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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
Q

What are some of the side effects of class 1b antiarrhythmics?

A
  • GI upset (most common)
  • CNS effects: dizziness, drowsiness
  • Less proarrhythmic than class 1a
26
Q

What are the effects of class 1c antiarrhythmics on cardiac activity?

A
  • Substantial decrease of phase 0 in normal tissue
  • decrease automacitiy
  • Increase refractory period
27
Q

What are the effects of class 1c antiarrhythmics on an ECG?

A
  • Increase PR interval
  • Increase QRS interval
  • Increase QT interval
28
Q

When would you use class 1C antiarrhythmics? (Flecainide, Propafenone)

A
  • Supraventricular arrhythmias (fibrillation and flutter)
  • Pemature ventricular contractions
  • Wolf-Parkinson-White syndrome
29
Q

What are the some the side effects of class 1C antiarrhythmics?

A
  • Proarrthymic and sudden death especially with chronic use and strucutal heart disease
  • Increase ventricular response to supraventricular arrhythmias
  • CNS and GI effects
30
Q

Describe the absorption and elimination of class 2 agents; propanolol, metoprolol, bisoprolol, esmolol

A

Propanolol: oral and IV

Metoprolol: oral (short acting), IV

Bisoprolol: oral only

Esmolol: IV only (v short acting t1/2 9 min)

31
Q

What are the cardiac effects of class 2 antiarrhythmics?

A
  • Increase refractory period in AV node to slow AV conduction velocity
  • Decrease phase 4 depolarisation
32
Q

When would you use class 2 antiarrhythmics?

A
  • 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
Q

What are some of the side effects of class 2 antiarrhythmics?

A
  • Bronchospasm
  • Hypotension
  • Not to be used in partial AV block or acute heart failure
34
Q

How can you administer amioderone (Class III agent)?

A

Oral or IV through a central line only

(T 1/2 of around 3 months)

35
Q

Why can amioderone not be given by IV peripherally?

A

Thromboplebitic if given peripherally

36
Q

What are the effects of giving amioderone (class 3 agent) on cardiac tissue?

A
  • Increases refractory period
  • Decreases phase 0 and conduction
  • Increases threshold for next AP
  • Decreased phase 4
  • Decreases speed of AV condution
37
Q

What are the effects of amioderone on the ECG?

A
  • Increase PR
  • Increase QRS
  • Increase QT
  • Decrease HR
38
Q

In what circumstances would you give amioderone?

A

Very wide spectrum, effective for most arrthymias

(especially life threatening ventricular tachycardia)

39
Q

What are some of the side effects of amioderone?

A
  • Pulmonary fibrosis
  • Hepatic injury
  • Increase LDL cholesterol
  • Thyroid disase
  • Photosensitivity
  • Optic Neuritis (transient blindness)

Risk of these increases with time

40
Q

How do you administer Class III antiarrhythmic sotalol?

A

Oral only

41
Q

What are the side effects of class III agent Sotalol?

A
  • Proarrhythmic
  • Fatgiue
  • Insomnia
42
Q

How do you administer the 2 class IV antiarrhythmics verapamil and diltiazem?

A

Verapamil: orally or IV

Diltiazem: orally only

43
Q

When would you use class IV antiarrhythmics?

A
  • Control the ventricles during supraventircular tachycardias
  • Stop re-entry loops around AV node
44
Q

What are some of the side effects of class IV antiarrhythmics?

A
  • Use with caution when AV block present
  • Can get asystole if given with Beta blockers
  • Hypotension
  • Decreased CO
  • GI problems (constipation)
45
Q

What is the mechanism of action of Adenosine in treating arrhythmia?

A
  • natural nucleoside binds to A1 receptors at AV/ SA node
  • Activates K+ currents
  • Hyperpolarisation of cell
  • Decreases heart rate by slowing AV conduction
46
Q

When would you give adenosine as an antiarrhythmic?

A
  • Re-entrant loops in supraventricular tachycardia
  • When scanning the heart to diagnose coronary artery disease
47
Q

What is the only way to administer adenosine

A

IV bolus dose

Very short acting half life of seconds

48
Q

What is the mechanism of action of ivabradine?

A

Blocks the If ion highly expressed in SA node

Slows the SA node but does not affect blood pressure

49
Q

When would you use ivabradine?

A
  • Reduce innapropriate sinus tachycardia
  • Reduce heart rate in heart failure and angina
50
Q

What is the mechanism of action of digoxin?

A

Slows AV conduction and slows HR by enhancing vagal activity

Used to reduce ventricular rates in atrial fibrillation and flutter

51
Q

What is the mechanism of action of atropine in treating bradycardia?

A

Selective muscarinic antagonist, blocks vagal activity to speed up AV conduction and increase HR

52
Q

Why should flecainide not be used alone to treat atrial flutter?

A

Flecainide alone causes pro-arrhythmic effect

Need to give alongside AV node blocking durgs to reduce ventricular rate

53
Q

What drug is used first line to treat ectopic beats?

A

Bisprolol

Clinical Pharmacology (25 decks)

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