Pharmacology: Arrhythmias

Question 1

two mechanisms behind cardiac arrhythmias

Answer 1

1. alterations in impulse formation

2. abnormalities in impulse conduction

Question 2

two alterations in impulse formation

Answer 2

• change in automaticity

- triggered activity

Question 3

describe change in automaticity

Answer 3

latent pacemakers take over the rhythm (faster than SA node) and there is a loss of overdrive suppression

Question 4

when does an escape beat happen in changing automaticity

Answer 4

slow AV node

Question 5

when does an ectopic beat happen in changing automaticity

Answer 5

if latent pacemakers fire faster e.g. ischaemia, hypokalaemia

Question 6

two forms of triggered activity

Answer 6

early afterdepolarisations

delayed afterdepolarisations

Question 7

describe early afterdepolarisations

Answer 7

occur in phase 2 or 3 and when the HR is slow, often stems from purkinje fibres and can lead to torsades de pointes

Question 8

what is torsades de pointes

Answer 8

polymorphic VT

Question 9

describe delayed afterdepolarisations

Answer 9

caused by increased Ca2+ and occurs when the heart rate is fast (can be caused by drugs e.g. digoxin

Question 10

three categories of abnormalities in impulse conduction

Answer 10

• re-entry
• conduction block
• accessory tract

Question 11

describe re-entry

Answer 11

re-entrant circuit with unidirectional block with retrograde conduction

Question 12

what does conduction block through the AV node cause?

Answer 12

heart block

Question 13

accessory tract

Answer 13

bundle of Kent is faster than the AV node and can trigger tachyarrhythmias

Question 14

anti-arrhythmic drug classification

Answer 14

Vaughn-Williams

Question 15

class 1A

Answer 15

Na+ channels at a moderate rate, slowing rise of AP and increasing refractory period

Question 16

examples of class 1A drugs

Answer 16

disopyramide

procainamide

Question 17

when are class 1A drugs used?

Answer 17

ventricular arrhythmias

Question 18

class 1B

Answer 18

Na+ channels at a rapid rate, preventing premature beats (ischaemic zone)

Question 19

when are class 1B drugs used

Answer 19

ventricular arrhythmias following MI

Question 20

class 1C

Answer 20

Na+ channels at a slow rate, depressing conduction

Question 21

when are class 1C used?

Answer 21

paroxysmal AF

Question 22

adverse of 1C

Answer 22

can trigger ventricular arrhythmias

Question 23

class II

Answer 23

beta blockers that decrease rate of depolarisation through SA and AV nodes

Question 24

when are class II drugs used?

Answer 24

SVT

Question 25

adverse of class II

Answer 25

excess sympathetic drive can trigger VT

Question 26

class III

Answer 26

K+ channel openers that prolong AP and increase refractory period suppressing re-entry

Question 27

when is class III used

Answer 27

SVT and VT(everything when other drugs are contradicted)

Question 28

adverse of class III, specifically amiodarone

Answer 28

pulmonary fibrosis
thyroid disorders
photosensitivity
peripheral neuropathy

Question 29

examples of class III

Answer 29

amiodarone and sotolol

Question 30

example of class 1B

Answer 30

lidocaine

Question 31

example of 1C

Answer 31

flecainide

Question 32

example of class II

Answer 32

metoprolol

Question 33

class IV

Answer 33

Ca2+ blockers, slow conduction in SA and AV and decrease force of cardiac contraction

Question 34

when is class IV used?

Answer 34

atrial flutter

AF

Question 35

adverse of Ca2+ blockers

Answer 35

can cause heart block (largely replaced by adenosine)

Question 36

example of a class IV drug

Answer 36

verapamil

Question 37

mechanism of action of adenosine

Answer 37

activates A1-adenosine receptors (Gi/o) opening ACh-sensitive K+ channels causing hyperpolarisation, suppressing conduction

Question 38

when is adenosine used?

Answer 38

paroxysmal SVT e.g. WPW

Question 39

role of digoxin

Answer 39

stimulates vagal activity slowing conduction and prolonging refractory period

Question 40

when is digoxin used?

Answer 40

AF

Question 41

when is digoxin used?

Answer 41

slow fast AF

Question 42

ECG in digoxin toxicity

Answer 42

reverse tick (downward sloping of ST wave with rapid upstroke back to isoelectric line with bradycardia)

Question 43

when should digoxin, amiodarone and verapamil be avoided (slow AV conduction)?

Answer 43

aberrant pathways

Question 44

SE of amiodarone

Answer 44

thyroid disease
liver disease
pulmonary fibrosis
peripheral neuropathy

Question 45

monitoring in amiodarone

Answer 45

TFTs and LFTs every 6 months