Arrhythmia Therapy

Question 1

What determines the resting membrane potential in the cardiac cells?

Answer 1

Uneven distribution of ions (Na, K, Ca) across membrane maintained but the Na-K ATPase pump

Produces a net negative charge inside the cells

Question 2

What are the Vaughan-Williams classification of drugs used to treat arrhythmias?

Answer 2

Class 1: 1a, 1b, 1c
Class II
Class III 
Class IV 
Other or class V

Question 3

What is the action of Class I drugs?

Answer 3

Stabilise membrane but vastly acting of Na channel blockers, slowing down rate of depolarisation

Question 4

What are the different Class I drugs?

Answer 4

Ia: quinidine
Ib: lidocaine (weakest of the 3 in blocking)
Ic: flecanide - strong blocker

Question 5

What is the action of Class II drugs?

Answer 5

Beta blockers - reduce or block the sympathetic NS and so reduce the transmission of impulses in heart

Act of phase 4 of action potential (resting potential)

Question 6

What are example of BB drugs and their clinical use?

Answer 6

Atenolol
Bisoprolol
Propranolol

Genre myocardial depressant for SVT and V dysrhythmias
Bisoprolol is first line for AF

Question 7

What is the actions of Class III drugs?

Answer 7

Increase the action potential duration by prolong depolarisation in phase 3

Question 8

What are example of class III drugs and their clinical use?

Answer 8

Amiodarone
Bretylium
Sotalol

Used for hard to treat dysrhythmias
VT or VF, AF or flutter - resistant to other drugs
Sustain VT

Question 9

What is the action of Class IV drugs?

Answer 9

CCB - slows the heart rate by depressing phase for depolarisation

Question 10

What are example of CCB drugs and their clinical use?

Answer 10

Verapamil
Diltiazem

Paroxysmal SVT
Rate control for AF and flutter

Question 11

Name other anti-dysrhythmic drugs

Answer 11

Digoxin

Adenosine

Question 12

What type of drugs is digoxin?

Answer 12

Cardiac glycoside

Question 13

What is the action of digoxin?

Answer 13

Inhibits the Na-K ATPase pump

Positive inotrope: improves the strengths of cardiac contraction by allowing more Ca to be available for contraction

Question 14

What is the clinical use for digoxin?

Answer 14

Heart failure
Atrial fibrillation

But important to monitor K levels, drug levels and toxicity

Question 15

Why can digoxin be toxic in patients with renal impairment?

Answer 15

Most of it is excretes by the kidneys, so in renal failure with reduced GFR, the half life is increase - so high conc. can remain in the body

Question 16

What are side effects of digoxin toxicity?

Answer 16

Nausea and vomiting 
Xanthopsia (yellow in vision)
Bradycardia 
Tachycardia 
Arrythmias: VT and VF

Question 17

What is the sign of digoxin toxicity on an ECG?

Answer 17

Depression of ST segment in lateral leads

Question 18

What is the treatment for digoxin toxicity?

Answer 18

Stop digoxin (still long half life so will stay in body after)
If levels very high and risk of significant arrhythmia: give Digibind

Question 19

What is the action of digibind?

Answer 19

Digoxin immune antibody - binds to digoxin, forming complex molecules which can be excreted in the urine

Question 20

What is the clinical use of Amiodarone?

Answer 20

Used for VT and SVT

Many drug-drug interactions esp digoxin)

Question 21

What are the side effects of amiodarone-drug interaction?

Answer 21

Hypo/hyper-thyroidism 
Pulmonary fibrosis 
Slate (grey pigmentation)
Corneal deposits 
LFT abnormalities

Question 22

What is the action of adenosine?

Answer 22

Slows the conduction through the AV node

Converts paroxysmal SVT to sinus rhythm

Question 23

What is a side effect of the anti-dysrhythmic drugs?

Answer 23

ALL anti-arrhythmics can cause arrhythmias

Question 24

What are indication for anticoagulation?

Answer 24

Atrial fibrillation (risk of stroke, peripheral emboli)
DVT/PE (for prophylaxis)
After surgery
Immobilisation (increased risk of DVT, given for prophylaxis)

Question 25

Name 5 anticoagulants

Answer 25

Warfarin

Dabigatran
Riveroxaban
Apixaban
Edoxaban

Question 26

What conditions may require anticoagulation?

Answer 26

Valvular heart disease
AF
Venous thromboembolism

Question 27

Describe the arterial thrombosis

Answer 27

Andhere of platelets to arterial walls
White
Associated with MI, stroke, ischaemia

Question 28

Describe venous thrombosis

Answer 28

Develops in areas of stagnated blood flow (DVT, L atrium)
Red
Associated with congestive heart failure
Cancer
Surgery

Question 29

What is the action of warfarin?

Answer 29

Inhibits vit K metabolism which is required to produce clotting factors

Question 30

What are mechanisms that will increase the activity of warfarin?

Answer 30

Decrease binding to albumin
Inhibit degradation
Decrease synthesis of clotting factors

Question 31

What are mechanism that will decreased the activity of warfarin?

Answer 31

Indiction of metabolising enzymes (cytochrome P450)
Promote clotting factor synthesis
Reduce absorption

Question 32

What is a way to monitor warfarin therapy?

Answer 32

Using International Normalised Ratio (INR) - to determine actual thromboplastin time (time taken for blood clots to form)

Question 33

What are the values of INR?

Answer 33

Normal: 1

Therapeutic INR: 2.5-4 depending of clinical indication

Question 34

What are the side effects to warfarin?

Answer 34

Bleeding

Teratogenic - avoid in 1st and 3rd trimester

Question 35

What are 4 ways to monitor warfarin therapy?

Answer 35

Regular INR
Watch if therapy altered
Patient education
Alcohol intake

Question 36

What are the benefits of Direct Oral Anticoagulants?

Answer 36

No required blood monitoring
No interaction with food or drugs
Given once/twice daily at fixed dose
As effective and safer than warfarin

Question 37

What are 4 different DOAC and their actions?

Answer 37

Direct thrombin inhibitor: Dabigatran and Apixaban

Factor Xa inhibitor (prevents formation of thrombin): Rivaoxaban and Edoxaban