Antiarrhythmics

Question 1

What is automaticity

Answer 1

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)

Question 2

What is abnormal automaticity

Answer 2

spontaneous depolarization of cells without pacemake current

Question 3

Triggered automaticity

Answer 3

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

Question 4

Sinus Tachycardia

Answer 4

An arrhythmia due to enhanced normal automaticity

Question 5

Three questions to ask of every arrhythmia

Answer 5

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

Question 6

Phase 4 depolarization of the SA node is slowed by

Answer 6

Vagal activity (Ach)

Question 7

Phase 4 depolarization of the SA node is accelerated by?

Answer 7

catecholamines (norep and ep)SNS

Question 8

Phase 0 depolarization is slowed by

Answer 8

Calcium channel blockers

Question 9

SA node is hyperpolarized by

Answer 9

adenosine

Question 10

Class II antiarrhythmics are?

Answer 10

Beta blockers

Question 11

Prototype Beta blocker anti-arrhythmic is

Answer 11

Propanolol

Question 12

Propanolol does what in regards to arrhythmias

Answer 12

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

Question 13

Why is propanolol not used as much anymore?

Answer 13

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

Question 14

Metoprolol used often why?

Answer 14

It is cardio-selective.

Question 15

Wide QRS complex means

Answer 15

premature ventricular beats

Question 16

Enhanced abnromal automaticity is best treated with>

Answer 16

Class I anti-arrhythmias drugs…Na blockers

Question 17

fast conducting tissue

Answer 17

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

Question 18

Slow conducting tissue

Answer 18

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

Question 19

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

Answer 19

This “recovery” time is prolonged

Question 20

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

Answer 20

true

Question 21

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

Answer 21

Normal to fast. intermeidate dissociation time

Question 22

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

Answer 22

Fast. Fast dissociation time

Question 23

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

Answer 23

basically any. Very slow dissociation time.

Question 24

Side effect of Na channel blockers

Answer 24

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

Question 25

Lidocaine for some reason does not work on atrial arrhythmias

Answer 25

true

Question 26

Toxicity of Lidocaine

Answer 26

CNS, confusion, seizures

Question 27

Class IC prototype

Answer 27

Flecanide

Question 28

Class IC agents are contraindicated in what situation?

Answer 28

Contraindicated in patients with structural heart disease. Very important

Question 29

Wide QRS complex tachycardia means what?

Answer 29

ventricular tacchy

Question 30

Ventricular Tacchycardia

Answer 30

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

Question 31

How do you treat ven tach

Answer 31

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

Question 32

What the hell is the problem in re-entry

Answer 32

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

Question 33

Class III drugs

Answer 33

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

Question 34

Amiodarone

Answer 34

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

Question 35

Electrocardiogram will show what when class III drug is given?

Answer 35

Elongation of PR, QRS, and QT interval

Question 36

Amiodarone used for what?

Answer 36

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

Question 37

side effects of Amiodarone

Answer 37

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

Question 38

Sotolol

Answer 38

K channel blocker and Beta blocker

Question 39

Sotolol useful in

Answer 39

Atrial, ventricular, AV nodal reentrant arrythmias including ven tach

Question 40

What Class III drug has only class III activity

Answer 40

Ibutilide

Question 41

Ibutilide used to treat

Answer 41

atrail fib

Question 42

Torsades de Pointe

Answer 42

Literally means turning of the point | Initiated by early afterdepolarization in setting of prolonged QT

Question 43

Torsades de pointe is seen most often in what antiarrhythmic drugs

Answer 43

K channel blockers class III

Question 44

Drugs that treat ventricular tachycardia in order of preference

Answer 44

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

Question 45

Sotolol should not be used to treat ventricular arrhythmias when

Answer 45

a pt is having an acute MI

Question 46

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

Answer 46

implantable defribrillator

Question 47

Narrow QRS complex

Answer 47

usually means you have something abnormal in the atrium

Question 48

Atrial fib mechanism

Answer 48

micro-reentry within the atrium

Question 49

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

Answer 49

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.

Question 50

What else could you use to slow the AV node

Answer 50

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

Question 51

Class IV antiarrhythmics

Answer 51

Calcium channel blockers...verapamil, Diltiazem

Question 52

What do class IV antiarrhythmics do>

Answer 52

Reduce SA node automaticity and AV node conduction | Very little effect on fast conduction tissue

Question 53

Adverse effects of Ca channel blockers

Answer 53

SA AV block, impaired myocardial contractility, hypotension

Question 54

Contraindicated in what patients

Answer 54

patients with CHF or LV dysfunction

Question 55

Ca channel blockers are useful in what patients

Answer 55

pateints with normal LV function, diabetics, pulmonary disease

Question 56

Adverse effects of Digoxin

Answer 56

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

Question 57

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

Answer 57

Digoxin intoxication

Question 58

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

Answer 58

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.

Question 59

Paroxysmla supraventricular tacchycardia

Answer 59

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

Question 60

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

Answer 60

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

Question 61

What is the preferred treatment in paroxysmal supraventricular tachycardia

Answer 61

Adenosine

Question 62

Adenosine

Answer 62

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

Question 63

What is Wolff-Parkinson White

Answer 63

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

Question 64

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

Answer 64

KNOW IT

Question 65

Procainemide toxicity

Answer 65

drug induced lupus and hypotension

Question 66

Lidocaine strictly works on what part of the heart?

Answer 66

Ventricles... Useful post-MI.

Question 67

What is the drug of choice for AV node arrhythmia

Answer 67

Adenosine