L16- Anti-dysrhythmic drugs 1

Question 1

In the ECG wave what do each of these correspond to?

P wave

QRS complex

T wave

Answer 1

P wave- atrial depolarization

QRS- ventricular depolarization and atrial repolarization

T wave- Ventricular repolarization

Question 2

What is likely to happen when bloods pumped back and forth between atria and ventricles?

Answer 2

Blood will clot

Question 3

What’s the difference between arrhythmia and dysrhythmia?

Answer 3

Arhythmia means absence of rhythm. (a subclass of dysrhythmia)

Dysrythmia is a disturbance of rhythm

Question 4

How are dyrhythmias classified?

Answer 4

According to their site of origin, effect and frequency of occurance. eg. supraventricular tachycardia, paroxysmal. In the AV node, too fast, occuring in attacks.

Question 5

What does true arrhythmia mean?

Answer 5

A very disogranized rhythm

Question 6

What are 5 main mechanisms that lead to dysrhythmia?

Answer 6

1. Ectopic pacemakers- heart develops extra pacemakers
2. Delayed after depolarization
3. Re-entry circuits- damage causes AP to travel in circles
4. Congenital abnormalities- additional conducting pathways between atria and ventricles
5. Heart block- damage to conducting pathway, disrupts A to V signalling, leads to bradycardia

Question 7

Where do re-entry dysrhuthmias arise?

Answer 7

At rings of cardiac tissue. Normally the wave branches around non-conducting region and mutual annihalation occurs where they meet. If there’s damage on one side, signal spreads back up th side.

Question 8

What is Wollf Parkinson White syndrome?

Answer 8

An inherited abnormality wher there are additional conducting pathways between the atria and the ventricles known as Kent bundles.

Question 9

What 2 problems does WPW syndrome cause?

Answer 9

1. The signal from the atria to ventricles go via Kent bundles too. Kent bundles can’t limit rate (like AVN) so causes atrial flutter and tachycardia
2. Can set up a giant re-entry circuit between atria and ventricles.

Question 10

Why are dysrhythmias often experienced by people who already have CVS problems?

Answer 10

Reduced O2 to cardiac muscle will depolarize cells slightly, making them more likely to fir innapropraite APs. Can also be due to damage and scarring to heart.

Question 11

How can drugs cause dysrhythmias?

Answer 11

Drugs to change the heart alter cardiac rhythm. If you give some to a healthy person, or too much drug is prescribed, can alter th heart rate too much.

Question 12

What effect would an ectopic pacemaker have?

Answer 12

If its rate exceeds that of the SAN then heart rate will increase. The P wave will have an odd shape too.

Question 13

How will the ECG change for someone with heart block?

Answer 13

As the ventricles can’t keep us with the atria, the P wave is probably normal. But the ventricles ar not depolarized and can’t contract so there’s no QRS complex. omg

Question 14

What is treated with shock paddles?

Answer 14

Ventricular fibrillation. (which is true arrhythmia- no real pattern in ECG)

Question 15

What does the Vaughan-Williams classificastion system do?

Answer 15

Divides anti dysrhythmia drugs into their mechanism, which channel they work at. 4 classes with class 1 subdivided into a, b and c

Question 16

What does each class target in the VW classification system?

Answer 16

1 = sodium channels

2 = Beta adrenoceptors

3 = potassium channels

4 = calcium channels

Question 17

Name one drug for each 4 classes of VW?

Answer 17

1. Lidocaine
2. Atenolol
3. Amiodarone
4. Verapamil

Question 18

In the cardiac AP what happens step by step?

Answer 18

Sodium channels cause depolarisation

Membrane brought to threshold

More sodium rushes in. Sodium closes

Calcium causes plateau phase

Calcium channels inactivated

Potassium channels open

Repolarization

Question 19

Which class is Amiodarone?

Answer 19

It’s formally class 3 blocks K channels.

However also blocks Na and Ca channels.

By blocking K channels, it prolongs the refractory period so slows down HR.

Question 20

WHat;’s a problem with Amiodarone?

Answer 20

It’s very lipophilic so gets into fats easily, forms microcrystals which can cause problems.

Takes a long time to get to steady plasma levels.

Then lasts a long time in the body.

Question 21

How is Amiodarone administered and what is its advantage?

Answer 21

Orally or by IV injection.

Although it slows the heart, does not alter the force of contraction.

Question 22

What does AMioderone do to the skin?

Answer 22

Builds up in skin and eyes and is photoreactive. Causes grey skin discolouration.

Question 23

What does sotalol do?

Answer 23

Blocks K channels. L isomers also work as class 2 (beta adrenoceptors). Prolongs AP.

If you block K then you prevent repolarization.

Question 24

What does adenosine do?

Answer 24

It activates K channels and slows pacemaker potential, slowing heart rate. Not in the VW class system.

Question 25

What does digoxin do? Which class?

Answer 25

Digoxin is unclassified in VW.

It can slow AV node conduction and improve ventricular filling during atrial fibrillation.

Has a very narrow therapeutic window.

Question 26

When is adenosine used for?

Answer 26

Suppressing tachycardias.

PSVT (paroxysmal supraventricular tachycardia) occure in attacks. General anaesthetics can provoke dysrhythmias in surgery, adenosine can treat this is emergencies.

Question 27

Why can adenosine only be used in emergencies?

Answer 27

Has a half life of 10 seconds. Given in a big dose by injection. Effects only last 20-30 seconds.

suppresses tachycardias

Question 28

What are the side effects of adenosine?

Answer 28

Dramatic slowing of heart can cause problems if patient has heart block.

Can cause bronchospasm in patients with asthma

Question 29

WHen should you not use adenosine?

Answer 29

asthma or heart block patients