Drugs Treating Cardiac Arrhythmias

Question 1

Outline the heart’s electrophysiological control mechanisms

Answer 1

transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell

Maintenance by ion selective channels, active pumps and exchangers

Question 2

Outline the electro conduction pathway through the heart

Answer 2

SA node

AV node

Bundle of his

R and L bundle branch

Purkinje fibres

Question 3

What are the phases of the cardiac action potential?

Answer 3

0 = rapid Na influx through open fast Na channels

1 = transient K+ channels open and K+ efflux return TMP to 0mV

2 = influx of Ca+ electrically balanced by K+ efflux

3 = Ca+ channels close but delayed rectifier K+ channels remain open and return TMP to -90mV

Question 4

What do arrhythmias result in?

Answer 4

rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output (CO)

Question 5

Briefly outline the classification of antiarrhythmic drugs

Answer 5

1 = Na channel blockers – slows conduction in tissue

2 = beta blockers – diminish phase 4 depolarisation

3 = K channel blockers – increase APD

4 = Ca channel blockers – decrease phase 4 spontaneous depolarisation

5 = unknown (adenosine)

Question 6

Describe the rate of AP in cardiac tissue vs SA/AV nodes

Answer 6

Cardiac tissue = fast AP

SA/AV = slow AP

Question 7

Outline the mechanisms of arrhythmogenesis

Answer 7

1) abnormal impulse generation:

Automatic rhythms = enhanced normal automaticity (increased AP from SA node), ectopic focus

Triggered rhythms = delayed afterdepolarisation, early afterdepolarisation

2) abnormal conduction:

Conduction block = 1st, 2nd, 3rd degree

Reentry = circus movement, reflection

Question 8

Describe Wolf-parkinson-white syndrome

Answer 8

Abnormal anatomic conduction between the atria and the ventricles

= provides re-entrant tachycardia circuit

Question 9

Briefly describe the actions of antiarrhythmic drugs

Answer 9

Cases of abnormal generation = decrease in phase 4 slope (pacemaker cells), raises threshold

Cases of abnormal conduction = decreased conduction velocity, increased effective refractory period

Question 10

Describe class 1A antiarrhythmics

Answer 10

Mechanism = reduce conduction, increase refractory period

Effect on the heart = increase QRS, PR and QT

Common uses = maintain sinus rhythm in AF

Common side-effects = hypotension, reduced CO

Quinidine

Question 11

Describe class 1B antiarrhythmics

Answer 11

Mechanism = APD decreased, increased threshold, decreased phase 0 conduction

Effect on heart = increased QRS

Uses = in scarred tissue, ventricular tachycardia

Side-effects = abdo upset, dizziness, drowsiness

Lidocaine

Question 12

Describe class 1C antiarrhythmics

Answer 12

Mechanism = decreased phase 0, decreased automaticity, increased APD

Effect on the heart = increased PR, QRS, QT

Uses = stop supraventricular arrhythmias

Side-effects = proarrhythmia and sudden death with chronic use and structural disease
Flecainide

Question 13

Describe class 2 antiarrhythmics

Answer 13

Mechanism = beta-blocker, increase APD, block the effects of adrenaline

Effect on the heart = increase PR, decreased HR, slows AV conduction

Uses = converting re-entrant at AV, protects ventricles from high atrial rates by slowing AV conduction

Side-effects = bronchospasm, hypotension, don’t use in AV block or ventricular failure
- Propranolol, bisoprolol

Question 14

Describe class 3 antiarrhythmics

Answer 14

Mechanism = increased APD, decrease phase 0 and conduction, decreased AV conduction

Effect on the heart = increased PR, QRS, QT, decreased HR

Uses = effective for most arrhythmias

Side-effects = pulmonary fibrosis, hepatic injury, increase LDL, thyroid disease, photosensitivity

Amiodarone, sotalol

Question 15

Describe class 4 antiarrhythmics

Answer 15

Mechanism = decreased AV conduction, increased refractory period in AV

Effect on the heart = increased PR

Uses = control ventricles during supraventricular tachycardia

Side-effects = caution when AV block present, decreased CO, GI problems

Verapamil

Question 16

Describe adenosine

Answer 16

Mechanism = decreased APD, decreased HR, slows AV conduction

Uses = convert re-entrant supraventricular arrhythmias, diagnosis of CAD

Question 17

Describe vernakalant

Answer 17

Mechanism = blocks atrial specific K+ channels

Uses = convert AF to normal sinus rhythm

Side-effects = hypotension, AV block

Question 18

Describe ivabradine

Answer 18

Mechanism = blocks If ion current in SA node slowing SA node

Uses = reduce sinus tachycardia, reduce HR in heart failure and angina

Side-effects = flashing lights, avoid in preg

Question 19

Describe digoxin

Answer 19

Mechanism = enhances vagal activity, slows AV conduction and HR

Uses = reduce ventricular rates in AF

Side-effects

Question 20

Describe atropine

Answer 20

Mechanism = muscarinic antagonist – block vagal activity to speed AV conduction and HR

Uses = treat vagal bradycardia

Question 21

Which drugs could be used in AF?

Answer 21

Rate control = bisoprolol

Rhythm control = sotalol, flecainide with bisoprolol

Question 22

Which IV drug first for VT?

Answer 22

metroprolol

Question 23

Should flecainide be used alone for atrial flutter?

Answer 23

No

Give AV nodal blocking drugs to reduce ventricular rates in flutter

Question 24

Best drug for WPW?

Answer 24

flecainide

Question 25

List drugs used in re-entrant SVT?

Answer 25

Acute = adenosine, verapamil, flecainide

Chronic = bisoprolol, sotalol

Question 26

Which drugs for ectopic atrial tachycardia?

Answer 26

Bisoprolol

Question 27

Which drugs for sinus tachycardia?

Answer 27

Ivabradine

Bisoprolol