Arrythmias and anti-arrythmic drugs

Question 1

What is another term for arrythmias?

Answer 1

Dysrhythmia

Question 2

What does arrythmia mean?

Answer 2

Disturbances in cardiac rhythm

Question 3

What are the different types of arrythmias?

Answer 3

Bradycardia

Atrial flutter
Atrial fibrillation

Tachycardia

Ventricular fibrillation

Question 4

What are the types of tachycardia? How are they different?

Answer 4

Ventricular tachycardia - arises from ventricles

Supraventricular tachycardia - arises from above ventricles

Question 5

What care the causes of ventricular tachycardia?

Answer 5

Ectopic pacemaker activity

Afterdepolarisations

Question 6

What causes ectopic pacemaker activity?

Answer 6

Damaged area of myocardium
Depolarised because sodium ions leak into cell
Generates action potentials

Dominates over SA node

Question 7

What is an afterpolarisation?

Answer 7

Abnormal depolarisations following the action potential

Question 8

What are the causes of supraventricular tachycardias?

Answer 8

Atrial flutter
Atrial fibrillation

Re-entry loop

• atria
• AV node

Question 9

What are the causes of bradycardia?

Answer 9

Sinus bradycardia

Conduction block

Question 10

What is sinus bradycardia?

Answer 10

Heart beat still in sinus rhythm

Just below 60bpm

Question 11

What are the causes of sinus bradycardia?

Answer 11

Intrinsic factors - SA node dysfunction

Extrinsic factors - drugs e.g. beta blockers, some Ca2+ channel blockers

Question 12

What is sick sinus syndrome?

Answer 12

Cardiac arryhtmias caused by intrinsic SA node dysfunction

Question 13

What are the causes of conduction block?

Answer 13

Intrinsic factors - problems with AV node, bundle of His

Extrinsic factors - drugs e.g. beta blockers, some Ca2+ ion blockers

Question 14

What are delayed after-depolarisations?

Answer 14

Membrane depolarises before next action potential

Question 15

When are delayed after-depolarisations more likely?

Answer 15

When intracellular Ca2+ conc. is high

Question 16

What are early after depolarisations?

Answer 16

Membrane depolarises during plateu phase of action potential

or during repolarisation phase

Question 17

What can early after-depolarisations lead to?

Answer 17

Oscillations in the membrane potential

Question 18

When are early after-depolarisations more likely?

Answer 18

Longer action potential

so a longer QT interval

Question 19

What happens when two impulses meet each other normally? Why?

Answer 19

Impulses cancel out

due to adjacent area being in refractory period

Question 20

What is a unidirectional block?

Answer 20

Impulse cannot be conducted in a certain direction along an area of myocardium

Question 21

How can a re-entry loop occur?

Answer 21

Unidrectional block prevents impulse conduction in a certain direction
Action potential travels via longer route
Goes the opposite way through the uridirectional block

Question 22

What causes atrial fibrillation?

Answer 22

Multiple re-entry loops in atria

Question 23

What causes the formation of multiple re-entry loops in the atria?

Answer 23

Stretching of atrial muscle

conductive tissue becomes damaged, irritated

Question 24

What is AV nodal re-entry?

Answer 24

Formation of re-entry loop within the AV node

Question 25

What is meant by ventricular pre-excitation?

Answer 25

Ventricles become depolarised before they normally should do

Question 26

What causes ventricular pre-excitation?

Answer 26

Accessory conductive pathway between atria and ventricles

Question 27

What else can the accessary conductive pathway cause?

Answer 27

Re-entry loops between atria and ventricles

Question 28

How does tachycardia affect output?

Answer 28

Reduces time in diastole reduces filling time of heart, EDV reduces SV, CO

Question 29

What are the different types of anti-arrythmic drugs?

Answer 29

1) Block VG Na+ channels 2) B-adrenoceptor antagonists 3) Block K+ channels 4) Block Ca2+ channels

Question 30

What is an example of a drug that blocks VG Na+ channels?

Answer 30

Lidocaine

Question 31

What mechanism does lidocaine use to block VG Na+ channels?

Answer 31

Use-dependent | blocks VG Na+ channels that are open or inactivated

Question 32

How does lidocaine affect the normal upstroke of the action potential?

Answer 32

It doesn't

Question 33

What can lidocaine be used to treat? Why?

Answer 33

Ventricular tachycardia | prevents action potentials being generated in damaged depolarised tissue

Question 34

How does lidocaine affect the next action potential?

Answer 34

It doesn't | dissociates in time for next action potential

Question 35

How is lidocaine given?

Answer 35

IV route

Question 36

What are some examples of B-adrenoceptor antagonists?

Answer 36

Propanolol Atenolol

Question 37

Where do B-adrenoceptor antagonists work in the heart

Answer 37

At B1 adrenoceptors

Question 38

What are the effects of B-adrenoceptor antagonists?

Answer 38

Decrease slope of pacemaker potential in SA node Slow down conduction at AV node

Question 39

When are B-adrenoceptors more effective?

Answer 39

Increased sympathetic input to heart

Question 40

What are B-adrenoceptor antagonists useful to treat?

Answer 40

Supraventricular tachycardia Following MI

Question 41

Why are B-adrenoceptor antagonists useful to treat supraventricular tachycardias?

Answer 41

Because they slow down conduction in AV node | Which slows down rate of ventricular depolarisation and contraction

Question 42

Why are B-adrenoceptor antagonists useful to treat MIs?

Answer 42

Block increased sympathetic drive, possible arrythmias Reduce oxygen demand, ischaemia by reducing heart rate, force of contraction

Question 43

How do drugs that block K+ cannels affect the action potential?

Answer 43

Delay repolarisation Delay the refractory period Delay the action potential

Question 44

Why are drugs that block K+ channels generally not used?

Answer 44

Because they can be pro-arrythmic

Question 45

How can drugs that block K+ channel be pro-arrythmic?

Answer 45

Longer repolarisation | prone to early-after depolarisations

Question 46

Which drug that blocks K+ channels is used frequently?

Answer 46

Amiodarone

Question 47

What are some other effects of amiodarone?

Answer 47

Blocks Ca2+ channels Beta blocker

Question 48

What is amiodarone used to treat?

Answer 48

Tachycardia by Wolff-Parkinson-White syndrome Ventricular arrythmias by MI

Question 49

What is an example of a drug that blocks Ca2+ channels in the heart?

Answer 49

Verapimil

Question 50

What are the effects of verapimil?

Answer 50

Decreases upstroke of action potential in SA node Decreases conduction of AV node Negative inotropy - decreases force of contraction

Question 51

Dihydropyridine Ca2+ channel blockers are not effective to treat...?

Answer 51

Arrythmias

Question 52

Dihydropyridine Ca2+ channel blockers act on...?

Answer 52

Vascular smooth muscle

Question 53

What is an example of a dihydropyridine Ca2+ channel blocker?

Answer 53

Nicarpidine

Question 54

What is another group of Ca2+ channel blockers?

Answer 54

Dihydropyridine Ca2+ channel blockers

Question 55

Where are adenosine receptors located in the heart?

Answer 55

AV node

Question 56

What are the adenosine receptors?

Answer 56

A1 receptors

Question 57

What type of receptor are A1 receptors?

Answer 57

GPCRs

Question 58

What are the effects of adenosine binding to A1 receptors?

Answer 58

Release of active beta-gamma subunit

Question 59

What does the active beta-gamma subunit do?

Answer 59

Increases conductivity of K+ channels | hyperpolarising the cells of the AV node

Question 60

What is adenosine useful to treat?

Answer 60

Re-entrant superventricular tachycardias

Question 61

How is adenosine given?

Answer 61

IV

Question 62

Is adenosine produced endogenously or not?

Answer 62

Yes it is