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*pharm exam 4 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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1
Q

How is WPW treated?

A

acutely with a 1B antiarrhythmic agent (particularly, lidocaine); can also treat long-term with a 1A or 1C agent (es

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2
Q

What are the 4 Vaughan-Williams Classes of antiarrhythmics?

A
  1. Na+ channel blockers (1A, 1B, 1C)
  2. Beta-blockers
  3. K+ channel blockers
  4. Ca2+ channel blockers
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3
Q

Why is prolonged QT so dangerous?

A

It may lead to Torsades de pointe or VF.

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4
Q

Na+ channel blockers affect which type of Na+ channels?

A

open or inactivated Na+ channels (NOT resting state ones)

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5
Q

Which class of Na+ channel blockers causes a shorter QT?

A

1B

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6
Q

Which of the Na+ channel blockers causes a prolonged QT?

A

1A

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7
Q

What are the main class 1A Na+ channel blockers?

A

procainamide, quinidine

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8
Q

What are the main class 1B Na+ channel blockers?

A

lidocaine

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9
Q

What are the main class 1C Na+ channel blockers?

A

flecainide, propafenone

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10
Q

Which of the Na+ channel blockers also has a class III (K+ blocking) effect?

A

1A (thus, prolonged APD and ERP)

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11
Q

Unique adverse effect associated with procainamide?

A

lupus-like syndrome (not permanent)

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12
Q

Unique adverse effect associated with quinidine?

A

tinnitus, seizure, thrombocytopenia

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13
Q

What is the exclusive clinical indication for class 1B Na+ channel blockers?

A

VT during ischemia

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14
Q

Which Na+ channel blocker has the weakest vs. strongest blockade effect?

A

1B < 1A < 1C

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15
Q

What is the clinical indication for class 1A antiarrhythmics?

A

AFib/flutter, VT (everything…SVT and VT)

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16
Q

What are the overall adverse effects of 1A antiarrhythmics?

A

prolonged QT leading to Torsades; anticholinergic effect

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17
Q

How do class 1B antiarrhythmics act as local anesthetics?

A

They block Na+ channel propagation by binding depolarized Na+, thereby inhibiting the pain signal to the brain.

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18
Q

Which antiarrhythmic can be used to treat digoxin arrhythmia?

A

Class 1B agents

19
Q

What are the main clinical indications for the class 1C agents?

A

refractory VT, WPW, SVT

20
Q

What is the main side effect associated with class 1C agents?

A

arrhythmias (due to delayed conduction speed)

21
Q

How do the beta blockers work?

A

They prevent epi and norepi from binding to their receptors (less cAMP=less Ca2+). They affect the NODAL action potential.

22
Q

What are the main adverse effects associated with beta blockers?

A

loss of energy (including libido) and bronchospasm (can affect beta-2 receptors as well)

23
Q

What is the physiologic effect of beta blockers?

A

They slow HR and decrease contractility. This ultimately decreases myocardial oxygen consumption.

24
Q

How is AFib treated in terms of rhythm and rate?

A
  • rhythm: class 1C antiarrhythmics

- rate: beta-blockers

25
Q

What is the main side effect associated with K+ channel blockers?

A

prolonged QT and Torsades risk (EXCEPT for amiodarone)

26
Q

Which drugs belong to the K+ channel blockers?

A

amiodarone, bretylium, sotalol, ibutilide

27
Q

Which are the main 2 classes of antiarrhythmics that we worry about in terms of prolonged QT?

A

class 1A and class III

28
Q

True or false: diltiazem in combination with metoprolol is an effective treatment for AFib.

A

FALSE! Giving a calcium channel blocker AND a beta-blocker can cause cardiac collapse because both affect the nodal action potential.

29
Q

Which drugs belong to the Ca2+ channel blockers?

A

verapamil and diltiazem (cardizem)

30
Q

What are the side effects associated with Ca2+ channel blockers?

A

hypotension and flushing

31
Q

What are the adverse effects associated with amiodarone?

A

Amiodarone is RIDDLED with side effects!

  • Toxic to lungs (pulmonary toxicity leading to fibrosis)
  • Toxic to liver (hypersensitive hepatitis)
  • Toxic to thyroid (source of inorganic iodine leading to hypo/hyperthyroidism)
  • Skin changes (blue/grey deposits)
  • Corneal deposits
  • Initially acts as a beta-blocker, potentially causing bradycardia, hypotension, and heart block
32
Q

What is the drug of choice for Torsades?

A

magnesium (relatively new treatment)

33
Q

What is the treatment of choice for Torsades?

A

cardioversion

34
Q

What are the main adverse effects of Digoxin?

A
  • GI (N/V/D + pain)
  • Hyperkalemia
  • Visual disturbances (yellow halos)
35
Q

What is Digoxin mainly used for clinically?

A

AFib and heart failure

36
Q

Describe the MOA of Digoxin.

A

It inhibits the Na+/K+ pump, leading to an increased driving force for Ca2+ into the cell (Na+ gets retained in the cell due to Na+/K+ pump blockade, and it is exchanged for Ca2+). Increased Ca2+ leads to increased inotropy. Digoxin also has parasympathetic effects, particularly on the SA and AV nodes, thus slowing conduction and decreasing HR.

37
Q

What is the difference between stable and unstable ventricular tachycardia?

A
  • Stable: BP is okay

- Unstable: BP is too low; need to cardiovert, then administer lidocaine and amiodarone

38
Q

What does amiodarone do?

A

It slows conduction through the AV node to treat SVT. However, it can cause transient heart block at the AV node. It is better to try a vagal maneuver first.

39
Q

Torsades is considered to be which type of arrhythmia?

A

V-tach

40
Q

What is an unintended adverse event associated with AFib cardioversion?

A

stroke due to dislodgment of clot in LA

41
Q

What do Ca2+ channel blockers treat?

A

SVT and AFib (atrial side stuff)

42
Q

Which classes of antiarrhythmics affect rate vs. rhythm?

A
  • rate: class II (beta-blockers) and IV (Ca2+ channel blockers)
  • rhythm: class I (Na+ channel blockers) and III (K+ blockers)
43
Q

What is the main physiological effect of Ca2+ channel blockers?

A

They decrease intracellular Ca2+ concentration, thereby decreasing inotropy and BP. They also decrease HR and therefore cardiac oxygen consumption.

*pharm exam 4 (12 decks)

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