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NUNA 680 - Pharm > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

1
Q

What is the incidence of arrhythmias during cardiac and non-cardiac surgery? Serious arrhythmias?

A

16.3-84%; less than 1%

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2
Q

What are the uses of antidysrhythmic drugs?

A

Control dysrhythmias perioperatively; maintenance therapy for a-fib and a-flutter refractory to ablation, and frequently shocked AICD patients

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3
Q

What are the two primary mechanisms of dysrhythmias?

A

Automaticity and re-entry

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4
Q

Explain the dysrhythmia mechanism of automaticity.

A

Condition where spontaneous depolarizations occur due to abnormal impulse generation in sinus or ectopic foci.

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5
Q

Explain the dysrhythmia mechanism of re-entry.

A

Impulses propagate more than one pathway (ex., WPW syndrome); seen more often with volatile agents because of suppression of SA node and conduction pathway

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6
Q

What factors promote dysrhythmias?

A 
Electrolyte imbalance
Hypoxemia
Acid base imbalance (alkalosis > acidosis)
Myocardial ischemia
Bradycardia
Increased mechanical stretch of myocardium
SNS stimulation
Drugs
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7
Q

Blocking ion channels manipulates various states of the action potential. Blocking Na+…

A

affects velocity of AP upstroke (ventricular tissue)

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8
Q

Blocking ion channels manipulates various states of the action potential. Blocking K+…

A

affects refractory

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9
Q

Blocking ion channels manipulates various states of the action potential. Blocking Ca+…

A

affects slope of phase 4 in nodal (pacemaker) tissue

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10
Q

What are prodysrhythmias?

A

Newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy (ex., Torsades, VT, wide complex ventricular rhythm)

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11
Q

What is phase 0 of the ventricular action potential?

A

Rapid depolarization as a result of opening of Na+ channels and closing K+ channels. Sodium rushes into the cell.

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12
Q

What is phase 1 of the ventricular action potential?

A

The period of initial repolarization that results from the closure of Na+ and opening of K+ channels. K+ begins to leave the cell. Na+ can no longer enter the cell.

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13
Q

What is phase 2 of the ventricular action potential?

A

The plateau phase that results from the sustained Ca++ current that began with the initial depolarization. Ca++ continues to enter the cell.

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14
Q

What is phase 3 of the ventricular action potential?

A

Repolarization due to opening of K+ and closure of Ca++ channels. K+ continues to leave the cell, but Ca++ can no longer enter the cell.

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15
Q

What is phase 4 of the ventricular action potential?

A

The resting potential during which time K+ channels are open and Na+ and Ca++ channels are closed.

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16
Q

What is the ERP of the ventricular action potential?

A

Effective refractory period during which the cell cannot be depolarized again. (Between phase 4s of the action potential cycle)

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17
Q

How do conduction cells vs. pacer cells differ in their action potentials?

A

Conduction myocytes have “fast” APs (dependent on Na+ for phase 0); pacemaker cells have “slow” APs (dependent on Ca++ for phase 0)

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18
Q

What is the resting charge for the ventricular AP?

A

-90 mV

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19
Q

What charge does the ventricular AP depolarize to?

A

+10 mV

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20
Q

What happens during phase 0 of the pacemaker AP?

A

Depolarization. L-Type Ca++ channels open; Ca++ rushes into the cell.

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21
Q

Pacemaker AP lacks which two phases?

A

1 and 2

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22
Q

Considering the lack of phases 1 and 2 in the pacemaker AP, what event causes the cell to begin repolarization?

A

For phase 3, K+ channels open and K+ leaves the cell.

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23
Q

Why is phase 4 of the pacemaker AP never a straight line?

A

There is always a slow Na+ leak into the cell.

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24
Q

Changing what aspect of the pacemaker AP changes heart rate?

A

The rate of phase 4 depolarization; steeper slope, by NE leads to faster HR; flatter slope by ACh leads to bradycardia or asystole

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25
Q

What are the Class I antidysrhythmic drugs known as?

A

Membrane Stabilizers; inhibit fast sodium channels

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26
Q

What are the Class II antidysrhythmic drugs known as?

A

Beta Adrenergic Antagonists; decrease rate of depolarization (phase 4)

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27
Q

What are the Class III antidysrhythmic drugs known as?

A

Refractory Prolongers; inhibit potassium ion channels

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28
Q

What are the Class IV antidysrhythmic drugs known as?

A

Ca+ Channel Blockers; inhibit slow calcium channels (calcium creep of SA cells)

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29
Q

What is the MOA of Class I antidysrhythmics?

A

Decrease depolarizations & conduction velocity by blocking Na+, moving the threshold potential farther away from the resting potential.

30
Q

What is the MOA of Class II antidysrhythmics?

A

Beta adrenergic antagonist; decreases magnitude of Ca+ influx, decreases K+ current (Na+/K+ pump), decreases pacemaker current (dec sinus rate), decrease rate of phase 4 depolarization, decrease epinephrine induced hypokalemia, decrease automaticity, decrease myocardial oxygen requirements, increase energy required to fibrillate the heart in ischemic tissue (dec ischemia related dysrhythmias), lengthen AV nodal conduction time and refractoriness which terminates re-entrant dysrhythmias, reduce mortality after MI

31
Q

What is the MOA of Class III antidysrhythmics?

A

Block K+ channels, increase absolute refractoriness, increase action potential duration, reduce automaticity, reduce re-entrant dysrhythmias, interact with beta blockers

32
Q

What is the MOA of Class IV antidysrhythmics?

A

Work primarily on sinus and AV nodal tissues; slow heart rate; decrease velocity of AV nodal conduction; useful in re-entrant dysrhythmias, rate control in RVR with a-fib and a-flutter, PSVT; v-tach; NOT been shown to reduce mortality after MI

33
Q

What risks must be considered when deciding whether to initiate antidysrhythmic therapy?

A

May increase risk of mortality
Risk of prodysrhythmias
Class Ia & Ib increased mortality and vent dysrhythmias
Class Ia & Ic can complicate CHF (weaken pump)
Lidocaine increases bradydysrhythmias & mortality after an MI

34
Q

Which antidysrhythmic drugs decrease mortality after MI?

A

Amiodarone & beta-blockers

35
Q

Indication for Quinidine

A

Prevent SVT, PVCs, maintain sinus rhythm in a-fib/a-flutter

36
Q

Quinidine MOA

A

Class I
Decrease phase 4 slope, prolong conduction
Blocks Na+, K+, alpha block, vagal inhibition

37
Q

Adverse effects of quinidine

A

Prolongs QRS, QT, PR, hypotension, may increase NMB

Depressant effect on contractility but may offset by increase in HR

38
Q

What class is procainamide?

A

Class I

39
Q

Indications of procainamide?

A
  • *ventricular and atrial tachydysrhythmias**

* *PVCs**

40
Q

MOA of procainamide?

A

Blocks Na+, K+ channels

Decreases automaticity, increases refractoriness

41
Q

Adverse effects of procainamide?

A

Slowed conduction times
Prolonged QRS, QT
Hypotension d/t myocardial depression
Lupus-like symptoms

42
Q

What class is disopyramide?

A

Class I

43
Q

Indications for disopyramide

A
  • *Atrial and ventricular tachydysrhythmias**

* *Maintain sinus rhythm in a-fib, a-flutter**

44
Q

MOA of disopyramide

A

Na+ channel block, anticholinergic actions

Slowed conduction

45
Q

Adverse effects of disopyramide

A

Myocardial depression
Depresses contractility, aggravates CHF
Prolongs QT

46
Q

What class is lidocaine?

A

Class I

47
Q

What are the indications for lidocaine?

A

Ventricular dysrhythmias, re-entry dysrhythmias (PVCs, V-tach)

Little effect on supraventricular dysrhythmias

48
Q

What is the non-dysrhythmic use for lidocaine?

A

ERAS multi-modal pain control
Infusion shown to be effective in colon surgery
Local anesthesia and IV regional blocks

49
Q

Lidocaine MOA

A

Delays phase 4 depolarizations (inhibits Na+ channels)

50
Q

What quality of lidocaine makes it appropriate for infusion?

A

Easily titrated

51
Q

What are some adverse implications of lidocaine use?

A

May increase mortality after MI
Myocardial depressant (bad for CHF)
Neurologic/seizures with toxicity
Prolonged PR, QRS

52
Q

Indications for beta adrenergic antagonists

A

Effective in dysrhythmias r/t increases in SNS

Ventricular rate control for a-fib, a-flutter

53
Q

Beta adrenergic antagonist MOA

A

Class II
Decrease spontaneous phase 4 depolarization
Decreased conduction through AV node

54
Q

Adverse effects of beta adrenergic antagonists

A

Prolonged PR, depressed myocardium

Bradycardia, hypotension, bronchospasm (since beta2 causes bronchodilation)

55
Q

Contraindications for beta adrenergic antagonists

A

CHF, reactive AW disease, AV block patients

56
Q

What class is amiodarone?

A

Class III

57
Q

Indications for amiodarone

A

Resistant v-tach, v-fib, a-fib, WPW

Acute termination of v-tach, v-fib (FIRST LINE TREATMENT)

58
Q

MOA of amiodarone

A

Blocks Na+, reduces currents of K+, Ca+
Prolongs AP, refractory, and conduction
Alpha and beta antagonist = vasodilation
Dilates coronary arteries (antianginal)

59
Q

Adverse effects of amiodarone

A

Hypotension (vasodilation, LV depression)
Pulmonary toxicity (d/t lipophilic, slow elimination)
Altered thyroid function (resembles thyroid hormone)
Marked QT prolongation, bradycardia, AV block
Resistant to catecholamines
Reduce O2 concentrations

60
Q

Describe dronedarone

A

Derivative of amiodarone (Class III)
Prevents return to a-fib/a-flutter (ONLY if pt is currently in sinus rhythm/after EP lab)
Potential to increase HF

61
Q

Drug class of verapamil and diltiazem

A

Class IV - Ca+ channel blockers

62
Q

Indications for verapamil and diltiazem

A

Rapid HRs - paroxysmal SVT, re-entrant tachydysrhythmias
Ventricular rate control in a-fib, a-flutter
NOT effective in reducing ventricular ectopy (bc dealing with SA tissue)

63
Q

MOA of verapamil and diltiazem

A

Block Ca+ in cardiac cells
Decreases spontaneous phase 4 depolarization
Vasodilation or coronary and peripheral arteries
Depresses AV node, negative chronotropic SA node

64
Q

Adverse effects of verapamil and diltiazem

A

AV block, aggravates reduced LV function
Hypotension
Myocardial depression
NMB may be exaggerated

65
Q

OTHER: Digitalis

A

Used to treat atrial tachydysrhythmias; slow AV node conduction slowing VR in a-fib; enhance accessory pathway conduction; increase Ca+ which enhances contractility
Risk of toxicity
Can cause any cardiac dysrhythmia

66
Q

OTHER: Adenosine

A

Slows sinus rate and conduction through AV node
NOT effective in a-fib, a-flutter, v-tach
RAPID BOLUS thru CVL
Transient asystole less than 5 seconds

67
Q

OTHER: Phenytoin

A

An anticonvulsant drug
Useful in VENTRICULAR but not atrial dysrhythmias and digitalis toxicity-induced ventricular dysrhythmias
Can depress sinus node

68
Q

OTHER: Magnesium

A

Prevent Torsades, digitalis-induced dysrhythmias, ventricular ectopy
ERAS analgesic effect, enhances opioid analgesia

69
Q

OTHER: Calcium

A

Increases threshold potential, protective against hyperkalemia dysrhythmias

70
Q

OTHER: Robinul/Glycopyrrolate

A

Muscarinic antagonist prevents ACh from producing negative chronotropic, inotropic, and dromotropic (conduction velocity) effects

71
Q

OTHER: Vasopressin

A

Produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction (bad for CAD)

NUNA 680 - Pharm (8 decks)

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