velocity and ERP?

Back 137

Decrease conduction

Increase ERP

Front 138

Would you use verapamil alone in a patient with a-fib and WPW?

Back 138

No

It may shorten the ERP of the accessory pathway --> enhances antegrade conduction --> worsens arrythmia

Front 139

Explain why CCBs are contraindicated in a wide-complex VT

Back 139

You must CONFIRM that the wide complex VT is of supraventricular origin

Verapamil and Diltazem will cause hemodynamic collapse and kill the patient if the tachy isn't SVT.

Front 140

Why can adenosine be used for wide-complex tachycardia dx?

Back 140

Adensoine is very short acting (10-sec)

If a tachycardia is of supraventricular origin (wide QRS) it will be stopped by adenosine --> BLOCKS AV NODE

Since the effects of adenosine are so short lived, it is used as a diagnostic tool

Front 141

Adenosine MOA

Back 141

Activates Adensoine receptors in atria, SA & AV nodes

Activate ACh sensitive K+ current
(hyperpolarization)

Inhibit cAMP-induced Ca++ influx
(Decrease conduction velocity in AV node)
(Increase refractoriness [AV node])

Front 142

What cardiac drugs are notable for causing AV block?

Back 142

Adenosine

Beta Blockers

Non-DHP CCBs

Digoxin

Front 143

"A,B,C,D"

Back 143

cardiac drugs are notable for causing AV block

Adenosine

Beta blockers

non-dhp CCBs

Digoxin

Front 144

Can Adensosine be used for chronic tx of arrythmias?

Back 144

No,

Half life is about 10 sec

Front 145

This drug, when used in WPW or AV nodal reentry patients restores NSR in 10-20 seconds in almost all cases

Back 145

IV Adenosine Bolus

Front 146

Why is adenosine not helpful in treating a-fib/flutter or ventricular tachycardia?

Back 146

Adensosine really only affects the AV node. A-Fib/Flutter or Ventricular Tachy are paced by the atrial and ventricular myocytes.

?????

Front 147

Side effects of this drug include Transient asystole, dyspnea, chest-pain and facial flushing

Back 147

Adenosine