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Pharmacology - Exam 3 > Anti-Arrhythmics Part 2 > Flashcards

Anti-Arrhythmics Part 2 Flashcards

1
Q

Where are reentry circuits most common?

A

In the ventricle (CHD)

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2
Q

What’s happening during Phase 0 of the ventricular myocyte depolarization?

A

The voltage-gated Na+ channels are open.

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3
Q

What does the slope of the Phase 0 portion of the depolarization curve tell you?

A

Conduction velocity Smaller slope = smaller velocity

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4
Q

Why is the depolarization curve relatively flat in Phase 2?

A

The influx of Ca++ equals effluent of K+

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5
Q

What do the funny channels affect?

A

Phase 4 or the rate of automaticity

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6
Q

What does the PR interval reflect?

A

index of conduction velocity + delay at the AV node

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7
Q

What does the QT interval reflect

A

Duration of ventricular AP

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8
Q

What kind of rhythm is flutter (atrial or ventricular)

A

organized tachycardia - 180-349 bpm

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9
Q

What kind of rhythm is fibrillation (atrial)?

A

disorganized tachycardia >350 bpm

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10
Q

What are the four causes of tachycardias?

A
  1. ectopic pacemakers 2. re-entry circuits 3. Early After Depolarizations (EADs) 4. Delayed after Depolarizations (DADs)
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11
Q

How does CHD lead to re-entry circuits?

A

hypoxia leads to decreased ATP generation, which in turn leads to less Na+/K+ ATPase and less depolarization. That creates a localized area with an increased refractory period

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12
Q

Which direction is the myocardium perfused

A

epicardium to endocardium

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13
Q

Where is the heart most at risk from CHD?

A

endocardium because muscle contraction reduces flow to to endocardium

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14
Q

What are the three requirements for a re-entry circuit?

A
  1. multiple conduction pathways 2. unidirectional conduction block 3. Conduction Time > Effective Refractory Period
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15
Q

What is an ectopic pacemaker? Where is it commonly located?

A

Cells that are acting as pacemakers that run faster than the SA node. The pulmonary vein has striated cardiac muscle that often forms an ectopic pacemaker.

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16
Q

What is the primary means of control in long-standing a fib?

A

Rate control - anesthetize the AV node and screw the P wave

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17
Q

How does rhythm control work in a fib?

A

abolish a fib with pharmacologic cardioversion and restore normal sinus rhythm

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18
Q

What drugs (class and name) are used for rate control in a fib?

A

Class II (beta blocker) - metoprolol Class IV (Ca 2+ channel blockers) - verapamil, digoxin

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19
Q

What drugs are used in rhythm control in a fib?

A

Class III (K+ blocker) - amiodorone Class IC (Na+ blocker) - flecainide

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20
Q

Who gets anticoagulation with a fib?

A

high risk of stroke CHADS-VASc score > or equal to 2

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21
Q

What anticoagulants can be used for A fib?

A

Warfarin RivaroXaban ApiXaban DabigaTran

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22
Q

what to drugs that treat tachyarrythmias do?

A
  1. decrease automaticity
  2. reduce conduction velocity for AV node
  3. increase AP duration (or ERP)
  4. Interfere with the sympathetic regulation of heart rate at SA and AV nodes
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23
Q

What part of the ventricular depolarization does each class of drugs effect?

A
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24
Q

Class I drugs block which type of channel and do they block all of them?

A

Na+ channels

fraction are blocked - 100% block = asystole

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25
Q

What is “use-dependent blockade”?

A

the channel must be open for the drug to bind to the site and block the channel

Class I more selective for “diseased tissue” - activated or unactivatable state - NOT resting

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26
Q

Na+ channel blockers _______(increase or decrease) conduction velocity which _________(increases or decreases) the PR interval and the QRS?

A

decreases conduction velocity

increases PR interval

Increases QRS (AP), which also increases refractory period

*overall, decreases channels available so you need lower resting potential to activate

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27
Q

Where are ectopic pacemakers usually located?

A

in the atria

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28
Q

Can ectopic pacemakers conduct directly to the ventricles?

A

No - there is fibrous tissue between the atria and ventricles, so the impulse must go through the AV node

29
Q

How does the AV node act as a brake?

A

It can only handle 250 bpm max, so it prevents tachycardia out of control

30
Q

If you block Na+ in inactivatable state, what happens to ERP?

A

Increases it to longer than the AP

31
Q

How do Class I drugs effect ectopic pacemakers?

A

by blocking Na+ Phase 4 funny channels, thereby making the cells less excitable

32
Q

Class IA also blocks which channels and increases the AP duration?

A

K+ out

increase the time to repolarize

33
Q

Class IB also keeps which channels open longer and decreases the AP duration?

A

K+ out increased

34
Q

Of the Class I drugs, what is the duration of the ERP from longest to shortest?

A

1C > 1A > 1B

35
Q

Which drug is best post-MI?

A

1B

1B is Best

Lidocaine I.V. acute VT post-MI

Mexiletine used to treat Long QT syndrome

36
Q

Why are 1B drugs best post-MI?

A

They are highly selective for diseased tissue (ischemic)

37
Q

What is flecainide used for?

A

VTs and SVT if no Hx of ischemic disease

THIS IS RHYTHM CONTROL

it is a very potent sodium channel blocker

38
Q

What is an important side effect of 1C drugs?

A

ataxia because they effect Na+ channels in the cerebellum

39
Q

Class 1A drugs are also what?

A

Anaesthetics

They also block sodium channels on pain and sensory neurons

40
Q

Other than blocking Na+ channels, what is a secondary effect of Class 1A drugs?

A

anticholingeric, so they decrease vagal influences on the SA and AV nodes

in other words, they increase nodal conduction velocity and automaticity

41
Q

What’s the danger with quinidine for a fib?

A

If you use it and lower the atrial tachyardia below the AV node rate “brake,” now the ventricles will beat much faster

solution: lower AV node conduction first with Ca 2+ blocker or Beta blocker

42
Q

What arrhythmia can Class IA cause?

A

Torsades de Pointes

contraindicated in incomplete AV block - excessive Na+ channel block can lead to asystole

QT prolongation leads to torsades females > males

43
Q

When is Class 1A drugs contraindicated?

A

Inherited Long QT Syndrome

44
Q

What channel mutation is seen in the most common form of prolonged QT Syndrome?

A

K+ channel mutation is “rectifying,” which means it takes longer to repolarize, prolonging the QT interval. Treat with Beta-blocker

45
Q

How do you treat Na+ channel inherited Long QT?

A

Class 1B - mexiletine

46
Q

What symptom should make you concerned about Long QT?

A

syncope

47
Q

How does amiodarone work?

A

blocks K+ efflux during Phase 3

also blocks Na+ channels

increases ERP

48
Q

What is amiodarone first line for at low doses?

A

rhythm control in atrial fibrillation

49
Q

what is amiodarone first line for in high doses?

A

VTs in structurally abnormal hearts

(especially VT post MI, post cardioversion for V-fib)

50
Q

What is the major risk with amiodarone?

A

prolonged QT - Torsades

51
Q

Amiodorone toxicity is a _________?

A

BITCH

Bradycardia/Blue Man

Interstitial Lung Disease

Thyroid (hypo/hyper)

Corneal/Cutaneous

Hepatic/Hypotension when IV (due to solvents)

52
Q

How does sotalol work?

A

Blocks K+ efflux during Phase 3, increases APD

53
Q

What is the first line use of sotalol?

A

Use for SVT and VT in patients with implanted ICD to reduce mortality and chance of shock

54
Q

What is ibutalide used for?

A

cardioversion of SVT

(blocks K+ efflux, increases APD)

55
Q

Summary table of Rx for Ventricular Arryhthmias

A
56
Q

In what disease are rate control drugs contraindicated?

A

WPW

All rate control drugs decrease AV conduction velocity, but in WPW the accessory pathway will allow AP to still enter the ventricle, creating potential for retrograde conduction, leading to AV reentrant tachycardia

57
Q

What do Calcium channel blockers do?

A

Block Ca++ channels in the AV node (selective for it, because no Na+ channels here)

decreases pacemaker current

increases ERP

decrease conduction velocity

58
Q

What are Ca 2+ blockers primarily used for?

A

SVTs (fibrillation or flutter)

59
Q

When is use of Ca++ blockers dangerous?

A

CHF - because they reduce contractility

60
Q

What are beta blockers used for?

A

SVTs

61
Q

What is the mechanism for beta blockers?

A

They block Beta 1 adrenergic receptors on the heart

They slow AV node conduction (rate control)

The decrease excitability (ectopic pacemakers)

lesser extent (due to Ca++ channel effects):

decrease SA node rate

decrease contractility

62
Q

What is the best choice in CHF?

A

Digoxin

63
Q

What is the mechanism of action for digoxin?

A

Inhibits Na+/K+ ATPase

lowers resting potential

lowers conduction velocity

Increases vagal activity, which causes:

decreased pacemaker activity

increased refractory period

decreased AV node conduction

64
Q

What’s the danger with digoxin?

A

toxicity because low TI

severe bradycardia

65
Q

How does adenosine work?

A

purine nucleoside acts at receptors on the hear

Increases K+ efflux, hyperpolarizes and causes less Ca2+ to come in

decreases: AV node conduction, SA pacemaker, automaticity

66
Q

What’s the 1/2 life of adenosine?

A

seconds

67
Q

What is adenosine used for?

A

diagnosis and acute termination of SVT

AV-node dependent narrow complex tachycardia

68
Q

Summary Table for Treatment of Arrhythmias

A

Pharmacology - Exam 3 (12 decks)

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