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Clinical Pharmacology > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

1
Q

What is torsades de pointes?

A

A life threatening form of ventricular tachycardia that arsises from long QT intervals

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2
Q

What can cause arrhythmia?

A

When there is a disturbance in:

  • Pacemaker impulse formation
  • Contraction impulse conduction (through tissues)
  • Or both
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3
Q

What is the consequence of arrhythmia?

A

Results in rate/ timing of contraction of the heart that may be insufficient to maintain normal cardiac output

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4
Q

Identify the movement of ions in cardiac action potentials in the ventricles

A
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5
Q

What is the MoA of class 1 antiarrythmics?

A

block Na+ channel

slows conduction through the tissue

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6
Q

Name 2 class 1 antiarrhythmics

A

Flecainide (1c)

Lidocaine (1b)

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7
Q

What is the mechanism of action of class 2 antiarrhythmics?

A

Beta adrenoreceptors blockers

Diminish phase 4 depolarisation and automaticity

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8
Q

Name a class 2 antiarrhythmic

A

Bisoprolol

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9
Q

What is the MoA of class 3 antiarrhythmics?

A

Block the K+ channel

Extend the refractory period increasing action potential duration

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10
Q

Name 2 class 3 antiarrhythmics

A

Amiodarone

Sotalol

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11
Q

What is the MoA of class 4 antiarrhythmics?

A

Calcium channel blockers

Prolong the plateu of the action potential and decrease spontaneous depolarisations

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12
Q

Name 2 class 4 antiarrhythmics

A

Diltiazem

Verapamil

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13
Q

Descibe the movement of ions in the SA/ AV node (slow action potential)

A
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14
Q

How do calcium channel blockers affect the SA/AV node action potential?

A

Slow conduction velocity by slowing pace maker cell depolarisation

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15
Q

What is Wolf-Parkinson- White syndrome?

A

A condition where accessory pathways exist within the heart called The Bundle of Kent

Causes re-entry loops that avoid the AV node → tachycardia

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16
Q

How can tachycardias arrise following myocardial infarcts?

A

Following M.I, scar issue is imperfect

Allows micro-re entry loops

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17
Q

What are the aims of drugs given if an arrhythmia is due to abnormal generation?

A
  • To decrease the action potentials in pacemaker cells (Beta blockers, Calcium channel blockers)
  • Raise the threshold for action potentials to occur
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18
Q

What are the aims of drugs given if an arrhythmia is due to abnormal conduction?

A
  • To reduce conduction velocity through the tissues (Class 1)
  • Increase the refractory period so cell can’t be reexcited again (Class 3)
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19
Q

What drugs fall in to each category of the Vaugh Williams Classification?

A
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20
Q

What are the effects of class 1A agents antiarrhythmics? (Procainamide, quinidine, disopyramide)

A
  • Decrease conduction of AP
  • Increase refractory period
  • Decrease autamaticity
  • Increase threshold for AP
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21
Q

What are the side effects of Class 1A antiarrhythmics?

A
  • Hypotension - reduced CO
  • Proarrhytmic due to increased QT interval
  • Dizziness, confusion, insomnia, seizure (at high doses)
  • GI effects (common)
  • Lupus like syndrome (esp procainamide)
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22
Q

What are the 2 class 1B antiarrhythmics, how must each be given?

A

Lidocaine: IV only

Mexiletine: oral

23
Q

What are the effects on cardiac activity of class 1b antiarrhytmics?

A
  • No change in phase 0 in normal tissue
  • Increase threshold for action potnetials
  • Decrease phase 0 in fast beating/ ischemic tissue
24
Q

In which situations would you use class 1b antiarrhythmics?

A

Acute ventricular tachycardia (especially during ischemia)

25
What are some of the side effects of class 1b antiarrhythmics?
* GI upset (most common) * CNS effects: dizziness, drowsiness * Less proarrhythmic than class 1a
26
What are the effects of class 1c antiarrhythmics on cardiac activity?
* Substantial decrease of phase 0 in normal tissue * decrease automacitiy * Increase refractory period
27
What are the effects of class 1c antiarrhythmics on an ECG?
* Increase PR interval * Increase QRS interval * Increase QT interval
28
When would you use class 1C antiarrhythmics? (Flecainide, Propafenone)
* **Supraventricular arrhythmias** (fibrillation and flutter) * Pemature ventricular contractions * Wolf-Parkinson-White syndrome
29
What are the some the side effects of class 1C antiarrhythmics?
* Proarrthymic and sudden death especially with **chronic** use and **strucutal heart disease** * Increase ventricular response to supraventricular arrhythmias * CNS and GI effects
30
Describe the absorption and elimination of class 2 agents; propanolol, metoprolol, bisoprolol, esmolol
**Propanolol**: oral and IV **Metoprolol:** oral (short acting), IV **Bisoprolol:** oral only **Esmolol:** IV only (v short acting t1/2 9 min)
31
What are the cardiac effects of class 2 antiarrhythmics?
* Increase refractory period in AV node to slow AV conduction velocity * Decrease phase 4 depolarisation
32
When would you use class 2 antiarrhythmics?
* Sinus and catecholamine dependent tachycardias * Converting reentrant arrhythmias at AV node * Protect ventricles from high atrial rates (slow AV conduction) in atrial flutter/ fibrillation
33
What are some of the side effects of class 2 antiarrhythmics?
* Bronchospasm * Hypotension * Not to be used in partial AV block or acute heart failure
34
How can you administer **amioderone** (Class III agent)?
Oral **or** IV through a **central line only** | (T 1/2 of around **3 months**)
35
Why can amioderone not be given by IV **peripherally?**
Thromboplebitic if given peripherally
36
What are the effects of giving amioderone (class 3 agent) on cardiac tissue?
* Increases refractory period * Decreases phase 0 and conduction * Increases threshold for next AP * Decreased phase 4 * Decreases speed of AV condution
37
What are the effects of amioderone on the ECG?
* Increase PR * Increase QRS * Increase QT * Decrease HR
38
In what circumstances would you give amioderone?
Very wide spectrum, effective for **most arrthymias** (especially life threatening ventricular tachycardia)
39
What are some of the side effects of amioderone?
* Pulmonary fibrosis * Hepatic injury * Increase LDL cholesterol * Thyroid disase * Photosensitivity * Optic Neuritis (transient blindness) Risk of these increases with time
40
How do you administer Class III antiarrhythmic **sotalol?**
**Oral** only
41
What are the side effects of class III agent Sotalol?
* Proarrhythmic * Fatgiue * Insomnia
42
How do you administer the 2 class IV antiarrhythmics verapamil and diltiazem?
Verapamil: orally or IV Diltiazem: orally only
43
When would you use class IV antiarrhythmics?
* Control the ventricles during **supraventircular tachycardias** * Stop re-entry loops around AV node
44
What are some of the side effects of class IV antiarrhythmics?
* Use with caution when AV block present * Can get **asystole** if given **with Beta blockers** * Hypotension * Decreased CO * GI problems (constipation)
45
What is the mechanism of action of Adenosine in treating arrhythmia?
* natural nucleoside binds to **A1 receptors** at AV/ SA node * Activates K+ currents * Hyperpolarisation of cell * **Decreases heart rate** by **slowing AV conduction**
46
When would you give adenosine as an antiarrhythmic?
* Re-entrant loops in supraventricular tachycardia * When scanning the heart to diagnose coronary artery disease
47
What is the only way to administer adenosine
**IV bolus dose** Very short acting half life of **seconds**
48
What is the mechanism of action of ivabradine?
Blocks the ***If *** ion highly expressed in SA node Slows the SA node but does not affect blood pressure
49
When would you use ivabradine?
* Reduce innapropriate sinus tachycardia * Reduce heart rate in heart failure and angina
50
What is the mechanism of action of digoxin?
Slows AV conduction and slows HR by **enhancing vagal activity** Used to reduce ventricular rates in atrial fibrillation and flutter
51
What is the mechanism of action of atropine in treating **bradycardia**?
Selective muscarinic **antagonist**, blocks vagal activity to **speed up** AV conduction and increase HR
52
Why should flecainide not be used alone to treat atrial flutter?
Flecainide alone causes **pro-arrhythmic effect** Need to give alongside AV node blocking durgs to reduce ventricular rate
53
What drug is used first line to treat ectopic beats?
Bisprolol

Clinical Pharmacology (25 decks)

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