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2-Pharm Exam 3 > Antiarrhytmics > Flashcards

Antiarrhytmics Flashcards

1
Q

Review antiarrhythmics diagram.

A
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2
Q

What occurs in phase 0 of myocyte AP?

A
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3
Q

What occurs in phase 1 of myocyte AP?

A
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4
Q

What occurs in phase 2 of myocyte AP?

A
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5
Q

What occurs in phase 3 of myocyte AP?

A
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6
Q

What occurs in phase 4 of myocyte AP?

A
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7
Q

What is the effective refractory period?

A

Effective or absolute (phase 2) (ERP) is the longest amount of time when cells cannot be depolarized again. The longest input that fails to conduct.

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8
Q

What are common factors that facilitate arrhythmias?

A
  • hypoxemia
  • electrolyte/acid-base abnormalities (acidosis, alkalosis, K+, Mg++)
  • myocardial ischemia
  • bradycardia
  • altered sympathetic nervous system various drugs
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9
Q

What are non-modifiable risk factors of Cardiac Arrhythmias?

A
  • dilated cardiac diseases
  • ischemic cardiomyopathy
  • autonomic changes of the conduction system
  • polymorphism of ion channels
  • congenital long-QT syndrome (LQTS).
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10
Q

Most arrhythmias occurring during anesthesia do not require treatment unless ____________

A

hemodynamic compromise

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11
Q

What is the mechanism of cardiac arrhythmias?

A
  • re-entry
  • enhanced/ectopic pacemaker activity
  • triggered activity
  • early after depolarization
  • delayed after depolarization
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12
Q

Mechanisms of Cardiac Arrhythmias: Define re-entry.

A
  • Due primarily to abnormality of conduction, an impulse may recirculate in the heart and cause repetitive activation without the need for any new impulse to be generated.
  • These are called reentrant arrhythmias.
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13
Q

Mechanisms of Cardiac Arrhythmias: Define Enhanced/ectopic pacemaker activity

A

Ectopic impulse may be increased pathologically in the automatic fibers or such activity may appear in ordinary fibers.

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14
Q

Mechanisms of Cardiac Arrhythmias: Define Triggered activity.

A

Secondary depolarizations accompanying a normal or premature action potential (AP).

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15
Q

Mechanisms of Cardiac Arrhythmias: Define Early after-depolarization.

A
  • Repolarization during phase-3 is interrupted and membrane potential oscillates.
  • If the amplitude of oscillations is sufficiently large, neighboring tissue is activated and a series of impulses are propagated.
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16
Q

Mechanisms of Cardiac Arrhythmias: Define Delayed after-depolarization.

A

After attaining resting membrane potential (RMP) a secondary deflection occurs which may reach threshold potential and initiate a single premature AP.

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17
Q

What are the two main causes of Mechanisms of Cardiac Arrhythmias?

A
  • Re-entry
  • Enhanced/ectopic pacemaker activity
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18
Q

What are the ECG changes with Hypomagnesemia?

A
  • prolonged PR QT intervals, diminished T-wave
  • Torsades
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19
Q

What are the ECG changes with Hypermagnesemia?

A

QRS widening, heart block, arrest

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20
Q

What does Hypomagnesemia often accompany?

A

hypoK+ and hypoCa

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21
Q

What are the ECG changes with Hypocalcemia?

A

Prolongation of QT

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22
Q

What are the ECG changes with Hypercalcemia?

A
  • QT shortening
  • widened or flattened T wave
  • J waves following QRS (early repolarization
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23
Q

What are the effects with Hypokalemia?

A
  • cellular level- hyperpolarizes (prolonged action potential)
  • This leads to Na+/Ca++ derangements that result in increased excitability
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24
Q

What are the ECG changes with Hypokalemia?

A
  • flattened T wave/inversion and U waves (repolarization)
  • PVC’s
  • tachyarrhythmias
  • Torsades
  • AF
  • VT/VF
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25
Q

What is hypokalemia associated with?

A

Associated with dig toxicity

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26
Q

What are the ECG changes with Hyperkalemia?

A
  • peaked T-waves
  • PR prolongation
  • QRS widening
  • VF
  • asystole
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27
Q

Review different classifications of arrhythmias.

A
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28
Q

Review the narrow and wide QRS complex.

A
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29
Q

What is the general MOA of Antiarrhythmic Drugs?

A

Block Na+, K+, Ca++ ion channels that constitute each phase of the cardiac action potential (AP)

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30
Q

What effects duration of Antiarrhythmic Drugs?

A

Duration of phase varies, atria vs ventricles

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31
Q

What is the inactive state?

A

unresponsive to a continued or new stimulus (plateau phase/repolarization

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32
Q

What is the resting state?

A

more prevalent during diastole

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33
Q

What is the active state?

A

more prevalent during systole (upstroke of the action potential)

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34
Q

What are the clinicsl effects of antiarrhymic drugs?

A
  • are targeted to specific phases (ions) of the AP and the effective refractory period (ERP)
  • leads to electrophysiologic effect on the myocardium
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35
Q

What is a component of the relative regractory period?

A

coincides with the T wave apex

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36
Q

What is the effect of Na+ blockade?

A

slow conduction and suppress upstroke velocity of the AP

37
Q

What is the effect of K+ blockade?

A

prolong repolarization by increasing the duration of the AP and ERP resulting in prolonged QT (Class III agents)

38
Q

What is the effect of Ca++ blockade?

A

by way of the α-subunits of L and T myocardial Ca++ channels

39
Q

Where do Class 1 drugs exert their effect on the cardiac AP?

A

Na+ Channel Blocker

  • Phase 0 (Na+ in)
40
Q

What are examples of Class 1 antidysrhymic medications?

A

Na+ Channel Blocker

  • 1a (moderate): Quinidine, Procainamide
  • 1b (Weak): Lidocaine, Phenytoin
  • 1c (strong): Flecainide, Propafenone
41
Q

What are examples of Class 4 antidysrhymic medications?

A

Ca2++ Channel blocker

  • Verapamil
  • Dilitiazem
42
Q

Where do Class 4 drugs exert their effect on the cardiac AP?

A

Ca2++ Channel blocker

  • Phase 2 (Ca2+ In)
43
Q

Where do Class 3 drugs exert their effect on the cardiac AP?

A

K+ Channel Blocker

  • Phase 3 (K+ Out)
44
Q

What are examples of Class 3 antidysrhymic medications?

A

K+ Channel Blocker

  • Amiodarone
  • Sotalol
45
Q

Where do Class 2 drugs exert their effect on the cardiac AP?

A

Beta-Blocker

  • Phase 4 (K+ rectifier)
46
Q

What are examples of Class 2 antidysrhymic medications?

A

Beta blocker

  • Propranolol
  • metoprolol
47
Q

Review cardiac antiarrhythmic drugs overview.

A
48
Q

Review efficacy of individual antiarrhythmic drugs.

A
49
Q

What is the MOA of Class I drugs?

A

These drugs inhibit fast sodium channels during depolarization (phase 0) of the cardiac AP

50
Q

What are the different types of Class I Drugs?

A
  • Class 1A
  • Class IB
  • Class IC
51
Q

What are the effects of Class 1A antidysrhythmics?

A

lengthen cardiac AP & ERP, Na+ channel inhibition, prolonged repolarization d/t K+ channel blockade

52
Q

What are the effects of Class 1B antidysrhythmics?

A

shorten the cardiac AP duration & refractory period

53
Q

What are the effects of Class 1C antidysrhythmics?

A

potent Na+ channel blockers, decrease rate of phase 0 depolarization & speed of conduction of cardiac impulses; little effect on AP or ARP; proarrhythmic effects

54
Q

What do class II drugs block?

A

These drugs primarily beta adrenergic blockers

55
Q

What are the effects of Class II drugs on the AP?

A
  • Decreased rate of spontaneous phase 4 depolarization
  • decreased autonomic nervous system activity
56
Q

What effect do Class II drugs have on the myocardial oxygen requirements?

A

Class 2: Beta Blockers

  • Drug-induced slowing of HR reduces myocardial oxygen requirements
57
Q

What affect do Class II Drugs have on the conduction of the heart?

A

Beta Blocker

  • Slows speed of conduction of impulses through atrium
  • prolongs PR interval on ECG
  • doesn’t alter duration of cardiac AP
58
Q

What is the MOA of Class III drugs?

A

K+ channel blocker

  • Block potassium ion channels, results in prolongation of cardiac depolarization, AP duration, & ERP
59
Q

What does Class III drugs decrease?

A

Decreases proportion of cardiac cycle during which myocardial cells are excitable & susceptible to a triggering event

60
Q

When are class III drugs useful?

A

Useful in suppressing reentrant tachycardias making the AP duration to be longer than that generated within the tachycardia circuit

61
Q

What are the effects of Amiodarone?

A
  • exhibits class III effects, class I, class II, and class IV effects
  • used in tx of supraventricular & ventricular arrhythmias
62
Q

What is the effects of Sotalol?

A

long acting, noncardioselective β-blocking drug w/ class III effects

63
Q

What are the effects of Dofetilide?

A

class III drug prescribed by cardiologists

64
Q

What are class IV drugs?

A

verapamil & diltiazem

65
Q

What is the MOA of Class IV drugs?

A

act by inhibiting inward slow calcium ion currents that may contribute to development of tachycardias

66
Q

Which Ca++ triggers contraction?

A

The L-type Ca++ channel is most abundant and is responsible for Ca++ entry into the cell that triggers contraction.

67
Q

What are T type Ca channels?

A

T-type Ca channels are most prevalent in the conduction system and are probably involved in automaticity

68
Q

What are Class IV drugs useful in treating?

A

Useful in tx of SVTs and idiopathic ventricular tachycardia

69
Q

Which CCBs do not possess Class IV drugs?

A

Dihydropyridine CCBs do not possess antiarrhythmic action (nifedipine, nicardipine, nimodipine)

70
Q

What is a Torsade de pointes more likely to develop?

A
  • More likely to develop with prolonged QTc
  • Drugs that increase duration of refractoriness; prolong the QTc d/t K+ channel blockade
71
Q

What medications likely to cause Torsades?

A

Class IA (quinidine, disopyramide); Class III (amiodarone)

72
Q

What is torsades often associated with?

A

Often asso/w bradycardia b/c the QTc interval is longer at slower heart rates

73
Q

What can exacerbate torsades de pointes?

A

Exacerbated by hypoK+, hypoMg++, poor LV function, and other QT prolongation drugs

74
Q

How does ventricular tachycardia occur?

A

Slowed conduction that allows for ventricular re-entry impulse

75
Q

What is the medications often associated with ventricular tachycardia?

A

Class IA (quinidine, procainamide), Class IC (flecainide, propafenone); (rarely class IB)

76
Q

What is true about ventricular tachycardia?

A

Tends to be slower and resistant to drug or electrical therapy

77
Q

What is true about wide complex ventricular rhythms?

A

re-entrant tachycardia that can degenerate into VF

78
Q

What drug class is associated with wide complex ventricular rhythms?

A

Class IC drugs (flecainide, propafenone)

79
Q

Chronic suppression of ventricular ectopy does not prevent future occurrence of ______________

A

life-threatening arrythmias

80
Q

What medication can prevent prevent future occurrence of life-threatening arrythmias?

A

Except amiodarone

81
Q

What precludes the use of Class IA/IC in CHF patients?

A
  • Proarrhythmic and negative inotropic effects
  • Amiodarone ok
82
Q

What increases mortality of with Class IA/IC?

A

Hx of MI and ventricular arrythmias: Mortality increased with Class IA/IC

83
Q

What decreases mortality of with Hx of MI and ventricular arrythmias?

A

Decreased with amiodarone and β-blockers

84
Q

What is not recommended in early stages of MI?

A
  • Lidocaine not recommended for prophylactic Tx in early stages of MI
  • CCB not recommended as first-line tx for acute MI
85
Q

What is treatment of torsades de pointes?

A

Magnesium

86
Q

What is true about amiodarone and heart failure patients?

A

Little role for drugs other than amiodarone for prevention of cardiac sudden death in patients with heart failure

87
Q

What is a common complication after cardiac surgery? What is prophylactic therapy?

A

Atrial fibrillation after cardiac surgery a common complication: Prophylactic therapy to reduce occurrence (& risk of stroke) often uses amiodarone, β-blockers, sotalol and Mg++

88
Q

The benefits of using an antiarrhythmic other than for ______ does not always outweigh the risks

A

acute use

2-Pharm Exam 3 (14 decks)

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