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Year 1 > Arrhythmia Drugs > Flashcards

Arrhythmia Drugs Flashcards

1
Q

Why do arrhythmias from?

A

Defects in impulse formation

Defects in impulse conduction

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2
Q

What are some defects in impulse formation?

A

Altered automacity

Triggered activity

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3
Q

What is physiological altered automacity?

A

Regulation of SA node activity by autonomic nevrous system

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4
Q

What is pathological altered automacity?

A

Latent pacemaker establishes HB instead of SA node (ectopic heart beat)

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5
Q

What are some causes of establishment of latent pacemaking?

A

If latent pacemaker fires at rate faster than SA node

If SA node firing frequency is pathologically low

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6
Q

What are some causes of latent pacemaker firing at rate FASTER than SA node?

A

Increased sympathetic acitvity, hypokalaemia and ischaemia trigger compensatory mechanisms in potential latent pacemakers i.e. cardiac myocytes

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7
Q

What are some causes of SA node firing frequency is pathologically low?

A

Ischaemia i.e. right coronary artery - no blood supply to SA node
Circulatory hormones i.e. hypothyroidism
Hypokalemia

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8
Q

What is triggered activity?

A

Afterdepolarizations triggered by normal action potential, two types
Early after depolarizations
Delayed after depolarizations

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9
Q

When do early after depolarisation occur?

A 
Phase 2 (terminal plateau) - AD mediated by Ca2+ L type channels 
Phase 3 (repolarization) - AD mediated by K+ channel opening (usually closed at this stage)
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10
Q

TRUE/FALSE

Delayed after depolarizations are associated with drugs such as sotalol

A

FALSE

EADs associated with sotalol - drugs that lengthen QT interval (Ventricular systole) and prolonging AP

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11
Q

When do delayed after depolarisation occur?

A

Occurs after complete repolarization

Caused by transient inward current involving Na+ channels

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12
Q

TRUE/FALSE

Delayed after depolarizations are associated with drugs such as digoxin

A

TRUE
Digoxin reverses action of Na+/K+ pump, allowing Na+ to enter cell. This results in activation of Ca2+ channels which provokes DADs

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13
Q

What are some causes of defects in impulse CONDUCTION?

A

Re-entry
Conduction block
Accessory tracts

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14
Q

What is a re-entry circuit?

A

Defect in self sustaining electric circuit with parallel conduction, resulting in cyclical stimulation of myocardium.
Caused by unidirectional block or slowed retrograde conduction velocity

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15
Q

What is heart block?

A

Fault in heart’s natural pacemaker due to block in electrical conduction (can be due to ischaemia , fibrosis etc)

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16
Q

What is partial block?

A

Tissue conducts all impulses, but more slowly than usual. Example is first degree AV block

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17
Q

What is intermittent block?

A

Tissue conducts some impulses but not others. Example is second degree AV block

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18
Q

What is Mobitz T1?

A 
Type of second degree heart block.
PR interval (atrial systole) lengthens from cycle to cycle until AV node fails and VENTRICULAR beat is missed.
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19
Q

What is Mobitz T11?

A

Type of second degree heart block.

PR interval is CONSTANT but every nth ventricular depolarization missing

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20
Q

What is complete block?

A

No impulses are conducted through affected area. Example is third degree AV block.
Atria and ventricles beat independently, governed by separate pacemakers.

21
Q

What is the significance of accessory tract pathways

A

Impulse conducted faster through accessory pathway than through AV node
predispose to reentrant loops and tachyarrhythmia

22
Q

What is disopyramide?

A

Class IA anti-arrhythmic drug

23
Q

What is lignocaine?

A

Class IB antiarrhythmic drug

24
Q

What is flecainide

A

Class IC antiarrhythmic drug

25
Q

What is the Vaughn Williams classification of antiarrhythmic drugs?

A 
Class 1 stimulates Na+ channels
Class 2 inhibits B-adrenoreceptors
Class 3 stimulates K+ channels
class 4 stimulates Ca2+ channels
26
Q

What does Class IA anti-arrhythmic drug do?

A

Associates with disassociates with Na+ channels at MODERATE rate.
Slow rise of AP (velocity)
PROLONGS refractory period.
This works to PREVENT REENTRY

27
Q

What does Class IB anti-arrhythmic drug do?

A

Associates with and disassociates with Na+ channels at FAST rate.
Depresses conduction velocity
This works to PREVENT PREMATURE BEATS and treat ventricular tachycardia

28
Q

What does Class IC anti-arrhythmic drug do?

A

Associates with and disassociates with Na+ channels at SLOW rate.
STRONGLY depresses conduction velocity (phase 0)
This leads to -ve chrono and inotropic effects

29
Q

TRUE/FALSE

Class I drugs bind preferentially to areas of the myocardium where AP firing frequency is highest

A

TRUE

During tachyarrhythmias Na+ channel spends most time in OPEN and ABSOLUTE inactivated state.

30
Q

How does adenosine work?

A

Stimulates A1 (adenosine) receptors in AVN

Opens GIRK channels (G protein coupled inwardly rectifying K+ channels) in the atrioventricular node

This HYPERPOLARIZES cells and slows conduction in the AVN.

31
Q

TRUE/FALSE

Adenosine is not used to terminate paroxysmal supraventricular tachycardia

A

FALSE

it is, slows conduction in AV node

32
Q

TRUE/FALSE

Paroxysmal supraventricular tachycardia is caused by reentry

A

TRUE

33
Q

What is the action of the Na+/K+ pump?

A

3 na+ pumped out of cell

2 K+ pumped into cell

34
Q

What is the mechanism of digoxin?

A

Inhibits Na+/K+ pump which results in more intracellular sodium
This activates the Ca2+/Na+ exchanger which increases intracellular Ca2+ levels
SOMEHOW indirectly causes inc. vagal activity

35
Q

TRUE/FALSE

Digoxin increases sympathetic activity to the heart and Is therefore contraindicated in the treatment of AF

A

FALSE
Digoxin actually increases vagal activity to the heart, the mechanism is unknown.
It IS used to treat AF

36
Q

TRUE/FALSE

Adenosine and Digoxin BOTH slow conduction in the AVN node

A

TRUE
Digoxin through stimulating vagal activity
Adenosine due to stimulation of A1 receptors (adenosine receptors) and GIRK (causing efflux K+ and hyperpolarizing cell)

37
Q

Why is digoxin used to treat atrial fibrillation & atrial flutter?

A

In AF&AF atria beats at such high rates that ventricles can only irregularily follow (chaotic reentry impulse)

Slowing the conduction of this impulse, slows and strengthens ventricular beat

38
Q

What is the mechanism of Verapamil?

A

blocks L-type voltage-activated Ca2+ channels

Slows conduction and prolongs refractory period in AV node and bundle of His

39
Q

TRUE/FALSE

Verapamil should be used with great caution in combination with other drugs that have a negative ionotropic effect

A

TRUE
can cause heart block in high dose - POWERFUL effect on AVN node conduction and already has negative inotropic effect - CAUTION with cumulative inotropic effects

40
Q

Why has adenosine replaced verapamil in treatment of supraventricular arrhythmias ?

A

Its safer, adenosine used for acute treatment, but verapamil used for prophylaxis

41
Q

What is lignocaine mainly used to treat?

A

Ventricular arrhythmias and premature beats - IV admin

42
Q

What is flecainide mainly used for?

A

prophylaxis of paroxysmal atrial fibrillation

43
Q

What is the main difference in pharm. use of disopyramide and procainamide?

A

Disopyramide is used (orally) to prevent recurrent ventricular arrhythmias,

procainamide (IV) to treat ventricular arrhythmias following myocardial infarction

44
Q

What are some problems associated with beta blockers?

A

excessive supression sympathetic drive that may trigger VT

45
Q

How do beta blockers work?

A

Control SVT by suppressing impulse conduction through the AV node

46
Q

TRUE/FALSE

Sotolol is a beta blocker

A

FALSE

it is a Type 3 agent (K+ blocker)

47
Q

How do class 3 drugs work?

A

block of voltage-activated K+ channels

slow repolarization of the AP =increase action potential

inc. duration the effective refractory period

48
Q 
TRUE/FALSE
Amiodarone has class IA, II and IV actions and also blocks β-adrenoceptors
A 
True
it is a class 3 drug but does other stuff 2
49
Q

Amiodarone is WAY more effective than other drugs, why is it not used in the long term?

A 
Long term use side effects
pulmonary fibrosis
thyroid disorders
photosensitivity reactions
peripheral neuropathy

Year 1 (15 decks)

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