Antiarrhythmics Flashcards

1
Q

What is automaticity

A

The ability of cardiac cells to sontaneously depolarize to threshold potential and initiate depolarization (pacemaker current). SA node, AV node, atrial conduction fibers, purkinjee fibers (ventricular conducting fibers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is abnormal automaticity

A

spontaneous depolarization of cells without pacemake current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Triggered automaticity

A

Echo depolarization in response to preceeding depolarization. Can occur early or late in repolarization (early afterdepolarization or delayed afterdepolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sinus Tachycardia

A

An arrhythmia due to enhanced normal automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Three questions to ask of every arrhythmia

A

Is the rhythm regular or irregular?
Is there evidence of atrial activity (p wave)?
Is the QRS complex narrow or widened?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phase 4 depolarization of the SA node is slowed by

A

Vagal activity (Ach)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Phase 4 depolarization of the SA node is accelerated by?

A

catecholamines (norep and ep)SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phase 0 depolarization is slowed by

A

Calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SA node is hyperpolarized by

A

adenosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Class II antiarrhythmics are?

A

Beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prototype Beta blocker anti-arrhythmic is

A

Propanolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Propanolol does what in regards to arrhythmias

A

reduces enhanced automaticity. Reduces atrial and ventricula rarrhythmias post MI and improves survival.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is propanolol not used as much anymore?

A

It is not cardio-selective which means that it can have effects in places outside the heart.
Also, it is lipid soluble so it can have effects on the brain like causing depression and nightmares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metoprolol used often why?

A

It is cardio-selective.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Wide QRS complex means

A

premature ventricular beats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Enhanced abnromal automaticity is best treated with>

A

Class I anti-arrhythmias drugs…Na blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

fast conducting tissue

A

Atrial and Ventricular fibers….Na dependent depolarization….thats why Na channel blockers are better for enhanced abnormal automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Slow conducting tissue

A

SA and AV node….Calcium dependent….thats why calcium channel blockers are better for enhanced normal automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What effect do Na blockers have on the movement of Na channels from inactive to resting

A

This “recovery” time is prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Na channel blockers cause a decreased rate of tise of phase 0 depolarization

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Class Ia agents (procaineamide) slow Conduction at what kinds of heart rate

A

Normal to fast. intermeidate dissociation time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Class Ib agents (lidocaine) slow conduction at what kinds of HR

A

Fast. Fast dissociation time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Class Ic agents (flecanide) slow conduction at what kinds of HR

A

basically any. Very slow dissociation time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Side effect of Na channel blockers

A

DRUG INDUCED LUPUS ( pleural and pericardial effusion), torsades de pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lidocaine for some reason does not work on atrial arrhythmias

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Toxicity of Lidocaine

A

CNS, confusion, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Class IC prototype

A

Flecanide

28
Q

Class IC agents are contraindicated in what situation?

A

Contraindicated in patients with structural heart disease. Very important

29
Q

Wide QRS complex tachycardia means what?

A

ventricular tacchy

30
Q

Ventricular Tacchycardia

A

an arrhythmia that results from organized re-entry of impulses most commonly around an anatomic barrier like infarction or ischemia

31
Q

How do you treat ven tach

A

interrupt re-entry with a Class Ia agent (not class I C) or a class III potassium channel blocker

32
Q

What the hell is the problem in re-entry

A

re-entry occurs when an impulse repetitively activates the same area of the heart. You must have some sort of block, it must be a unidirectional block, and the conduction time must exceed the effective refractory period

33
Q

Class III drugs

A

Potassium channel blockers….increases the time it takes to repolarize. Increase the refractory period. Interrupts re-entry. good for treating re-entry issues like Ven tach

34
Q

Amiodarone

A

Class III AA, blocks K, Na, Ca, and Beta receptors

35
Q

Electrocardiogram will show what when class III drug is given?

A

Elongation of PR, QRS, and QT interval

36
Q

Amiodarone used for what?

A

atrial and vent arrhythmias. IV used for life threatening arrhythmias. Used in cardiac resucitation

37
Q

side effects of Amiodarone

A
Significant and serious. 
Pulmonary fibrosis (fatal in 1 out of 400)
photosensitivity dermatitis
Corneal microdeposits
Optic neuritis
thyroid issues
38
Q

Sotolol

A

K channel blocker and Beta blocker

39
Q

Sotolol useful in

A

Atrial, ventricular, AV nodal reentrant arrythmias including ven tach

40
Q

What Class III drug has only class III activity

A

Ibutilide

41
Q

Ibutilide used to treat

A

atrail fib

42
Q

Torsades de Pointe

A

Literally means turning of the point

Initiated by early afterdepolarization in setting of prolonged QT

43
Q

Torsades de pointe is seen most often in what antiarrhythmic drugs

A

K channel blockers class III

44
Q

Drugs that treat ventricular tachycardia in order of preference

A

Amiodarone, Lidocaine, Procainemide (all IV mostly except amiodarone can be given orally)

45
Q

Sotolol should not be used to treat ventricular arrhythmias when

A

a pt is having an acute MI

46
Q

Most effective treatment for pts at risk of sudden death due to ventricular tacchycardia and V fib

A

implantable defribrillator

47
Q

Narrow QRS complex

A

usually means you have something abnormal in the atrium

48
Q

Atrial fib mechanism

A

micro-reentry within the atrium

49
Q

What kinds of drugs are used to control ventricular rates in patients with rapid supraventricular arrhythmias?

A

drugs that block impulse conduction through the AV node…remember, the AV node is slow conducting cardiac tissue so it is calcium dependent which means you would need to use Calcium cahnnel blockers to slow it.

50
Q

What else could you use to slow the AV node

A

Beta blocker b/c the AV node is innervated and regulated by the SNS
Or…Digoxin…vagal stimulation

51
Q

Class IV antiarrhythmics

A

Calcium channel blockers…verapamil, Diltiazem

52
Q

What do class IV antiarrhythmics do>

A

Reduce SA node automaticity and AV node conduction

Very little effect on fast conduction tissue

53
Q

Adverse effects of Ca channel blockers

A

SA AV block, impaired myocardial contractility, hypotension

54
Q

Contraindicated in what patients

A

patients with CHF or LV dysfunction

55
Q

Ca channel blockers are useful in what patients

A

pateints with normal LV function, diabetics, pulmonary disease

56
Q

Adverse effects of Digoxin

A

It can trigger increased normal automaticity, delayed afterdepolarizations, APC’s, VPCs, Paroxysmal atrial tachycardia, ventricular tachycardia.

57
Q

Delayed afterdepolarizations occur following repolarization and result from Calcium overload . They are a sign of what

A

Digoxin intoxication

58
Q

In patients with A-fib, is a rate control or rhythm control better?

A

Studies show that there is no clear advantage to a rhythm control and that simply controlling the rate is good enough and leads to fewer adverse effects.

59
Q

Paroxysmla supraventricular tacchycardia

A

re-entry occurring within the AV node. Rapid activation of ventricle and atria

60
Q

Drugs that affect or interrupt re-entry in the AV node

A

You must know this….Calcium channel blocker, Beta blocker, DIgoxin

61
Q

What is the preferred treatment in paroxysmal supraventricular tachycardia

A

Adenosine

62
Q

Adenosine

A

Used for PSVT b/c it blocks AV node. Works rapidly: half life is ten seconds

63
Q

What is Wolff-Parkinson White

A

Connection between the atrium and ventricle. This can form a big re-entry circuit

64
Q

KNOW THIS…Digoxin is contraindicated in pts with Wolf Parkinson White Syndrome because Digoxin increases vagal stimulation of the atrium which actually increases conduction in the atrium and can lead to atrial flutter or a-fib, this can increase transmission of atrail impulses across the WPW accesssory pathway and lead to ventricular fib

A

KNOW IT

65
Q

Procainemide toxicity

A

drug induced lupus and hypotension

66
Q

Lidocaine strictly works on what part of the heart?

A

Ventricles… Useful post-MI.

67
Q

What is the drug of choice for AV node arrhythmia

A

Adenosine