Antiarrhythmatics

Question 1

Briefly outline the normal cardiac conduction

Answer 1

• SAN triggers atrial depolarisation
• AVN receives signal and through the Bundle of His, LBB/RBB, and Purkinje fibres causes ventricular depolarisation. AVN is is the only pathway for action potential to enter the ventricles (due to nonconducting band)

Question 2

What is slow conduction?

What is fast conduction?

Answer 2

• Slow: complete atrial systole before ventricular systole starts
• Fast: His Bundles and Purkinje fibers (–> ventricular depolarisation and contraction)

Question 3

Give three reasons why arrhythmias occur?

Answer 3

1. changes in automaticity of the natural pacemaker (SAN)
2. Ectopics
   - due to excitable groups of cells or;
   - hypoxic/ischaemic tissue that undergoes spontaneous depolarization and can become ectopic pacemaker
3. interruption of normal conduction pathwya
4. Abnormal conduction pathway
5. Electrolyte disturbance and drugs

Question 4

What is cardiac reentry?

Answer 4

Propagating impulse fails to die out after normal activation of the heart and persist to re-excite the heart after the refractory period has ended

“Loop” continues to excite the muscle over and over again

Question 5

What is anatomically defined reentry?

What is functionally defined reentry?

Answer 5

1. Impulse propagation by more than anatomical pathway between two points in the heart e.g. WPW syndromes, atrial flutter, paroxysmal SVT
2. Can occur in the absence of anatomically defined pathways e.g. AF/VF/Torsades de pointes

Question 6

Generally speaking, how do antiarrhythmics work?

Answer 6

Reduce the excitability of ectopics

Work by altering ion fluxes within excitable tissues

Na+, Ca+, K+

Question 7

Consider the Vaughan Williams classification of antiarrhythmics

What are class 1 antiarrhythmics? How do they work?

E.g

Answer 7

Sodium channel blockers

They increase the QRS interval

Lidocaine, Flecainaide

Question 8

Consider the Vaughan Williams classification of antiarrhythmics

What are class 2 antiarrhythmics? How do they work?

E.g

Answer 8

B-blockers

They decrease heart rate (increase diastolic filling which is why its used in IHD) and increase the PR interval

Nonselective (propranolol, atenolol)
Bisoprolol **

Highly selective: carvedilol, esmolol (IV, short-acting)

Question 9

Consider the Vaughan Williams classification of antiarrhythmics

What are class 3 antiarrhythmics? How do they work?

E.g

Answer 9

Potassium channel blockers

They increase the QT interval

Amiodarone, Sotalol (class 2/3 function)

Question 10

Consider the Vaughan Williams classification of antiarrhythmics

What are class 4 antiarrhythmics? How do they work?

E.g

Answer 10

Calcium channel blockers

Reduce heart rate, vasodilation increase PR interval

Verapamil, Diltazem

Question 11

How does digoxin exert antiarrhythmic effects?

What is it used for?

Answer 11

Causes sodium inhibition and K-ATPase inhibition

Increases PR interval, decreases QT interval

Rate controlling AF

Question 12

How does adenosine exert antiarrhythmic effects?

Answer 12

Purinergic receptor agonist

Decreases HR

Increases PR interval

Question 13

When might you use class 1A agents?

Side effects?

Answer 13

Quinidine, Disopyramide, Procainamide

Useful in supraventricular and ventricular arrhythmias
-only in those with good ventricular function due to negative inotropic effects, (they weaken the force of contractions)

Anticholinergic side effects
Can cause AV block

Question 14

Compare the route of administration between Lidocaine and Mexiletine

Answer 14

Used for VT storm (uncontrolled by amiodarone=1st line)

Lidocaine must be given IV due to FPHM

Mexiletine is its orally active sister
- it also doesn’t prolong QT interval and can be used in patients with history of VT

Question 15

Side effects of class 1b drugs

Answer 15

CNS side effects

• tinnitis
• seizures
• hallucinations
• drowsiness
• coma

Question 16

How do class 1c agents works

When is flecainide used?

Answer 16

Most potent Na channel blockers

FLECAINIDE
Used in new-onset fast AF to rhythm control
Should be used with preserved LV function

Should be used with caution in those with pacemakers

Question 17

Give three side effects of class two agents

Answer 17

• bronchospasm (asthmatics, COPD)
• hypotension
• bradycardia
• HF
• impotence
• exacerbation of PVD

Question 18

How do you manage class two overdose?

Answer 18

• glucagon
• temporary pacing (quicken heart)
• inotropic support (maintain BP)

Question 19

When is sotalol used?

Give three side effects

Answer 19

Paroxysmal AF
“Pill in pocket” strategy- used when patient feels episode of AF

Hypokalaemia, hypomagnesia, bronchospasm, pulmonary oedema, HF, AV block, QT prolongation, bradycardia, torsades

Question 20

What is it used for?

Side effects of amiodarone (class 3)

Answer 20

SV and ventricular arrhythmias
- 1st line for VT

Structurally related to thyroid hormone –> hypo/hyperthyroidism
- monitor TFTs

Question 21

How do you manage a paroxysmal SVT?

Answer 21

• Carotid massage
• Valsalva maneouvre
• IV adenosine

Question 22

How is the electrical conduction in WPW?

How do you treat WPW?

Answer 22

In WPW, there is normal conduction and accessory pathway conduction

Class three drugs

if hypotensive, cardiovert immediately

Question 23

What does VT look like on ECG

Answer 23

• Broad complex
• WiLLiaM MaRRoW
• AV dissociation
• extreme axis deviation

Question 24

Give three causes of VF

Answer 24

• acute MI
• Drug overdose e.g. TCA
• Hypokalaemia

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