Antidysrhythmics

Question 1

What is arrhythmia?

Answer 1

Absence of rhythm

Question 2

What is dysrhythmia?

Answer 2

Disturbance in rhythm

Question 3

How are dysrhythmias classified?

Answer 3

Site of origin, effect and frequency of occurrence

Question 4

What are the possible sites of origin of dysrhythmias?

Answer 4

Atrial
Ventricular
Junctional (supraventricular)

Question 5

What is meant by a true dysrhythmia?

Answer 5

A very disorganised rhythm

Question 6

What is meant by tachycardia?

Answer 6

Heart beat too fast

Question 7

What is meant be bradycardia?

Answer 7

Heart beat too slow

Question 8

What is paroxysmal supraventricular tachycardia?

Answer 8

Happens in attacks, rapid but regular heart beat

Question 9

What are ectopic heartbeats?

Answer 9

Skipped or extra heartbeats leading to irregular heart rate and heart rhythm

Question 10

What is multifocal atrial tachycardia?

Answer 10

electrical impulses arriving from multiple locations within atria

Question 11

What is ventricular fibrillation?

Answer 11

Rapid heartbeat initiated within ventricles. It is characterised by 3 or more consecutive premature ventricular beats

Question 12

What is the most common type of bradydysrhythmia?

Answer 12

Heart block - communication between atria and ventricles is disrupted

Question 13

What is the difference between first, second and third degree heart block?

Answer 13

First: slowed conductance through AVN
Second: some atrial impulses fail to make it through to ventricles
Third: no conduction from atria to ventricles - complete heart block

Question 14

What is asystolic arrest?

Answer 14

Complete cessation of electrical activity - bradydysrhythmia

Question 15

What are the five main mechanisms that lead to dysrhythmia?

Answer 15

Ectopic pacemakers - conducting tissue other than SAN initiate heart beat
Delay after depol - build up on Ca2+ in cells leading to train of APs
Re-entry circuits - Tissue damage leads to AP travelling in circles
Congenital abnormalities - additional conducting pathways between atria and ventricles
Heart block - damage to conducting pathways disrupts signalling between atria and ventricles

Question 16

Ectopic foci lead to an odd shaped ___ wave on ECG

Answer 16

P

Question 17

Heart rate increase if rate of ectopic focus exceeds rate of SAN. True or false?

Answer 17

True

Question 18

What takes place in AF that leads to abnormal impulse generation?

Answer 18

Atrial myocytes contract independently, each atria potentially acts as ectopic focus so there is no coordinated contraction of atria so QRS complex occurs at irregular intervals

Question 19

Ventricular fibrillation can be a result of ectopic foci or re-entry circuits. True or false?

Answer 19

True

Question 20

Ventricular fibrillation is a true arrhythmia. True or false?

Answer 20

True

Question 21

In ventricular fibrillation, the ventricles are not coordinated in contraction and there is no ____ wave on ECG

Answer 21

QRS

Question 22

What is Wolff-Parkinson-White syndrome?

Answer 22

A congenital abnormality where there are additional conducting pathways between the atria and ventricles known as Kent bundles.
Signals go via AVN and Kent bundles leading to atrial flutter - ventricles try to keep up pace with atria - sudden death possible
Kent bundles can also set up re-entry circuits

Question 23

Can Kent bundles be surgically removed?

Answer 23

Yes - if one or two present usually surgically removed

Question 24

All dysrhytmias are abnormal and dangerous. True or false?

Answer 24

False - sinus dysrhythmia is an alteration of HR brought about by breathing - particularly common in young people

Question 25

What is the VW system?

Answer 25

main classification system used for anti-dysrhythmic drugs

Question 26

In the VW system, which receptors are targeted in the different classes?

Answer 26

``` Class I - Na channels Class 2 - B1 receptor Class 3 - K channel Class 4 - Calcium channel Unclassified - various ```

Question 27

What are the main drugs in the classes of VW system?

Answer 27

Class I - Lidocaine Class 2 - Atenolol Class 3 - Amioderone Class 4 - Verapamil

Question 28

Which class of the VW system is further subdivided into a, b and c?

Answer 28

Class 1

Question 29

How do class 1 drugs in the VW system work?

Answer 29

They block sodium channels in a use-dependence manner (preferentially block open and inactivated channels). They share this mechanism with local anaesthetics

Question 30

Which class does lidocaine belong to and how is it administered?

Answer 30

Class 1b - IV because metabolised by the liver so not given orally

Question 31

What is lidocaine's clinical use?

Answer 31

Ventricular dysrhythmia

Question 32

What class do procainamide and disopyramide belong to?

Answer 32

1a

Question 33

What class does flecainide belong to?

Answer 33

1c

Question 34

Class 1c drugs are useful in preventing paroxysmal atrial fibrillation. True or false?

Answer 34

True

Question 35

Class 1c drugs should be used after heart attacks. True or false?

Answer 35

False - avoid after heart attacks - sudden death likely

Question 36

B1 antagonists are particularly useful if sympathetic nervous system is involved in dysrhythmia. True or false?

Answer 36

True

Question 37

B1 blockers are useful for supraventricular and ventricular disrhythmia. True or false?

Answer 37

True

Question 38

What are the unwanted side effects of beta blockers?

Answer 38

``` Bronchoconstriction Heart block Hypoglycaemia Cold extremities Vivid dreams ```

Question 39

What is one of the weaknesses of VW system?

Answer 39

Some drugs act by more than one mechanism

Question 40

How does amiodarone work?

Answer 40

By blocking potassium channels (also blocks sodium and calcium)

Question 41

What is amiodarone useful for treating?

Answer 41

Supraventricular, ventricular dysrhythmias and WPW syndrome, AF

Question 42

How do potassium channel blockers work in reducing heart rate?

Answer 42

Potassium channel activation contributes to repolarisation so by blocking the channels, action potentials are prolonged and so is the refractory period therefore there is a decrease in heart rate

Question 43

Which drug is an analogue of the thyroid hormone?

Answer 43

Amioderone

Question 44

Amioderone is very lipophilic. True or false?

Answer 44

True

Question 45

What are the ways in which amioderone is administered?

Answer 45

Orally or IV into a central vein

Question 46

Although amioderone reduces heart rate, it alters the force of contraction, which isn't good. True or false?

Answer 46

False - doesn't alter the force of contraction

Question 47

What does cardiac rhythm depend on?

Answer 47

Ion channel activity and calcium ion concentration

Question 48

What is the structure of calcium channels (and sodium channels)?

Answer 48

Large proteins formed from an alpha subunit and a beta subunit. The alpha subunit consists of 4 pseudo-subunits. The pseudo-subunits have 6 transmembrane domains with a membrane dipping domain between the 5th and 6th transmembranes. The 4th transmembrane is charged and acts as a voltage sensor

Question 49

Voltage gated channels can exist in three states. What are they?

Answer 49

Resting Open Inactivated

Question 50

What is verapamil used for?

Answer 50

Prophylactically for paroxysmal supraventricular tachycardia and also in patients with AF to decrease ventricular rate

Question 51

Is Verpamil safe to use for patients with WPW?

Answer 51

No - dangerous

Question 52

Class IV drugs act on which type of calcium channel?

Answer 52

L-type

Question 53

What are unwanted side effects of amiodarone?

Answer 53

Thyrotoxicosis Hepatoxicity Bradycardia Micro-crystals in the cornea

Question 54

What are the major side effects of verapamil?

Answer 54

AVN block | Reduction in CO

Question 55

Which drug has a mechanism of reducing after-depolarisations?

Answer 55

Verapamil

Question 56

What causes after-depolarisations to take place?

Answer 56

Build up of calcium in cell due to repeated stimulation which triggers chain of APs

Question 57

Ziconotide is a drug that blocks which type of calcium channel?

Answer 57

N-type

Question 58

What are weaknesses of VW system?

Answer 58

Excludes some potential sites for antidysrhythmic drugs Doesn't allow for the fact that some drugs have multiple mechanisms of action Does not all for the fact that drug action on diseased tissue may differ from that on healthy tissue

Question 59

What is digoxin used for?

Answer 59

Heart failure

Question 60

Antidysrhytmic effects of digoxin are largely mediated by which nerve?

Answer 60

Vagus

Question 61

Ziconotide requires intrathecal delivery. True or false?

Answer 61

True

Question 62

Ziconotide has a narrow therapeutic window. True or false?

Answer 62

True

Question 63

How does digoxin work?

Answer 63

It increases vagus nerve activity which: reduces SAN firing rate reduces AVN conduction velocity reduces ventricular rate

Question 64

Digoxin has a narrow therapeutic index. What happens if it is given at a toxic dose?

Answer 64

Increases sympathetic tone - dysrhythmia - depolarisation increases afterdepolarisations increases ectopic beats

Question 65

How is digoxin toxicity treated?

Answer 65

Stop digoxin administration Correct hypokalaemia by giving KCl orally/infusion Give propranolol/phenytoin

Question 66

How does adenosine work?

Answer 66

Activation of adenosine leads to activation of K+ channels and so hyperpolarisation, reducing AP duration and inhibiting Ca2+ channels.

Question 67

What can adenosine be used for?

Answer 67

Supression of: Supraventricular tach Ventricular tach - WPW PSVT

Question 68

Why can't adenosine be used chronically?

Answer 68

Because it's plasma half life is 10s