Arrhythmia: therapies Drugs for irregular heart rhythms, and anticoagulation

Question 1

What is an arrhythmia

Answer 1

Deviation from the normal rhythm of the heart

Question 2

Types of arrhythmias

Answer 2

Sinus
Tachycardia
Bradycardias

Question 3

Tachycardias

Answer 3

Supraventricular (atrial fibillation and SVT (junctional)
Ventricular arrhythmia (Tachycardia and fibrillation)

Question 4

Resting Membrane Potential

Answer 4

• During RMP the inside of the cell is a net negative charge relative to the outside
• Dependent on the sodium-potassium ATPase pump (requires energy)

Question 5

Action Potential (3)

Answer 5

1. Na+ enters the cell causing depolarisation once the threshold hits -40 mV
2. Ca++ enters the cell, initiation of contraction
3. K+ exits the cell causing repolarisation

Question 6

Vaughan-Williams Classification antiarrhythmics

Answer 6

Class I- V

Question 7

Class IA electrophysiological property

Answer 7

(moderate) sodium-channel blockade, thus reducing amplitude of AP and conduction velocity

Question 8

Class IA examples (3)

Answer 8

Quinidine
Procainamide
Dispyramide

Question 9

Class IB electrophysiological property

Answer 9

(Weak) sodium-channel blockades, thus reducing amptitude of AP and conduction velocity

Question 10

Class IB drugs examples (3)

Answer 10

Lidocaine
Mexeletine
Tocainide

Question 11

Class IC electrophysiological properties

Answer 11

(strong) sodium-channel blockade thus reducing amplitude of AP and conduction velocity

Question 12

Class IC drug examples

Answer 12

Flecainide

Propafenone

Question 13

Class II electrophysiological properties

Answer 13

B-Adrenergic receptor antagonism

Question 14

Class II examples

Answer 14

Atenolol

Bisoprolol

Question 15

Class III electrophysiological peoperties

Answer 15

Prolong refractoriness (slow K flow out of cells)

Question 16

Class III drug examples

Answer 16

Amiodorane
Bretylium
Sotalol

Question 17

Class IV electrophysiological properties

Answer 17

Calcium channel blockade

Question 18

Class IV drug examples

Answer 18

Diltiazem

Verapamil

Question 19

Class V drug

Answer 19

Other

Digoxin

Question 20

Class I drug most commonly used

Answer 20

Fleicanide

Question 21

Action of Class II (2)

Answer 21

Prolongs phase 4 depolarisation (slows SA discharge and AV conduction and reduces excitability in non-nodal cardiac tissues)
Shortens phase 2- negative effect on contractility

Question 22

First line for atrial fibrillation

Answer 22

Class II drugs

Question 23

Class III drugs are used for

Answer 23

dysrhythmias that are difficult to treat

• Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter- resistant to other drugs

Question 24

Use of Amiodarone

Answer 24

VT and supraventricular tachycardia

Question 25

Drug interactions of Amidodarone

Answer 25

Digoxin

Question 26

Side effects of Amiodarine (5)

Answer 26

``` Thyroid (hypo or hyper) Pulmonary fibrosis Slate grey pigmentation Corneal deposits LFT abnormalities ```

Question 27

Class IV (4)

Answer 27

* Calcium channel blockers- bind to Lcard- type voltage gated Ca++ channels * Depress phase 4 depolarisation in SA and AV nodes * Slow the HR (decrease automaticity and slows AV conduction) * Shortens phase 2 plateau phase (reduce contractility)

Question 28

Digoxin (class 5) properties

Answer 28

have properties of several classes and are not present in a particular class

Question 29

Action of Digoxin (5)

Answer 29

* Cardiac glycoside * Inhibits the sodium-potassium ATPase pump * Increases vagal tone- slows SA/AV node conduction * Complex effect on the cardiac action potential- reduces the refractory period in the myocardium * Increases Ca++ intracellular- positive inotropic effect

Question 30

Indications for Digoxin (2)

Answer 30

Atrial dysrhythmias | Heart failure

Question 31

Digoxin Toxicity (6)

Answer 31

* Nausea and vomiting * Xanthopia- objects appear yellow * Bradycardia * Tachycardia * Arrhythmias: VT and VF * Reverse tick appearance of ST segment in lateral leads

Question 32

Digoxin Toxicity Treatment (3)

Answer 32

Stop digoxin Give Digibind More serious is potassium levels are low

Question 33

Action of Adenosine

Answer 33

Slows/blocks conduction through AV node

Question 34

Use of Adenosine

Answer 34

Used to convert paroxysmal supraventricular tachycardia to sinus rythm

Question 35

Features of Adenosine (4)

Answer 35

Very short half life Only administered as fast IV push May cause asystole for a few seconds Minimal side effects

Question 36

All antiarrhythmics can cause___

Answer 36

arrhythmias

Question 37

Indications for anticoagulation

Answer 37

Atrial fibrillation- risk of stroke and pulmonary embolism Metallic heart valves DVT/PE

Question 38

Thrombosis in AF is caused when what 3 things are compromised

Answer 38

Stasis Abnormal blood Abnormal vessels

Question 39

Characteristics of the ideal anti-coagulant (6)

Answer 39

* Oral * No need for monitoring * No interaction with food or drugs * Given once or twice a day/fixed dose irrespective of body weight/age * As effective as warfarin * Safer than warfarin

Question 40

Oral anticoagulants and their function (3)

Answer 40

* Warfarin- Vitamin K reductase antagonist- prevents the production if active clotting factors * Dabigatran- Direct Thrombin Inhibitor * Rivaroxaban, Apixaban, Edoxaban- Direct Xa inhibitors

Question 41

Production of Clotting factors (5)

Answer 41

1. Vitamin K epoxide reductase 2. Reduced vitamin K 3. Vitamin K epoxide 4. Clotting factor precursors 5. Complete clotting factors (II, VII, IX and X)

Question 42

INR

Answer 42

Prothrombin Time Time it takes for blood to clot International normalised ratio

Question 43

Normal INR

Answer 43

1

Question 44

Therapeutic INR is normally

Answer 44

2.5-4.0

Question 45

Adverse effects of Warfarin (6)

Answer 45

``` • Bleeding (dose related) • Interaction with multiple drugs • Pregnancy  Teratogenic (chondrodysplasia)  Retroplacental bleeding and foetal intracerebral bleeding  Avoid in first and third trimester ```

Question 46

What enzyme metabolises Warfarin and what are the consequences of this (4)

Answer 46

Cytochrome P450 Interacts with drugs such as macrolide AB Antifungals Antiepileptic drugs

Question 47

Drugs that increase warfarin activity (5)

Answer 47

``` Aspirin Sulfonamides Cimetidine Erythromycin Antibiotics (oral) ```

Question 48

How does Aspirin | Sulfonamides increase warfarin activity

Answer 48

Decrease binding of warfarin to albumin

Question 49

How does Cimetidine | Erythromycin increase warfarin activity

Answer 49

Inhibit degradation of warfarin

Question 50

How does Antibiotics (oral) increase warfarin activity

Answer 50

Decrease synthesis of clotting factors

Question 51

Drugs that promote bleeding (2)

Answer 51

Aspirin | Heparin

Question 52

How does aspirin promote bleeding

Answer 52

Inhibition of platelets

Question 53

How does Heparin promote bleeding

Answer 53

Inhibition of clotting factors

Question 54

Drugs that decrease Warfarin activity (4)

Answer 54

Barbiturates Phenytoin Vitamin K Cholestyramine

Question 55

How does Barbiturates and Phenytoin decrease warfarin activyt

Answer 55

Induction od metabolising enzyme cytochrome P450

Question 56

How does Vitamin K decrease warfarin activity

Answer 56

Promote clotting factor synthesis

Question 57

How does Cholestyramine decrease warfarin activity

Answer 57

Reduces absorption

Question 58

Inhibitors of Cytochrome P450 (8) (increases effect of warfarin)

Answer 58

* Omeprazole * Disulfiram * Erythromycin * Valproate * Isoniazid * Ciprofloxacin and Cimetidine * Ethanol (acutely) * Sulphonamides

Question 59

Inducers of Cytochrome P450 (reduced effect of Warfarin)

Answer 59

* Alcohol (chronic use) * Barbiturates * Carbamazepine * Phenytoin * Rifampicin * Sulphonylureas

Question 60

Monitoring warfarin therapy (4)

Answer 60

* Regular INR * Watch if therapy altered * Patient education * Alcohol intake