LAB - 7.1 - Antiarryhtmic Agents Flashcards

1
Q

The activation gates on the Na+ and K+ channels are closed, and the membrane’s resting potential is maintained.

A

Resting state

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2
Q

A stimulus opens the activation gates on some Na+ channels. Na+ influx through those channels depolarizes the membrane. If the depolarization reaches the threshold, it triggers an action potential.

A

Depolarization

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3
Q

Depolarization opens the activation gates on most Na* channels, while the K* channels’ activation gates remain closed. Na* influx makes the inside of the membrane positive with respect to the outside.

A

Rising phase of the action potential

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4
Q

The inactivation gates on most Na+ channels close, blocking Na* influx. The activation gates on most K+ channels open, permitting K+ efflux which again makes the inside of the cell negative.

A

Falling phase of the action potential

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5
Q

Both gates of the Na+ channels are closed, but the activation gates on some K+ channels are still open. As these gates close on most K+ channels, and the inactivation gates open on Na* channels, the membrane returns to its resting state.

A

Undershoot

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6
Q

is a problem with the rate or rhythm of your heartbeat.

A

Arrhythmia

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7
Q

it means that the heart beats too quickly, too slowly, or with an irregular pattern.

A

Arrhythmia

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8
Q

When the heart beats faster than normal, it is called .

A

tachycardia

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9
Q

When the heart beats too slowly, it is called .

A

bradycardia

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10
Q

The most common type of arrhythmia is ___, which causes an irregular and fast heart beat.

A

atrial fibrillation

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11
Q

Electrical changes associated with atrial depolarization

A

P wave

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12
Q

Electrical changes associated with ventricular depolarization

A

QRS complex

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13
Q

Electrical changes associated with ventricular repolarization

A

T wave

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14
Q

The electrical changes associated with atrial repolarization normally coincide with the ___ complex and are obscured by it.

A

QRS

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15
Q

___ drugs affect the action potential of the cardiac cells, altering their automaticity, conductivity, or both

A

Antiarrhythmic

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16
Q

Can Anti-arrhytmic drugs cause arryhytmia?

A

YES

17
Q

Classification of Antiarrhythmics (Based on Mechanisms of Action)

A

Class I – Blocker’s of Fast Na+ Channels

18
Q

Which Class I Sublass features:
Prolong repolarization
Increased duration of action potential

A

Subclass IA

19
Q

Examples of Subclass IA Medications

A

Quinidine
Procainamide
Disopyramide

20
Q

Class I Antiarryhtmic Drugs are ___ blockers

A

Sodium

21
Q

Which Class I Sublass features:
Shortened depolarization
Decreased action potential duration

A

Subclass IB

22
Q

Examples of Subclass IB Medications

A

Lidocaine
Mexiletine
Phenytoin

23
Q

This Subclass IB Medication is approved only for use in life-threatening ventricular arrhythmias in adults

A

Mexiletine

24
Q

Which Class I Sublass features:
No effect of depolarization and on action potential duration

A

Subclass IC

25
Q

Examples of Subclass IC Medications

A

Flecainide
Propafenone

26
Q

This Subclass IC Medication was initially developed as a local anesthetic. It slows conduction in all parts of heart

A

Flecainide (Tambocor)

27
Q

This Subclass IC Medication:
- Also slows conduction
-Weak β – blocker

A

Propafenone

28
Q

affect predominantly slow-channel tissues (sinoatrial [SA] and atrioventricular [AV] nodes), where they decrease rate of automaticity, slow conduction velocity, and prolong refractoriness

A

Class II – β–adrenergic blockers

29
Q

Examples of Class II – β–adrenergic blockers

A

Propranolol
Metoprolol
Atenolol
Pindolol

30
Q

This Class II – β–adrenergic blocker:

Slows SA node and ectopic pacemaking
Can block arrhythmias induced by exercise or apprehension
Other β–adrenergic blockers have similar therapeutic effect:

A

Propranolol

31
Q

Block potassium channels and slow the outward movement of potassium during phase 3 of the action potential, thereby prolonging it

A

Class III – K+ channel blockers

32
Q

Developed because some patients are sensitive to Na channel blockers (they died!)

A

Class III – K+ channel blockers

33
Q

Examples of Class III – K+ channel blockers

A

Amiodarone
Bretylium
Dofetilide
Sotalol

34
Q

This Class III – K+ channel blocker is the drug of choice for treating ventricular fibrillation or pulse less ventricular tachycardia in cardiac arrest situations

A

Amiodarone

35
Q

Block the movement of calcium ions across the cell membrane thereby decreasing the excitability and contractility of the myocardium

Slow the rate of AV-conduction in patients with atrial fibrillation

A

Class IV – Ca+ Channel Blockers

36
Q

Examples of Class IV – Ca+ Channel Blockers

A

Verapamil
Diltiazem

37
Q

This Class IV – Ca+ Channel Blocker blocks Na+ channels in addition to Ca2+, also slows SA node in tachycardia

A

Verapamil (Isoptin)

38
Q

There is a risk of severe cardiac effects if Class IV drugs are given IV within ___ hours of IV beta-adrenergic drugs. The combination should be avoided.

A

48

39
Q

Nursing Implementation for Antiarryhtmic Agents

A

Titrate the dose to the smallest amount needed to achieve control of the arrhythmia to decrease the risk of severe adverse effects.

Continually monitor cardiac rhythm when initiating or changing dose to detect potentially serious adverse effects and to evaluate drug effectiveness.

Ensure that emergency life support equipment is readily available to treat severe adverse reactions that might occur.

Administer parenteral forms as ordered only if the oral form is not feasible; expect to switch to the oral form as soon as possible to decrease the potential for severe adverse effects.

Consult with the prescriber to reduce the dose in patients with renal or hepatic dysfunction; reduced dose may be needed to ensure therapeutic effects without increased risk of toxic effects.

Establish safety precautions, including side rails, lighting, and noise control, if CNS effects occur to ensure patient safety.

Arrange for periodic monitoring of cardiac rhythm when the patient is receiving long-term therapy to evaluate effects on cardiac status.