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Clinical Pharmacology > 17) Cardiac Arrhythmias > Flashcards

17) Cardiac Arrhythmias Flashcards

1
Q

Describe some abnormal impulse generations in the heart:

A

Delayed or early afterpolarisation

Ectopic focus

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2
Q

Describe some abnormal conduction that can occur in the heart:

A

Conduction block

Re-entry loops

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3
Q

What is circus movement (in terms of conduction)?

A

Part of conduction pathway is blocked so impulse travels in retrograde fashion, re-exciting some cells

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4
Q

Describe Wolf-Parkinson-White syndrome:

A

Accessory pathway between atria and ventricles (bundle of Kent), that doesn’t have rate slowing properties of AVN

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5
Q

What are the general actions of arrhythmia drugs on impulse generation and conduction?

A

Decrease funny current slope in pacemaker cells
Raise threshold to prolong action potential
Decrease conduction velocity
Increase refractory period

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6
Q

What are examples of class Ia anti-arrhythmics?

A

Quinidine and procainamide

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7
Q

What is the mechanism of action of class Ia anti-arrhythmics?

A

Decrease conduction, increase refractory period and increase AP threshold by sodium channel blocking

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8
Q

When are class Ia anti-arrhythmics indicated?

A

Prevent AF

Ventricular arrhythmias

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9
Q

What are the side effects of class Ia anti-arrhythmics?

A 
Hypotension 
Proarrthymia
Dizziness
Confusion 
Lupus like syndrome (procainamide)
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10
Q

What are examples of class Ib anti-arrhythmics?

A

Lidocaine, mexiletine

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11
Q

What are examples of class Ic anti-arrhythmics?

A

Flecainide, propafenone

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12
Q

What are examples of class II anti-arrhythmics?

A

Propanolol, metoprolol, bisoprolol, esmolol

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13
Q

What are examples of class III anti-arrhythmics?

A

Amiodarone, sotalol

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14
Q

What are examples of class IV anti-arrhythmics?

A

Verapamil, diltiazem

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15
Q

What is the mechanism of action of class Ib anti-arrhythmics?

A

Sodium channel blockers (fast association) - decrease Na+ conduction in fast beating or ischemic tissue

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16
Q

When are class Ib anti-arrhythmics indicated?

A

Ventricular tachycardia

17
Q

What are the side effects of class Ib anti-arrhythmics?

A

Dizziness, drowsiness, abdominal upset

18
Q

What is the mechanism of action of class Ic anti-arrhythmics?

A

Sodium channel blockers (slow association) - decrease sodium entry, increase refractory period

19
Q

When are class Ic anti-arrhythmics indicated?

A

Supraventricular arrhythmia (fib and flutter)
Premature ventricular contractions
WPW

20
Q

What are the side effects of class Ic anti-arrhythmics?

A

Pro-arrhythmic
Sudden death in previous MI
CNS and GI effects

21
Q

What is the mechanism of action of class II anti-arrhythmics?

A

Beta blockers
Decrease conduction through AVN
Decrease depolarisation

22
Q

When are class II anti-arrhythmics indicated?

A

Tachycardia
Protect ventricles from high atrial rate
Convert re-entrant arrhythmias

23
Q

What are the side effects of class II anti-arrhythmics?

A

Bronchospasm, hypotension

24
Q

What is the mechanism of action of class III anti-arrhythmics?

A

Increase refractory period and prolong repolarisation by blocking K+ channels

25
Q

When are class III anti-arrhythmics indicated?

A

Ventricular tachycardia

WPW

26
Q

What are the side effects of class III anti-arrhythmics?

A

Amiodarone: pulmonary fibrosis, hepatic injury, thyroid disease, optic neuritis
General: pro-arrhythmic, fatigue, insomnia

27
Q

What is the mechanism of action of class IV anti-arrhythmics?

A

Ca2+ channel blockers - slow conduction through AVN, increase refractory period

28
Q

What are the side effects of class IV anti-arrhythmics?

A

Hypotension, decreased CO, GI problems

29
Q

When are class IV anti-arrhythmics indicated?

A

Supraventricular tachycardia, convert re-entry

30
Q

What is the mechanism of action of adenosine?

A

Activation of K+ channels in AVN and SAN causing hyperpolarisation and decrease HR

31
Q

When is adenosine used?

A

Convert re-entrant supraventricular arrhythmias

32
Q

What is the mechanism of action of vernakalant?

A

Blocks atrial specific K+ channels to slow atrial conduction

33
Q

When is vernakalant used?

A

Convert AF to sinus

34
Q

What is the mechanism of action of ivabradine?

A

Blocks the funny current in sinus node to slow HR

35
Q

When is ivabradine used?

A

Sinus tachycardia, angina, heart failure

36
Q

What is the mechanism of action of digoxin? And when is it used?

A

Decreases conduction at AVN, increases vagal activity

Reduce ventricular rate in AF

37
Q

What is the mechanism of action of atropine? When is it used?

A

Selective muscarinic antagonist that blocks vagal activity to increase HR in vagal bradycardia

38
Q

What are the principles of AF treatment?

A

Rate control

Rhythm control

Clinical Pharmacology (24 decks)

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