Cardiac Arrhythmia Drugs

Question 1

The P wave of an ECG corresponds to what event in the cardiac cycle?

Answer 1

Contraction of the atria

Question 2

The R wave of an ECG corresponds to what event in the cardiac cycle?

Answer 2

Contraction of the ventricles

Question 3

The T wave of an ECG corresponds to what event in the cardiac cycle?

Answer 3

Repolarization of the ventricles

Question 4

Arrhythmias can be defined as disturbances in what?

Answer 4

Pacemaker impulse formation (SA/AV node)

Contraction impulse conduction (Bundle of His)

Both of these

Question 5

Arrthymias can result in “blackouts” as a result of what?

Answer 5

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

Question 6

Draw a graph (action potential vs. time) showing the fast action potential of cardiac myocytes over time
Explain what is happening at each stage

Answer 6

Question 7

Using the graph you have drawn showing cardiac action potential to show where drugs blocking Na+ channels act

Answer 7

Phase 0

Question 8

Using the graph you have drawn showing cardiac action potential to show where drugs beta blockers act

Answer 8

Phase 4

Question 9

Using the graph you have drawn showing cardiac action potential to show where drugs blocking K+ channels act

Answer 9

Late phase 3 (refractory period)

Question 10

Using the graph you have drawn showing cardiac action potential to show where drugs blocking calcium channels act

Answer 10

Phase 2

Question 11

Draw a graph showing the slow action potential of the SA/AV node

Where in the heart does this type of AP originate?

Answer 11

In the pacemakers (SA or AV node) of the heart

Question 12

Where would a fast actional potential occur within the heart?

Answer 12

In ventricular cardiac myocytes

Question 13

Where would a slow actional potential occur within the heart?

Answer 13

Atrium (specifically SA/AV nodes)

Question 14

Give two general types of abnormal impulse generation

Answer 14

Abnormal automaticity- spontaneous firing

Triggered rhythms- myocytes contract twice when stimulated once

Question 15

Give two examples of abnormal automaticity

Answer 15

1. Enhanced normal automaticity

Increased number of action potentials from the SA node

2. Ectopic foci

Action potentials arise from sites other than the SA node

Question 16

Give two types of triggered rhythm and explain the difference between the two

Answer 16

1. Delayed afterdepolarization

AP arises from the resting potential

2. Early afterdepolarization

AP arises from the plateau phase

e.g. Torsade de Pointes

Question 17

What are the two general types of abnormal conduction?

Answer 17

Conduction block

Reentry

Question 18

Describe the four types of conduction block

Answer 18

1st degree- slowed impulses through the conducting system (usually asymptomatic and does not require treatment)

2nd degree, Mobitz Type I- electrical impulses are delayed further and further with each subsequent heartbeat until a beat fails to reach to the ventricles entirely

2nd degree, Mobitz Type II- some electrical impulses are unable to reach the ventricles

3rd degree- none of the electrical impulses from the atria reach the ventricles

Bundle branch block- electrical impulses are slowed or blocked as they travel through His in one of the two ventricles.

Question 19

Descibe how first degree heart block might look on an ECG

Why might you see these changes?

Answer 19

Prolonged P-R interval (>200ms)

Everything else is normal

Why: Problem at the AV node-conducton from here to ventricles is slowed, everything else is functioning ok

Question 20

Describe how second degree type I heart block might look on an ECG

Why might you see these changes?

Answer 20

Progressive prolongation of the P-R interval until a QRS complex is completely dropped

Why? Problem most likely functional deficit at the AV node structurally intact

Question 21

Describe how second degree type II heart block might look on an ECG

Why might you see these changes?

Answer 21

Intermittent non-conducted P waves without progressive prolongation of the PR interval

PR interval remains the same

Wide QRS

Dropped QRS, P waves remain

Why: Block is below the AV node (in the His or Purkinje system), more likely due to structural damage

Question 22

Describe how thrid degree heart block might look on an ECG

Why might you see these changes?

Answer 22

P waves and R waves are independent

(Atrial and ventriclar activities are not synchronous)

No PR to QRS relationship

Why: Complete AV dissociation from the ventricles

Perfusing rhythm is maintained by a junctional or ventricular escape rhythm

Question 23

Explain what is meant by “re-entry” in relation to abnormal conduction leading to arrhytmias

Answer 23

Re-entry is a defect which occurs when the action potential fails to extinguish itself and reactivates a region that has recovered from the previous AP

Image B

Question 24

What is reflection type reentry in relation to abnormal AP conducton?

Answer 24

Reflection is when an AP front travels in a forward direction through tissue that is then re-excited by a wave front that propagates backward.

A on the image

Question 25

What is Wolff-Parkinson-White syndrome?

Answer 25

The commonest form of ventricular preexcitation Presence of an acessory pathway (Bundle of Kent) which provides an alternative route for ventricular depolarisation (avoids AV node, exciting the ventricles) Intermitted tachycardia results

Question 26

At which points could we use drugs for the treatment of: 1) Abnormal AP generation 2) Abnormal AP conduction

Answer 26

1) Decrease the slope of phase 4 in the pacemakers cells - making it harder for the rhythm to be generated Raise the threshold 2) Decrese conduction velocity Increase effective refractory period (harder for the cell to be re-excited)

Question 27

What are the two main goals of pharmacological treatment of arrhytmias?

Answer 27

Restore normal sinus rhythm and conduction Prevent more serious and possibly lethal arrhythmias from occuring

Question 28

What are the three main ways in which drugs can act to improve arrhytmias?

Answer 28

1) Decrease conduction velocity 2) Change ERP duration 3) Supress abnormal automaticity

Question 29

Where do class I A antiarrhytmic drugs have their action? Give some examples of such drugs

Answer 29

Moderate reduction in conduction of phase 0 (Na+) e.g. Quinidine, procainmide

Question 30

Where do class I B antiarrhytmic drugs have their action? Give some examples of such drugs

Answer 30

No change in phase 0 Increased threshold of (Na+) e.g. Lidocaine

Question 31

Where do class I C antiarrhytmic drugs have their action? Give an example of such

Answer 31

Marked reduction in phase 0 through **strong** blockade of Na+ channels Increased AP duration through blockade of K+ channels e.g. Flecainide

Question 32

Where do class II antiarrhytmic drugs have their action? Give some examples of such drugs

Answer 32

Beta-adrenergic receptor blockers Increase the action potential duration and refractory period in AV node to SLOW AV conduction velocity Decrease phase 4 repol. e.g. Propanolol, bisoprolol, esmolol

Question 33

Where do class III antiarrhytmic drugs have their action? Give some examples of such drugs

Answer 33

Increase the refractory period and the action potential duration (K+ channel block) Decrease phase 0 and coduction (Na+ channel block) Decrease pahase 4 (beta block and Ca2+ block) e.g. Amiodarone, Sotalol, Dofetalide, Ibutilide

Question 34

Where do class IV antiarrhytmic drugs have their action? Give some examples of such drugs

Answer 34

Calcium channel blockers Slow conduction through the AV node Increase refractory period in AV node Increase phase 4 slope e.g. Verapamil, Diltiazem

Question 35

Why is it important to check if a patient is asthmatic before starting them on a Class II antiarrhythmic drug?

Answer 35

These drugs block b-adrenergic receptors and cause bonchospasm which may worsen their asthma symptoms

Question 36

Which drugs could be used to treat AF?

Answer 36

Rate control (reduce ventricular response): Bisoprolol Verapamil Diltiazem +/- Digoxin Rhythm control (stop AF): Sotalol Flecainide + bisoprolol Amiodarone (central line)

Question 37

Which IV drugs might you use to treat ventricular tachycardia?

Answer 37

Depending on what is already prescribed: (All IV): Metoprolol Lignocaine Amiodarone

Question 38

Should Flecainide be used alone to treat atrial flutter?

Answer 38

No If you slow the flutter rate to that the AV node takes the beat "flecainide flutter" which is a one to one conduction- patient will go into asystole NEED Bisoprolol with this

Question 39

Which is the best drug to use to treat WPW syndrome?

Answer 39

Flecainide - oral, long-term Amiodarone- NOT long-term

Question 40

Which drugs could be used to treat re-entrant SVT both 1) Acutely 2) Chronically

Answer 40

1) Acutely: (IV) Adenosine Verapamil Flecainide 2) Chronic: (Oral) Bisoprolol Verapamil Sotalol Flecainide Procainamide

Question 41

Which drugs would you use to treat ectopic beats?

Answer 41

First line: Bisoprolol Flecanide, Sotalol, Amiodarone (ONLY IF NO structural/IHD)

Question 42

Which drugs would you use to treat sinus tachycardia?

Answer 42

Ivabradine Bisoprolol Verapamil