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Maddie’s Pharm > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

Define arrhythmia. (5)

A

A heart condition where disturbances in pacemaker impulse formation (SA/AV node) or ectopic impulse conduction (or a combination) lead to a rate / contraction pattern that is inadequate to maintain cardiac output.

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2
Q

Describe the stages of the fast action potential. (5)

A 
0 = initial depolarisation due to sodium influx.
1 = plateau due to potassium efflux
2 = plateau due to calcium influx 
3 = repolarisation due to potassium efflux and calcium influx 
4 = maintenence off resting membrane potential by Na+/K+ ATPase
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3
Q

Describe the stages of the slow action potential. (5)

A 
0 = depolarisation due to calcium influx 
2 = peak due to calcium influx
3 = repolarisation due to potassium efflux
4 = setting up of the If with sodium and potassium influx.
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4
Q

Describe the pathophysiology of Wolff-Parkinson-White Syndrome. (4)
Explain the causes. (3)

A

A disorder of abnormal conduction due to an accessory pathway called the Bundle of Kent between the Bundle of His and the atria, meaning impulses travelling down the Bundle of His get recirculated to the atria to be sent again. This is called a re-entry loop, and leads to pre-excitation.
This can occur congenitally, or due to infarction, because infarcted tissue transmits electrical current differently.

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5
Q

Explain the two main ways that drugs can affect arrhythmic hearts. (6)

A

Abnormal current generation - decrease the phase 4 slope (If) in pacemaker cells or raise the threshold so not all impulses get transmitted.
Abnormal conduction - decrease conduction velocity or increase essential refractory period.

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6
Q

Describe class 1 drugs and their effects. (3)

A

Na+ channel blockers.

Slows conduction of phase 0 (fast ap) in tissues, and have a minor increase to action potential duration.

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7
Q 
Name three class 1A drugs. (3)
What is their administration route? (2)
A

Procainamide
Quinidine
Disopyramide
All oral or IV.

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8
Q

Describe the effects in cardiac tissue of class 1A agents. (7)

A

Decreases conduction speed by descreasing the speed of phase 0.
Increase refractory period (increased action potential duration and increased Na+ channel inactivation)
Decrease automaticity (decreased slope of phase 4)
Increased threshold

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9
Q

Describe the effects of class 1A drugs on the ECG. (2)

A

Increased QRS interval

Increased QT interval.

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10
Q

Describe the use of two class 1A drugs. (4)

A 
Quinidine = maintain sinus rhythm in AF
Procainamide = given IV acutely for SVT and ventricular tachycardia.
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11
Q

Describe the main side effects of class 1A drugs. (7)

A

Hypotension (reduces CO)
Proarrhythmic (Torsades des Points from increased QT interval).
Dizziness, confusion, headache, seizures.
GI upset.

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12
Q 
Name two class 1B drugs. (2)
Describe their administration route. (2)
A

Lidocaine - IV only

Mexiletine - oral

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13
Q

Describe the effects on cardiac tissue of class 1B drugs. (3)

A

Increase the threshold

Decrease phase 0 conduction in tachycardic or ishcaemic tissue only.

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14
Q

Describe the effects of class 1B drugs on an ECG. (2)

A

None if normal speed

Increased QRS interval in faster beating.

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15
Q

Describe the uses of class 1B drugs. (2)

A

Ventricular tachycardia esp during ischaemia

Not for use in atrial arrhythmias

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16
Q

Describe the side effects of class 1B drugs. (3)

A

Less proarrhythmic than class 1A
Dizziness, drowsiness
GI upset.

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17
Q 
Name two class 1C drugs. (2)
Describe their administration route. (2)
A

Flecainide
Propafenone
IV or oral

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18
Q

Describe the effects on cardiac tissue of class 1C drugs. (4)

A

Highly decreased phase 0 to slow action potential
Increased threshold to decrease automaticity
Increased action potential duration
Increased refractory period

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19
Q

Describe the effects on ECG of class 1C drugs. (3)

A

Increased PR interval
Increased QRS interval
Increased QT interval

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20
Q

Describe the uses of class 1C drugs (3)

A

Supraventricular tachydardia
Ectopic ventricular contractions
Wolff-Parkinson-White Syndrome

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21
Q

Describe the side effects of class 1C drugs. (6)

A

Proarrhythmic and sudden death associated with prolonged use, or structural heart disease.
Increases ventricular rate due to increased transmission of the slowed atrial rate.
Dizziness, drowsiness
GI upset

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22
Q

Describe class 2 drugs. (1)
Name two examples. (2)
Describe the method of administration. (2)

A

Beta blockers.
Propanolol - oral or IV
Bisoprolol - oral

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23
Q

Describe the effects on cardiac tissue of class 2 drugs. (4)

A

Increased action potential duration and increased refractory period in the AV node to decrease AV node conduction.
Decrease phase 4 depolarisation (blocks catecholamine effects).

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24
Q

Describe the effects of Class 2 drugs on ECG. (2)

A

Increase PR interval

Decreased HR.

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25
Q

Describe uses of class 2 drugs. (3)

A

Sinus and catecholamine dependent tachycardia
Converting re-entrant arrhythmias at AV node (eg WPW)
Slows AV conduction in AF.

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26
Q 
Describe the  side effects of class 2 drugs. (2)
Explain who these side effects exclude. (4)
A

Bronchospasm
Hypotension
Asthmatics (bronchospasm would cause attack) and those in heart block or unstable heart failure (hypotension would make these worse).

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27
Q

Describe class 3 drugs. (1)

A

K+ channel blockers.

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28
Q

Give two examples of a class 3 drug. Describe their method of administration and their half lives. (6)

A

Amioderone - Oral or IV - t1/2 = 3 months

Sotalol - oral - t1/2 = 10 ish hours

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29
Q

Describe the effects of amioderone on an ECG. (4)

A

Increased PR interval
Increased QRS interval
Increased QT intervals
Decreased heart rate

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30
Q

Describe the effects of Amioderone on cardiac tissue. (4)

A

Increased action potential duration and increased refractory period.
Increased threshold
Decreased speed of AV conduction.

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31
Q

Describe the main use for Amioderone. (3)

A

Shockable but otherwise drug resistant VF.

Can work in most arrhythmias.

32
Q

Describe the side effects for Amioderone. (7)

A 
Pulmonary fibrosis 
Hepatic injury 
Increased LDL cholesterol
Thyroid disease
Photosensitivity 
Optic neuritis (transient blindness) 
Needs monitoring of warfarin and digoxin esp.
33
Q

Describe the cardiac effects of sotalol. (3)

A

Increased action potential duration and increased refractory period by closing AV conduction.

34
Q

Describe the effects on an ECG of sotalol.

2

A

Increased QT interval

Decreased heart rate.

35
Q

Describe the uses of Sotalol. (2)

A

Wide spectrum use for ventricular and supraventricular tachycardia.

36
Q

Describe the side effects of sotalol. (2)

A

Proarrhythmic

Insomnia and fatigue.

37
Q

Describe class 4 drugs. Give two examples and their methods of administration. (5)

A

Calcium channel blockers.
Verapamil - oral or IV
Diltiazem - oral

38
Q

Describe the cardiac effects of class 4 drugs. (4)

A

Slows AV conduction
Increased refractory period in the AV node
Increased slope of phase 4 in the SA node to slow HR.

39
Q

Describe the ECG effects of class 4 drugs. (2)

A 
Increased PR interval 
Changes HR (direction dependent on BP).
40
Q

Describe the uses of class 4 drugs. (2)

A

Supraventricular tachycardia

Convert SVT if caused by re-entry.

41
Q

Describe the side effects of class 4 drugs. (2)

A

Do not give with a beta blocker - asystole.

GI upset.

42
Q

Describe the effects of class 1 drugs on the drawing of the fast action potential. (2)

A 
Peaks slower (more to the right) 
Repolarises slower (more to the right.
43
Q

Describe the effects of class 2 drugs on the drawing of the fast action potential. (2)

A 
Peaks slower (more to the right)
Repolarises slower (more to the right)
44
Q

Describe the effects of class 2 drugs on the drawing of the slow action potential. (2)

A

Increased slope of the If - faster depolarisation.

45
Q

Describe the effects of class 3 drugs on the drawing of the fast action potential. (2)

A

Initially the same.

Repolarises much slower.

46
Q

Describe the effects of class 4 drugs on the drawing of the fast action potential. (3)

A

Peaks much slower and of less amplitude.

Repolarises slower.

47
Q

Describethe effects of class 4 drugs on the slow action potential. (2)

A

If the same

Depolarises slower

48
Q

Explain the administration of adenosine. (2)

A

Give rapid IV bolus because t1/2 is only seconds.

49
Q

Describe the MoA of adenosine.(5)

A

Natural nucleotide that binds to A1 receptors and activates K+ Efflux, which hyperpolarises cells. This hyperpolarisation inhibits calcium movement, which decreases the action of the pacemaker, to decrease the heart rate.

50
Q

Describe the cardiac effects of adenosine. (2)

A

Slows AV conduction - will temporarily “stop the heart”

51
Q

Describe the uses of adenosine. (2)

A

Converts re-entrant supraventricular arrhythmias

Diagnosis of coronary artery disease with scans.

52
Q

Describe the contraindication of adenosine. (4)

A

Accessory pathways.
Asthma
Heart block
HF

53
Q

Describe the MoA of Vernakalant. (2)

A

Blocks atrial specific K+ channels.

54
Q

Describe the cardiac effects of Vernakalant. (2)

A

Slows atrial conduction,

Increases potency with higher heart rates

55
Q

Describe the side effects of Vernakalant (3)

A

Hypotension
AV block
Sneezing

56
Q

Describe the uses of Vernakalant. (2)

A

Convert recent onset atrial fibrillation to normal sinus rhythm.

57
Q

Describe the MoA of Ivabradine. (3)

A

Blocks If current if highly expressed in the SA node. Doesn’t affect BP.

58
Q

Describe the side effects of Ivabradine. (2)

A

Flashing lights

Teratogenic

59
Q

Describe the uses of Ivabradine. (3)

A

Reduces sinus tachycardia

Reduces HR in heart failure and angina while avoiding BP drops.

60
Q

Describe the MoA of digoxin. (3)

A

Enhances vagal activity to increase refractory period.

Slows AV conduction to reduce HR.

61
Q

Describe the uses of digoxin. (1)

A

Reduces ventricular rates in AF.

62
Q

Describe the MoA of atropine. (3)

A

Selective muscarinic antagonists to speed up AV conduction to increase HR.

63
Q

Describe the effects of adenosine on the slow action potential drawing. (1)

A

Slows the If (decreased slope)

64
Q

Describe the uses of atropine. (1)

A

Treat vagal bradycardia.

65
Q

Describe the effects of atropine on the slow action potential drawing. (1)

A

Slows the If (decreased slope).

66
Q

Describe the relationships between efficacy and tolerability in regards to cardiac drugs. (2)

A

Often the most efficatious drugs are the least tolerable.

67
Q

Describe the drugs that fit the patten for the relationship of efficacy and tolerability. (8)

A

Bisoprolol, verapamil, diltiazem - least efficacious, but highly tolerable.
Soltalol, flecainide, mexiletine - middle for both.
Amioderone - life threatening ADRs but highly efficacious.

68
Q

Describe the drug prescription options in AF if rate control is needed. (8)

A 
Bisoprolol - Beta blocker (class 2) 
Verapamil - CCB (class 4) 
Diltiazem - CCB (class 4) 
Digoxin - slows AV conduction
69
Q

Describe the drug prescription options in AF if rhythm control is needed. (4)

A 
Soltalol - KCB (class 3)
Flecainide with Bisoprolol - NCB (class 1C) and beta blocker (class 2) 
Amioderone - KCB (class 3)
70
Q

Describe the drug prescription options in Atrial flutter (2)

A

AV node blocking drugs to reduce ventricular rates eg digoxin.

71
Q

Describe the drug prescription options in Wolff-Parkinson-White Syndrome. (2)

A 
Flecainide - NCB (class 1C) 
Amioderone - KCB (class 3)
72
Q

Describe the drug prescription options in Acute re-entrant SVT. (4)

A

Adenosine - slows AV conduction
Verapamil - CCB (class 4)
Flecainide - NCB (class 1C)
IV

73
Q

Describe the drug prescription options in Chronic re-entrant SVT. (5)

A 
Bisoprolol - Beta blocker (class 2) 
Verapamil - CCB (class 4) 
Flecainide - NCB (class 1C) 
Amioderone - KCB (class 3) 
Oral
74
Q

Describe the drug prescription options with Ectopic beats. (3)

A 
Bisoprolol - Beta blocker (class 2) 
Flecainide - NCB (class 1C) 
Amioderone - KCB (class 3)
75
Q

Describe the drug prescription options in Sinus tachycardia. (3)

A 
Ivabradine - slows the sinus node 
Bisoprolol - Beta blocker (class 2) 
Verapamil - CCB (class 4)

Maddie’s Pharm (23 decks)

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