Pharmacology: Chapter 14 Agents Used In Cardiac Arrythmias

Front 1

On the action potential curve what does phase 0 represent?

Back 1

influx of Na through fast Na channels initiating depolarization

Front 2

What is unique about AP's in pacemaker and ectopic pacemaker cells? How does it occur?

Back 2

1) the AP occurs spontaneously during diastole
2) occurs from a gradual increase of depolarizing current through special hyperpolarization activated ion channels

Front 3

In someone with ectopic pacemaker what is the result of giving them extra K+?

Back 3

it will hyperpolarize them and slow or stop their firing. Note that decreased extracellular K+ can increase their rate of firing

Front 4

What occurs during the upstroke of the AP?

Back 4

this is phase 0 and corresponds to an in rush of Na into the atrial, purkinje, and ventricular cells

Front 5

What are the effects of hyperkalemia on the heart?

Back 5

1) reduced AP duration
2) slowed conduction
3) decreased pacemaker rate
4) decreased arrythmias

Front 6

What are the effects of hypokalemia on the heart?

Back 6

1) prolonged AP
2) increased pacemaker rate
3) arrythmias at pacemaker

Front 7

What is the effect of K+ channel blocking antiarrythmic agents? What is a side effect? What drugs use this mechanism?

Back 7

1) prolonged AP, mimics hyerkalemia
2) torsade de pointes
3) quinidine and sotalol

Front 8

What occurs during phases 1 and 2 of an AP?

Back 8

it is the turning off of most of the Na current and the waxing and waning of Ca current with a slow development of repolarization from K+

Front 9

What occurs during phase 3 of an AP?

Back 9

Na and Ca channels close and K+ approaches equilibrium helping to repolarize the cell. This is when the major K+ current occurs

Front 10

hyperkalemia has what effect on the upstroke of an AP?

Back 10

it decreases upstroke

Front 11

What do arrythmias result from?

Back 11

1)disturbances in impulse formation
2) disturbances in impulse conduction
3) both of the above

Front 12

What is the interval between depolarizations of a pacemaker cell equal to?

Back 12

the duration of the AP and the duration of the diastolic interval

Front 13

What phase of the AP determines the diastolic interval?

Back 13

phase 4 (the pacemaker potential)

Front 14

What AP phase is reduced by vagal and beta blockers?

Back 14

4

Front 15

What does acetylcholine do to the maximum diastolic potential?

Back 15

makes it more negative

Front 16

Increased phase 4 depolarization slope does what? What can cause this?

Back 16

1) accelerates pacemaker rate
2) hypokalemia, beta agonists, positive chronotropic drugs, fiber stretch and acidosis

Front 17

What is a chronotropic drug?

Back 17

Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate.

Front 18

What phase do early afterdepolarizations (EAD) effect? What about delayed afterdepolarizations?

Back 18

1) EADs interrupt phase 3
2) DADs interrupt phase 4

Front 19

Do EADs or DADs occur with increased Ca?

Back 19

DADs

Front 20

What does acetylcholine do to the maximum diastolic potential?

Back 20

makes it more negative

Front 21

Increased phase 4 depolarization slope does what? What can cause this?

Back 21

1) accelerates pacemaker rate
2) hypokalemia, beta agonists, positive chronotropic drugs, fiber stretch and acidosis

Front 22

What is a chronotropic drug?

Back 22

Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node. Positive chronotropes increase heart rate; negative chronotropes decrease heart rate.

Front 23

What phase do early afterdepolarizations (EAD) effect? What about delayed afterdepolarizations?

Back 23

1) EADs interrupt phase 3
2) DADs interrupt phase 4

Front 24

Do EADs or DADs occur with increased Ca?

Back 24

DADs, they also occur with fast heart rate

Front 25

Under what conditions do EADs generally occur?

Back 25

slow heart rate

Front 26

Do EADs or DADs arise the plateau of the AP? Which arises from the resting potential?

Back 26

1) EADs
2) DADs

Front 27

Why are DADs and EADs referred to as triggered automaticity?

Back 27

because they require a normal AP for their initiation

Front 28

What is present in Wolff-parkinson-white syndrome?

Back 28

reentry of an impulse causes contraction excitation of atrial tissue, AV node, ventricular tissue because of an accessory AV connection (bypass tract)

Front 29

What are the conditions that must exist for reentry to occur?

Back 29

1) there must be an obstacle around which a reentrant wave can penetrate
2) there must be unidirectional block but not bidirectional
3) conduction time around the circuit needs to be long enough so that the reentry impulse does not reenter tissue during the refractory period. During the refractory period no new signal can be propagated

Front 30

If conduction velocity is too slow is there bidirectional or unidirectional block?

Back 30

bidirectional

Front 31

If conduction velocity is too rapid is there bidirectional or unidirectional block?

Back 31

bidirectional

Front 32

What can depress conduction velocity?

Back 32

hyponatremia and hypocalcemia

Front 33

What type of block do drugs that impede sodium or calcium cause?

Back 33

bidirectional because they slow conduction velocity

Front 34

Would impact would lengthened refractory periods have on reentry?

Back 34

they would make reentry less likely

Front 35

What are the 4 MOA to combat arrythmias?

Back 35

1) Na channel blockade
2) Ca channel blockade
3) sympathetic blockade
4) prolonging the refractory period

Front 36

In which phase are channels in the activated state?

Back 36

phase 0

Front 37

In which phase are the channels in the inactivated state?

Back 37

phase 2

Front 38

Therapeutically channel blocking drugs do not target resting channels but do target activated or inactivated channels. Which phases are targeted?

Back 38

phases 0 and 2

Front 39

Drugs that affect cells with abnormal automaticity reduce the slope of which phase of the AP? How?

Back 39

1) phase 4
2) they block either Na or Ca channels thereby reducing the ratio of Na permeability to K+ permeability

Front 40

How do beta blockers indirectly reduce phase 4 slope?

Back 40

by blocking the positive chronotropic action of norepi in the heart

Front 41

Antiarrythmic agents have different classes what are they?

Back 41

Class 1: Na channel blockade
Class 2: sympatholytic action
Class 3: prolongation of APD usually with delayed rectifier K+ current
Class 4: blockade of cardiac Ca current

Front 42

What is an example of a drug that uses all 4 antiarrythmic classes?

Back 42

amidorone

Front 43

What part of the AP does procainimide slow?

Back 43

the upstroke and slows conduction

Front 44

On EKG what is seen in someone taking procainamide?

Back 44

prolonged QRS

Front 45

How is the AP prolonged in someone taking procainamide?

Back 45

it also does nonspecific blockage of K+ channels

Front 46

Does procainamide work at the SA or AV node?

Back 46

both

Front 47

What are some of the extracardiac effects of procainamide?

Back 47

ganglion blocking effects resulting in hypotension

Front 48

What toxicities are seen with procainamide?

Back 48

1) Excessive AP prolongation
2) QT interval prolongation
3) induction of tosade de pointes and syncope
4) precipitation of new arrythmias
5) SLE LIKE SYMPTOMS OF ARTHRALGIA AND ARTHRITIS

Front 49

What class is procainamide?

Back 49

class 1 subgroup 1A meaning it prolongs APD and dissociates from the channel

Front 50

What class is quinidine?

Back 50

Class 1 subgroup 1A meaning it prolongs APD and dissociates from the channel

Front 51

How does quinidine work and what does it effect?

Back 51

slows upstroke of AP and conduction and prolongs QRS by blocking Na channels

Front 52

How does quinidine prolong the action potential?

Back 52

by blocking several K+ channels

Front 53

What are the toxic effects of using quinidine?

Back 53

1) prolonged QT interval
2) torsades de pointes
3) cinchonism: headache, dizziness, and tinnitus

Front 54

disopyramide is what class of antiarrythmic?

Back 54

class 1 subgroup 1A meaning it prolongs APD and dissociates from the channel

Front 55

What are the effects of disopyramide?

Back 55

similar to procainamide and quinidine

Front 56

What are some of the adverse effects of disopyramide?

Back 56

similar to procainamide and quinidine but also has atropine like effects that produce urinary retention, dry mouth, blurred vision and constipation

Front 57

What antiarrythmic group is lidocaine in?

Back 57

class 1 subgroup 1B which means shortened APD and dissociates from channel with rapid kinetics

Front 58

Lidocaine is particularly effective against arrythmias caused by what condition?

Back 58

acute MI

Front 59

What is the MOA of lidocaine?

Back 59

block both activated and inactivated Na channels

Front 60

When Lidocaine blocks the inactivated state, which cells are primarily being effected?

Back 60

purkinje and ventricular cells have a longer AP which means a longer phase 2 compared to atrial cells

Front 61

What are some of the toxicities associated with lidocaine use?

Back 61

paresthias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions, seizures. remember this is also a local anesthetic and these side effects are correspond to local anesthetics

Front 62

What is the lidocaine the agent of choice to terminate?

Back 62

v tach and prevention of v fib, however it is used most to treat arrhythmias

Front 63

what class is mexiletine?

Back 63

Class 1: subgroup1 B meaning it shortens APD and dissociates rapidly from the channel

Front 64

What is mexiletine used for?

Back 64

treatment of ventricular arrythmias

Front 65

What class is flecainide?

Back 65

class 1 subgroup 1C meaning they have minimal effects on APD and dissociate slowly

Front 66

What is flecainides effect on the QT interval?

Back 66

does not prolong even though it is potent blocker of both Na and K channels

Front 67

What is flecainide currently used for?

Back 67

people with relatively normal hearts but who have supraventricular arrhythmias. it is effective at suppressing premature ventricular contractions.

Front 68

What class is propafenone?

Back 68

class 1 subgroup 1C meaning that it has minimal effects on APD and dissociates slowly

Front 69

What is propafenone used for?

Back 69

supraventricular arrythmias

Front 70

What beta blocker is used as an antiarrythmic? What class would this be in?

Back 70

esmolol is in class 2 because it is a sympatholytic

Front 71

What effect do class III drugs show on the EKG?

Back 71

prolonged QT interval

Front 72

When is amiodarone given?

Back 72

serious ventricular and supraventricular arrhythmias and atrial fib

Front 73

What are the cardiac effects of amiodarone?

Back 73

prolonged APD by blocking K rectifyer channel. it also blocks inactive Na channels. Both effects result in slowed heart rate and decreased AV node conduction

Front 74

What are extracardiac effects?

Back 74

vasodilation

Front 75

What are the toxic effects of amidarone?

Back 75

1) symptomatic bradycardia and heart block in people with preexisting sinus or AV nodal disease
2) pulmonary fibrosis
3) photodermatitis with grey blue skin
4) blocks conversion of thyroxine to T3 in periphery (can cause hypo/hyperthyroid)

Front 76

What liver enzyme is amiodarone inactivated by? What is a common GI drug that inhibits this enzyme and results in accumulation of amiodarone? What liver enzymes does amiodarone inhibit?

Back 76

1) CYP3A4
2) cimetidine inhibits CYP3A4
3) apparently all others

Front 77

Why was dronedarone created?

Back 77

to decrease the thyroid effects of amiodarone

Front 78

What is dronedarones MOA and what is more effective for than amiodarone?

Back 78

1) it blocks K+ channels and beta adrenoceptors
2) reduces mortality of atrial fib

Front 79

How dronedarone classified?

Back 79

class 3

Front 80

What is unique about sotalol?

Back 80

it has class 3 and class 2 properties so it prolongs ADP and has beta blocking effects

Front 81

what is sotalol used to treat?

Back 81

ventricular arrythmias and maintanence of sinus rhythm in people with atrial fib

Front 82

What class is dofetilide in?

Back 82

Class 3. it acts only on K+ rectifier channels

Front 83

What class is ibutilide? What is it used to treat?

Back 83

1)class 3 it acts by blocking the K+ rectifier channel
2) atrial flutter and atrial fib

Front 84

Which Ca channel blockers precipitate arrythmias and are contraindicated in their treatment?

Back 84

dihydorpyridines

Front 85

What is the MOA of verapamil?

Back 85

blocks both activated and inactivated L-type Ca channels so its effects are more marked in tissues that fire frequently and those in which activation depends exclusively on Ca current like the SA and AV node

Front 86

Can verapamil effect DAD or EADS?

Back 86

can suppress both

Front 87

What are extracardiac effects of verapamil?

Back 87

vasodilation and other effects where smooth muscle is present

Front 88

In large doses what can verapamil do?

Back 88

produce an AV block

Front 89

What is verapamil primarily used for?

Back 89

supraventricular tachy, can reduce rate in atrial flutter and fib

Front 90

What is the mechanism of adenosine?

Back 90

activation of an inward K+ rectifier current and inhibition of calcium current causing hyperpolarization and suppression of calcium dependent AP. Meaning it slows AV nodal firing, less so at SA node

Front 91

Under what condition is adenosine employed?

Back 91

prompt conversion of paroxysmal supraventricular tachy to sinus rhythm

Front 92

What is a common side effect of adenosine?

Back 92

chest burning and SOB

Front 93

What are the effects of Mg?

Back 93

it has antiarrhythmic properties particularly in people with digitalis induced arrythmias

Front 94

What are the effects of increasing K+ concentration?

Back 94

1) a resting potential depolarizing action
2) membrane potential stabilizing action caused by increased K+ permeability

Front 95

what can hypokalemia result in?

Back 95

DADs and ectopic pacemaker activity

Front 96

What is the concern with someone given verapamil who is diagnosed with supraventricular tachy but really has ventricular tachy?

Back 96

hypotension and cardiac arrest

Front 97

Can antiarrythmics be beneficial for CHF or IHD?

Back 97

only a few, generally not

Front 98

What are the effects of adenosine on 1) blocking Na channels in normal cells 2) depolarized cells 3) the refractory period in normal cells 4) depolarized cells 5) Ca channel blockade 6) effect on pacemaker activity 7) sympatholytic activity?

Back 98

1)none
2)none
3) none
4) none
5) yes
6) none
6) yes

Front 99

What are the effects of amiodarone on 1) blocking Na channels in normal cells 2) depolarized cells 3) the refractory period in normal cells 4) depolarized cells 5) Ca channel blockade 6) effect on pacemaker activity 7) sympatholytic activity?

Back 99

1) some
2) a lot
3) increases refractory
4) increases refractory
5) some
6) decreases
7)some

Front 100

what can hypokalemia result in?

Back 100

DADs and ectopic pacemaker activity

Front 101

What is the concern with someone given verapamil who is diagnosed with supraventricular tachy but really has ventricular tachy?

Back 101

hypotension and cardiac arrest

Front 102

Can antiarrythmics be beneficial for CHF or IHD?

Back 102

only a few, generally not

Front 103

What are the effects of adenosine on 1) blocking Na channels in normal cells 2) depolarized cells 3) the refractory period in normal cells 4) depolarized cells 5) Ca channel blockade 6) effect on pacemaker activity 7) sympatholytic activity?

Back 103

1)none
2)none
3) none
4) none
5) yes
6) none
6) yes

Front 104

What are the effects of amiodarone on 1) blocking Na channels in normal cells 2) depolarized cells 3) the refractory period in normal cells 4) depolarized cells 5) Ca channel blockade 6) effect on pacemaker activity 7) sympatholytic activity?

Back 104

1) some
2) a lot
3) increases refractory
4) increases refractory
5) some
6) decreases
7)some

Front 105

What is the effect of adenosine on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 105

1) increase/decrease
2) increased
3) increased
4) none
5) none
6) effective
7) unknown

Front 106

What is the effect of amiodorone on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 106

1) decreases
2) increases
3) variable
4) increased
5) increased
6) effective
7) effective

Front 107

What is the effect of disopyramide on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 107

1) increase/decrease because of anticholinergic effect
2) increase/decrease
3) increase/decrease
4) increased
5) increased
6) effective
7) more effective

Front 108

What is the effect of dofetilide on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 108

1) decreased
2) none
3) none
4) none
5) increased
6) effective
7) none

Front 109

DWhat is the effect of dronedarone on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 109

1) unknown
2) unknown
3) unknown
4) unknown
5) increased
6) effective
7) none

Front 110

What is the effect of esmolol on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 110

1) decreased
2) increased
3) increased
4) none
5) none
6) effective
7) effective

Front 111

What is the effect of flecainide on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 111

1) decreased
2) increased
3) increased
4) increased
5) none
6) effective
7) more effective

Front 112

What is the effect of ibutilide on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 112

1) decreased
2) none
3) none
4) none
5) increased
6) effective
7) unknown

Front 113

What is the effect of lidocaine on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 113

1) none
2) none
3) none
4) none
5) none
6) none
7) effective

Front 114

What is the effect of procainamide on 1) SA node rate 2) AV refractory period 3) PR interval 4) QRS duration 5) QT interval 6) usefulness in supraventricular arryth and 7) ventricular arryth

Back 114

1) decreased
2) increased/decreased
3) increased/decreased
4) increased
5) increased
6) effective
7) more effective