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Anesthesia Pharmacology II > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

2
Q

What are the 2 major mechanisms that cause ectopic cardiac dysrhythmias?

A

Automaticity

Reentry

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3
Q

What is automaticity in the myocardium?

A

The ability of the cardiac muscles to depolarize spontaneously without electrical stimulation from the nervous system.

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4
Q

The discharge rate of normal or abnormal pacemaker activity may be accelerated by what: (4)

A
  • Drugs
  • Various forms of cardiac disease
  • Reduced potassium
  • Alterations of autonomic nervous system tone
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5
Q

What does enhanced normal automaticity result in?

What does abnormal automaticity result in?

A

Sinus tachycardia

Accelerated idioventricular rhythm

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6
Q

Reentry is responsible for most of the clinically important arrhythmias, including a-fib, a-flutter, AV nodal reentry, AV reentry involving a bypass tract, ventricular tachycardia after MI, and v-fib. True or false?

A

True.

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7
Q

What are other underlying mechanisms that can cause dysrhythmias? (7)

A

Myocardial Ischemia
Hypoxemia
Bradycardia–>ventricular dysrhythmias
Hypokalemia, hypomagnesemia–>ventricular dysrhy.
Volatile agents and other drugs
Acid-Base Changes–>**alkalosis **
ANS Changes

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8
Q

What are the following antidysrhythmic classes?

Class I
II
III
IV

A

I. Membrane stabilizers

II. Beta blockers

III. Prolong repolarization

IV: Ca channel blockers

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9
Q

How do Class I agents work? (3)

A

Decrease automaticity

Decrease conduction through bypass tracts by blocking “fast” Na channels

Decrease Phase 0 depolarization

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10
Q

What is Phase 0?

A

Rapid depolarization via Na channels

Gates close when 0 mV reached

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11
Q

What is Phase 1?

A

Partial repolarization (K moves out the cell)

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12
Q

What is Phase 2?

A

Plateau (slow Ca movement into cell to neutralize K out)

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13
Q

What is Phase 3?

A

Rapid repolarization

(Ca channel close and K continues to move out unopposed)

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14
Q

What is Phase 4?

A

Resting phase, repolarization

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15
Q

The Class I drugs are the membrane stabilizers that block _______ channels thereby inhibiting Phase ___ .

A

Sodium

0

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16
Q

What do Class IA drugs do? (3)

A

Depress Phase 0 depolarization

Prolong action potential duration

Slow conduction velocity

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17
Q

What are the Class IA drugs? (3)

A

Procainamide

Disopyramide

Quinidine

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18
Q

When is QUINIDINE indicated? (3)

What class drug is it?

A
  • A-fib
  • WPW
  • PVC’s

Class IA

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19
Q

What do Class IB drugs do? (2)

A

Shorten AP conduction

Have little effect on Phase 0

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20
Q

What are the Class IB drugs? (3)

A

Phenytoin

Lidocaine

Tocainide

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21
Q

What do Class IC drugs do? (3)

A

Greatly depress Phase 0 depolarization

Minimally affect AP duration

Slow conduction

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22
Q

What class of agents bind most rapidly to the receptors?

What class of agents have the slowest binding and dissociation from the receptor?

A

Class IB

Class IC

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23
Q

What % of patients with a-fib taking quinidine, procainamide, and disopyramide will convert to NSR?

A

25%

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24
Q

Class IA drugs can be given IM and are preferred to be given IV? True or false?

A

False

Not IM because of pain.

Limited via IV because of vasodilation and myocardial depression can result.

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25
Q

What drug is effective in the treatment of acute and chronic supraventricular dysrhythmias?

A

Quinidine

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26
Q

What are the side effects of quinidine? (5)

A
  • Prolonged QT
  • Syncope or sudden death
  • Hypotension
  • Allergic reaction (itch, hives)
  • Diarrhea
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27
Q

We use quinidine in the OR. True or false?

A

False.

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28
Q

What EKG changes will indicate that quinidine should be discontinued or the dose should be decreased?

A

50% increase in QRS duration or heart block will ensue

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29
Q

What pts should not be prescibed quinidine? (2)

A

prolonged QT interval

AV heart block

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30
Q

What are the indications for procainamide? (3)

A
  • PVT
  • PVC
  • Ventricular dysrhythmias

Note: Not as effective in treating atrial tachydysrhythmias as quinidine.

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31
Q

What are the side effects of procainamide? (5)

A
  • Myocardial depression
  • Hypotension (by direct myocardial depression)
  • Asystole or v-fib (heart block or high conc. of drug)
  • Lupus-like symptoms (SLE-like syndrome)
  • Rash

Note: SLE is systemic lupus erythematasous

Also, incidence of side effects are high!

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32
Q

What are the indications for disopyramide?

A

Atrial and ventricular tachydysrhythmias

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33
Q

What is the adminiatration for disopyramide?

A

Oral

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34
Q

What is the mechanism of disopyramide?

When is the peak effect?

A

Simiar to quinidine, membrane stabilizing

2 hours

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35
Q

What are the side effects of disopyramide? (3)

A

Direct myocardial depression–precipitating CHF, hypotension

Anticholinergic activity–dry mouth, urinary hesitancy

Prolonged QT and paradoxical VT

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36
Q

What are the indications for lidocaine relating to dysrhythmias? (2)

A

PVC

V-tach

Note: Minimal atrial effects!

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37
Q

Lidocaine has significant 1st pass metabolism. True of false?

A

True.

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38
Q

What is the dose for lidocaine?

IV
IM
IV infusion rate

A

2 mg/kg

4 - 5 mg/kg

1 - 4 mg/min

39
Q

What is the mechanism of lidocaine? (2)

A

Delays the rate of Phase 4 depolarization

Blocks Na channels in depolarized tissues

Note: Not able to alter rate of atrial cells so not good for atrial tach.

40
Q

What are the side effects of lidocaine? (3)

> 5 mcg/ml (in plasma)
5-10 mcg/ml
> 10 mcg/ml

A

Stimulation of CNS

Seizures, hypotension

CNS depression, apnea, cardiac arrest

41
Q

What are the indications for phenytoin? (3)

A

Paradoxical VT

Torsade de Pointes

Digitalis toxicity

42
Q

How can phenytoin be administered?

What is the IV dose?

What is the max dose?

A

PO, IV

1.5 mg/kg q5 min or 10-15 mg/kg

1 gram

43
Q

What is the mechanism of phenytoin? (2)

A

Shortens QT interval

Improved conduction through the AV node

Note: Similar effects are lidocaine, but more profound.

44
Q

What drug shortens the QT interval more than any other drug?

A

Phenytoin

45
Q

What are the side effects of phenytoin? (4)

A

Bone marrow suppression

Increased blood sugar

CNS disturbances: cerebellar symptoms

Hypotension

46
Q

What is the indication for MEXILETINE and TOCAINIDE?

A

V-tach

47
Q

What is the mechanism of MEXILETINE and TOCAINIDE?

A

Similar to lidocaine

48
Q

What are the side effects of MEXILETINE and TOCAINIDE? (2)

A

Epigastric burning

Neurologic effects

49
Q

ON BOARDS

What are rare effects of TOCAINIDE? (2)

A

Bone marrow depression

Pulmonary fibrosis

50
Q

When is FLECAINIDE indicated? (3)

A

Atrial tachdysrhythmias

WPW

Ventricular premature beats (sometimes)

51
Q

What is the mechanism of FLECAINIDE? (2)

A

AV conduction block

Decreased SA node function

52
Q

What are the side effects of FLECAINIDE? (4)

A

Moderate negative inotropic effect

Prodysrhythmic effect

Vertigo

Visual accomadation problems

53
Q

What drug is most effective at suppressing premature ventricular beats and v-tach?

A

FLECAINIDE

54
Q

What are the indications for beta blockers? (4)

A

A-fib

A-flutter

Paroxysmal AT

Digitalis induced ventricular dysrhythmias

55
Q

What are the common beta blockers? (3)

A

Propanolol

Metoprolol

Esmolol

56
Q

What is the mechanism of Class II (beta blocking) drugs? (3)

A

Block sympathetic activity

Decreased rate of Phase 4 depolarization

Decreased rate of SA node discharge

57
Q

What are the side effects of beta blockers? (5)

A
  • Allergic rash
  • Bradycardia
  • Bronchospasm
  • CHF (worsen)
  • Mental depression, fatigue
58
Q

What is a Class III drug?

A

Amiodarone

59
Q

What is the indication for amiodarone? (2)

A

Refractory supraventricular / V tach

WPW

60
Q

Amiodarone is not very effective for atrial tach. True or false?

A

True.

61
Q

What is the dose of amiodarone?

initial IV dose
IV infusion rate

A

150 mg/ 10 min

1 mg/min

62
Q

What is the mechanism of amiodarone?

A

Prolongs refractory period in all cardiac tissue

63
Q

What must you do when giving amiodarone?

A

Give slowly because it can cause hypotension.

64
Q

What are the side effects of amiodarone? (3)

A

Pulmonary toxicity

Ventricular tachydysrhythmias

Hypotension

65
Q

If the daily dose of amiodarone exceeds 400mg, what side effect is likely to occur?

What is the course of treatment?

A

Pulmonary alveolitis

Decrease FiO2 at lowest possible to maintain adequate oxygenation because of increased production of free oxygen radicals.

66
Q

What are other side effects from chronic use of amiodarone? (10)

A
  • Bradycardia (resistance to atropine)
  • Heart block
  • Neurologic abnormalities like muscle weakness, ataxia
  • Pulmonary fibrosis
  • Hypo/hyper thyroidism
  • Corneal deposits
  • Phytosensitivity
  • Cyanotic discoloarion of the face
  • Increased plasma transaminase
  • Displacement of digoxin from binding sites
67
Q

What are the Class IV drugs? (2)

A

Verapamil

Diltaizem

68
Q

What are known as the supraventricular antidysrhythmics?

A

Class IV, Ca channel blockers

69
Q

What are the indications for calcium channel blockers? (3)

A

Paroxysmal SVT

Afib

A-flutter

70
Q

What drug may decrease the response to catecholamines and sympathetic stimulation which may manifest as sinus arrest, AV heart block, and result in low CO?

A

AMIODARONE

71
Q

The use of what drug may indicate the potential need for a temporary pacemaker?

A

AMIODARONE

72
Q

What is the dose of verapamil?

PO
IV

A

80 - 120 mg PO q 6-8 hours

5 - 10 mg IV

73
Q

What is the dose of diltiazem?

IV

A

20 mg IV

Note: This is 2nd line drug to be used in beta blocker doesn’t work.

74
Q

What is the mechanism of action of Class IV drugs? (2)

A

Decrease phase 4

Depresses AV node

75
Q

What is the metabolism and excretion of Class IV drugs?

A

Hepatic metabolism

Renal excretion

76
Q

What are the side effects of Class IV drugs? (3)

A

Hypotension

AV block

Direct myocardial depression (usually with chronic therapy)

77
Q

What class of drug increases:

effective refractory period
action potential duration
QT duration

A

Class IA

Quinidine, Procainamide, Disopyramide

78
Q

What class of drug decreases:

depolarization rate
conduction velocity

A

Class IA

79
Q

What class of drug decrease:

effective refractory period
action potential duration

A

Class IB

Lidocaine, Phenytoin, Mexiletine, Tocainide

80
Q

What class of drug:

decrease depolarization rate and conduction velocity
increase PR, QRS, and QT duration

A

Class IC

Flecainide

81
Q

What class of drug decrease:

conduction velocity
automaticity
QT duration

A

Class II

Beta blockers

82
Q

What class of drug:

decrease conduction
decrease automaticity
increase refractory period
increase PR duration
increase QT

A

Class III

Amiodarone

83
Q

What class of drug decreases action potential duration?

A

Class IV

Verapamil, Diltiazem

84
Q

What are the indications for digitalis? (2)

A

Atrial tachydysrhythmias

Heart failure

85
Q

What is the oral dose of digitalis?

A

0.5 - 1 mg over 12-24 hours

86
Q

What is the mechanism of digitalis?

A

Increase phase 4 slope

Increased AV node refractoriness

87
Q

What are the side effects of digitalis? (5)

A
  • Digitalis toxicity
  • EKG changes–digitalis effect
  • Cardiac dysrhythmias
  • Nausea
  • Disturbance of cognitive function
88
Q

When is adenosine indicated? (2)

A

PSVT (atrial tach)

WPW

89
Q

What is the dose of adenosine IV?

A

6 mg

Repeat in 3 min with 6-12 mg

90
Q

What is the mechanism of adenosine? (2)

A

Similar to Ca blocker

Hyperpolarize the cell

Note: Will see flat line on ECG!

91
Q

What are the side effects of adenosine? (5)

A
  • Headache
  • Facial flushing
  • Bronchospasm
  • Dyspnea
  • Transient AV block

Anesthesia Pharmacology II (11 decks)

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