Cardiac Arrhythmia Drugs Flashcards

1
Q

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

A

Contraction of the atria

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2
Q

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

A

Contraction of the ventricles

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3
Q

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

A

Repolarization of the ventricles

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4
Q

Arrhythmias can be defined as disturbances in what?

A

Pacemaker impulse formation (SA/AV node)

Contraction impulse conduction (Bundle of His)

Both of these

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5
Q

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

A

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

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6
Q

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

A
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7
Q

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

A

Phase 0

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8
Q

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

A

Phase 4

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9
Q

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

A

Late phase 3 (refractory period)

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10
Q

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

A

Phase 2

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11
Q

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

Where in the heart does this type of AP originate?

A

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

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12
Q

Where would a fast actional potential occur within the heart?

A

In ventricular cardiac myocytes

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13
Q

Where would a slow actional potential occur within the heart?

A

Atrium (specifically SA/AV nodes)

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14
Q

Give two general types of abnormal impulse generation

A

Abnormal automaticity- spontaneous firing

Triggered rhythms- myocytes contract twice when stimulated once

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15
Q

Give two examples of abnormal automaticity

A
  1. Enhanced normal automaticity

Increased number of action potentials from the SA node

  1. Ectopic foci

Action potentials arise from sites other than the SA node

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16
Q

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

A
  1. Delayed afterdepolarization

AP arises from the resting potential

  1. Early afterdepolarization

AP arises from the plateau phase

e.g. Torsade de Pointes

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17
Q

What are the two general types of abnormal conduction?

A

Conduction block

Reentry

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18
Q

Describe the four types of conduction block

A

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.

19
Q

Descibe how first degree heart block might look on an ECG

Why might you see these changes?

A

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

20
Q

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

Why might you see these changes?

A

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

21
Q

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

Why might you see these changes?

A

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

22
Q

Describe how thrid degree heart block might look on an ECG

Why might you see these changes?

A

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

23
Q

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

A

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

24
Q

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

A

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

25
Q

What is Wolff-Parkinson-White syndrome?

A

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

26
Q

At which points could we use drugs for the treatment of:

1) Abnormal AP generation
2) Abnormal AP conduction

A

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)

27
Q

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

A

Restore normal sinus rhythm and conduction

Prevent more serious and possibly lethal arrhythmias from occuring

28
Q

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

A

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

29
Q

Where do class I A antiarrhytmic drugs have their action?

Give some examples of such drugs

A

Moderate reduction in conduction of phase 0 (Na+)

e.g. Quinidine, procainmide

30
Q

Where do class I B antiarrhytmic drugs have their action?

Give some examples of such drugs

A

No change in phase 0

Increased threshold of (Na+)

e.g. Lidocaine

31
Q

Where do class I C antiarrhytmic drugs have their action?

Give an example of such

A

Marked reduction in phase 0 through strong blockade of Na+ channels

Increased AP duration through blockade of K+ channels

e.g. Flecainide

32
Q

Where do class II antiarrhytmic drugs have their action?

Give some examples of such drugs

A

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

33
Q

Where do class III antiarrhytmic drugs have their action?

Give some examples of such drugs

A

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

34
Q

Where do class IV antiarrhytmic drugs have their action?

Give some examples of such drugs

A

Calcium channel blockers

Slow conduction through the AV node

Increase refractory period in AV node Increase phase 4 slope

e.g. Verapamil, Diltiazem

35
Q

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

A

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

36
Q

Which drugs could be used to treat AF?

A

Rate control (reduce ventricular response):

Bisoprolol

Verapamil

Diltiazem

+/- Digoxin

Rhythm control (stop AF):

Sotalol

Flecainide + bisoprolol

Amiodarone (central line)

37
Q

Which IV drugs might you use to treat ventricular tachycardia?

A

Depending on what is already prescribed:

(All IV):

Metoprolol

Lignocaine

Amiodarone

38
Q

Should Flecainide be used alone to treat atrial flutter?

A

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

39
Q

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

A

Flecainide - oral, long-term

Amiodarone- NOT long-term

40
Q

Which drugs could be used to treat re-entrant SVT both

1) Acutely
2) Chronically

A

1) Acutely: (IV)

Adenosine

Verapamil

Flecainide

2) Chronic: (Oral)

Bisoprolol

Verapamil

Sotalol

Flecainide

Procainamide

41
Q

Which drugs would you use to treat ectopic beats?

A

First line: Bisoprolol

Flecanide, Sotalol, Amiodarone (ONLY IF NO structural/IHD)

42
Q

Which drugs would you use to treat sinus tachycardia?

A

Ivabradine

Bisoprolol

Verapamil

43
Q
A