Ch 49: Antidysrhythmic Drugs Flashcards

1
Q

Virtually all of the drugs used to treat dysrhythmias can also…

A

…cause dysrhythmias.

p. 534

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2
Q

What type of therapies are beginning to replace drugs as the preferred treatment for many dysrhythmias?

A

nonpharmacologic therapies such as implantable defibrillators and radiofrequency ablation

(p. 534)

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3
Q

What term is actually more appropriate than “arrhythmia”?

A

dysrhythmia

p. 534

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4
Q

What is the term for the electrical pathways between the SA node and AV node?

A

internodal pathways

p. 535

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5
Q

Fast potentials occur in…

A

…fibers of the His-Purkinje system and in atrial and ventricular muscle.

(p. 535)

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6
Q

Drugs that reduce calcium entry during phase 2 (of fast potentials) do not…
However, they can…

A

…influence cardiac rhythm.
…reduce myocardial contractility.

(p. 535)

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7
Q

In phase 3 (of fast potentials), rapid ______________ takes place. This is caused by…

A

repolarization

extrusion of potassium from the cell.

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8
Q

Phase 3 repolarization can be delayed by drugs that…

A

…block potassium channels.

p. 535

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9
Q

During phase 4, two types of electrical activity are possible:

A

1) the membrane potential may remain stable
2) the membrane may undergo spontaneous depolarization

(p. 535)

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10
Q

All cells which have the capacity for self-excitation (automaticity)…

A

…are potential pacemakers.

p. 536

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11
Q

Under normal conditions, ____________ cells undergo very slow spontaneous depolarization, and __________ cells do not undergo any.

A

His-Purkinje; myocardial

p. 536

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12
Q

Under pathologic conditions, significant _____ _ ______________ may occur in all of these cells, and especially in ________ ______. When this happens, a ___________ can result.

A

phase 4 depolarization; Purkinje fibers
dysrhythmia

(p. 536)

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13
Q

Slow potentials occur in cells of the…

A

…SA node and AV node.

p. 536

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14
Q

Spontaneous phase 4 depolarization in the SA node normally determines…

A

…heart rate.

p. 536

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15
Q

Phase 0 of fast potentials is caused by…

In contrast, phase 0 of slow potentials is caused by….

A

…a rapid influx of sodium.
…a slow influx of calcium.

(p. 537)

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16
Q

Slow potentials lack…

A

… a phase 1.

p. 537

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17
Q

The P wave is caused by…

A

…depolarization of the atria.

p. 537

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18
Q

The QRS complex is caused by…

A

…depolarization of the ventricles.

p. 537

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19
Q

The T wave is caused by…

A

…repolarization of the ventricles, and is not associated with overt physical activity of the heart.

(p. 537)

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20
Q

Lengthening of the PR interval indicates…

A

…a delay in conduction through the AV node.

p. 537

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21
Q

What drug depresses the ST segment?

A

Digoxin

p. 537

22
Q

Dysrhythmias arise from 2 fundamental causes:

A

1) disturbances of impulse formation (automaticity)
2) disturbances of impulse conduction

(p. 537)

23
Q

Dysrhythmias may be produced if tissues that do not normally express automaticity…

A

…develop spontaneous phase 4 depolarization.

p. 537

24
Q
Excessive discharge of \_\_\_\_\_\_\_\_\_\_\_ neurons can augment automaticity to cause tachycardia; 
excessive \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ (\_\_\_\_\_) discharge can suppress automaticity to cause bradycardia.
A

sympathetic
parasympathetic (vagal)

(p. 537)

25
Q

Degrees of AV block:
If impulse conduction is…
If some impulses pass through but…
If all traffic through…

A

….delayed, but not prevented, the block is a 1st degree.
…but others do not, the block is a 2nd degree.
…the AV node stops, the block is a 3rd degree.

(p. 537)

26
Q

The phenomenon of reentrant activation can result in…

A

…repetitive ectopic beats.

p. 538

27
Q
According to the Vaughan Williams classification scheme, which antidysrhythmic drugs are in Class I?
Class II?
Class III?
Class IV?
Other antidysrhythmic drugs?
A
Class I: Sodium channel blockers
Class II: Beta blockers
Class III: Potassium channel blockers (drugs that delay repolarization)
Class IV: Calcium channel blockers
Other: adenosine and digoxin

(p. 538)

28
Q

What are the effects of beta and calcium channel blockers in the SA node?
AV node?
in the atria and ventricles?

A

..they reduce automaticity
…they slow conduction velocity
…they reduce contractility

(p. 539)

29
Q

Amiodarone is an important potassium channel blocker. It works by…
It prolongs both the…

A

…delaying repolarization of fast potentials.
…action potential duration and the effective refractory period.

(p. 539)

30
Q

Which classes of antidysrhythmic drugs cause QT prolongation?

A

Class IA and class III

p. 540

31
Q

What are the 2 major groups of dysrhythmias?

A

supraventricular dysrhythmias
ventricular dysrhythmias

(p. 540)

32
Q

Group I antidysrhythmic drugs block cardiac sodium channels. By doing so, they decrease…

A

…conduction velocity in the atria, ventricles and His-Purkinje system.

(p. 542)

33
Q

What are the primary differences between Class 1A and Class 1B antidysrhythmic drugs?

A
Class IA agents delay polarization, and class IB agents accelerate repolarization.
Class IB agents have little or no effect on the ECG.  

(p. 542, 545)

34
Q

Class I drugs are similar in action and structure to the…

A

…local anesthetics.

p. 542

35
Q

Like quinine, quinidine has…

A

…antimalarial and antipyretic properties.

p. 543

36
Q

Quinidine is strongly…

A

…anticholinergic (atropine-like) and blocks vagal input to the heart.

(p. 543)

37
Q

To prevent excessive ventricular stimulation by quinidine, patients are usually pretreated with…

A

…digoxin, verapamil, or a beta blocker, all of which suppress AV conduction.

(p. 543)

38
Q

Quinidine (along with fellow Class IA agents procainamide and disopyramide) have 2 pronounced effects on the ECG:

A

1) widening of the QRS complex
2) prolongation of the QT-interval

(p. 543)

39
Q

Quinidine is a also a drug of choice for…

A

…severe malaria.

p. 543

40
Q

Quinidine and quinine are both known as cinchona alkaloids because their natural source is the bark of the South American cinchona tree.
Cinchonism is a term for the adverse effects which can be caused by these drugs. It is characterized by…

A

…tinnitus, headache, nausea, vertigo, and disturbed vision.

(p. 544)

41
Q

Procainamide is only weakly…

A

…anticholinergic, and hence is not likely to increase ventricular rate.

(p. 544)

42
Q

Lidocaine is used only for…

A

…ventricular dysrhythmias.

p. 545

43
Q

Lidocaine works by:

1) blocking ______ ______ ________ and thereby slowing…
2) it reduces ____________ in the ventricles and His-Purkinje system
3) it accelerates ______________ by shortening the action potential duration and ___

A

1) cardiac sodium channels; …conduction in the atria, ventricles, and His-Purkinje system
2) automaticity
3) repolarization; ERP

(p. 545)

44
Q

Phenytoin is also used to treat…

A

…digoxin-induced dysrhythmias.

p. 545

45
Q

In contrast to lidocaine and many other antidysrhythmic drugs, phenytoin…

A

…increases AV nodal conduction.

p. 545

46
Q

What are the only two Class IC agents available right now?

A

flecainide and propafenone

p. 546

47
Q

What effects do class IC agents have on the ECG?

A

widening of the QRS and prolongation of the PR

p. 546

48
Q

What are the 3 members of Class II?

A

propranolol, acebutolol, esmolol

p. 546

49
Q

Propranolol is a ____________ beta-adrenergic antagonist.

A

nonselective

p. 546

50
Q

What are the effects of Class II agents on the ECG?

A

bradycardia, prolongation of the PR interval

p. 546

51
Q

The reduction in AV conduction velocity translates to a…

A

…prolonged PR interval.

p. 546