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Cardio Block > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What are the 2 major mechanisms for arrhythmias?

A

1) ABNORMAL AUTOMATICITY - pacemaker activity that originates anywhere other than in the SA node.
2) ABNORMAL (REENTRANT) CONDUCTION - conduction of an impulse that does not follow the defined path or that reenters tissues previously excited by the same impulse.

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2
Q

What is Torsades de pointes?

A

Ventricular arrhythmia that is often INDUCED by antiarrhythmic and other drugs that change the shape of the AP and prolong the QT interval. EKG morphology of a polymorphic ventricular tachycardia, often displaying waxing and waning QRS amplitude

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3
Q

What syndrome is Torsades associated with?

A

Long QT syndrome - heritable abnormal prolongation of the QT interval caused by mutations in the I(K) and I(Na) channel proteins.

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4
Q

What are the classes of drugs used in cardiac arrhythmias?

A 
Group 1 - sodium channel blockers
Group 2 - beta-adrenoceptor blockers
Group 3 - potassium channel blockers
Group 4 - calcium channel blockers 
Miscellaneous - adenosine, potassium ion, magnesium ion
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5
Q

How are Group 1 Antiarrhythmics subdivided?

A

Subdivided on the basis of their effects on AP duration.

ALL group 1 drugs reduce both phase 0 and phase 4 sodium currents. They all prolong ERP by slowing recovery of sodium channels from inactivation.

Group 1A drugs also reduce phase 3 potassium current and prolong AP duration, resulting in significant prolongation of ERP.
Group 1B/1C drugs have no effect on potassium current and thus shorten or have no effect on AP duration.

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6
Q

Explain the Group 1A classification

A 
Group 1A (procainamide) PROLONG THE AP!
Increase PR, Increase QRS, Increase QT

Slow conduction in ischemic and depolarized cells and slow or abolish abnormal pacemakers whenever these processes depend on sodium channels.

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7
Q

Explain the Group 1B classification

A

Group 1B (lidocaine) shorten the AP in some cardiac tissues!

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8
Q

Explain the Group 1C classification

A 
Group 1C (flecainide) no effect on AP duration!
Slightly increase PR, Increase QRS
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9
Q

What Group 1 subdivision is most selective and why? Least selective?

A

Group 1B is the MOST selective agents and have significant effects on sodium channels in ischemic tissue, but negligible effects on channels in normal cells.

Groups 1A and 1C are LESS selective and cause some reduction of I(Na) even in normal cells

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10
Q

What type of “dependence” does Group 1 drugs have?

A

USE-DEPENDENT or STATE DEPENDENT - selectively depress tissue that is frequently depolarizing (eg during fast tachycardia) or tissue that is relatively depolarized during rest (eg by hypoxia)

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11
Q

MOA of Procainamide (Group 1A)

A

Use- and state-dependent block of I(Na) channels; some block I(K) channels

Slowed conduction velocity (in the atria, Purkinje fibers, and ventricular cells) and pacemaker activity

Prolonged AP duration and refractory period

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12
Q

Clinical Applications of Procainamide (Group 1A)

A

Atrial and ventricular arrhythmias, especially after MI

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13
Q

PK of Procainamide (Group 1A)

A

Oral and parenteral (oral slow-release forms available)

Duration 2-3h

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14
Q

Toxicities/Interactions of Procainamide (Group 1A)

A

Increased arrhythmias, hypotension, lupus-like syndrome

Hyperkalemia usually exacerbates the cardiac toxicity of these drugs. Treatment of overdose uses sodium lactate (to reverse drug-induced arrhythmias) and pressor sympathomimetics (to reverse drug-induced hypotension)

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15
Q

What is the difference between Disopyramide and Procainamide?

A

Disopyramide is similar but longer duration of action; toxicity includes antimuscarinic effects and HF

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16
Q

What is the difference between Quinidine and Procainamide?

A

Quinidine is similar but toxicity includes cinchonism (headache, vertigo, tinnitus), cardiac depression, GI upset, and autoimmune reactions (e.g. thrombocytopenic purpura).
Also reduces the clearance of digoxin and may increase its concentration significantly. Torsades de pointes is particularly associated with quinidine.

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17
Q

MOA of Lidocaine (Group 1B)

A

Highly selective use- and state-dependent I(Na) block; minimal effect in normal tissue; no effect on I(K)

Selectively affect ischemic or depolarized Purkinje and ventricular tissue and have little effect on atrial tissue; the drugs reduce AP duration in some cells, but because they slow recovery of sodium channels from inactivation, they do not shorten (and may even prolong) the ERP.

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18
Q

Clinical Applications of Lidocaine (Group 1B)

A

Ventricular arrhythmias post-myocardial infarction and digitalis-induced arrhythmias.

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19
Q

PK of Lidocaine (Group 1B)

A

IV and IM
Duration 1-2h
Never given orally because it has a very high first-pass effect and its metabolites are potentially cardiotoxic.

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20
Q

Toxicities of Lidocaine (Group 1B)

A

CNS sedation or excitation

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21
Q

What is the difference between Mexiletine and Lidocaine?

A

Mexiletine is similar but oral activity and longer duration of action

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22
Q

What is the difference between Phenytoin and Lidocaine?

A

Phenytoin (anticonvulsant) is sometimes classified with group 1B agents because it can be used to reverse digitalis-induced arrhythmias. It resembles lidocaine in lacking significant effects on EKG.

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23
Q

MOA Flecainide (Group 1C)

A

Selective-use and state-dependent block of I(Na)
Slowed conduction velocity in atrial and ventricular cells.
No effect on ventricular AP or QT interval. They increase QRS duration.

24
Q

Clinical Application Flecainide (Group 1C)

A

Refractory ventricular arrhythmias.

25
Q

PK of Flecainide (Group 1C)

A

Oral

Duration 20h

26
Q

Toxicities of Flecainide (Group 1C)

A

Increased arrhythmias

CNS excitation

27
Q

What group of drugs is more likely than other antiarrhythmic drugs to exacerbate or precipitate arrhythmias (proarrhythmic effect)

A

Flecainide (Group 1C drugs)

28
Q

What are the prototypic antiarrhythmic Beta Blockers (Group 2)

A

Propranolol

Esmolol and Metoprolol (B1 selective)

29
Q

MOA of Group 2

A

Cardiac B-adrenoceptor blockade and reduction in cAMP, which results in reduction of both sodium and calcium currants and the suppression of abnormal pacemakers.

AV node is particularly sensitive to BB and the PR interval is usually prolonged.

30
Q

Clinical Applications of Group 2

A

Post-MI as prophylaxis against sudden death ventricular fibrillation; thyrotoxicosis

31
Q

PK of Group 2

A

Oral, parenteral

Duration 4-6h

32
Q

Toxicities of Group 2

A

Bronchospasm, cardiac depression, AV block, hypotension

33
Q

What are prototype Group 3 drugs

A

Dofetilide and Ibutilide

34
Q

MOA of Group 3

A

AP prolongation by blockade of I(K) channels that are responsible for the repolarization (phase 3) of the AP. Main effect is to prolong the ERP. INCREASE QT interval!

35
Q

Clinical Applications and PK of Group 3

A

Ibutilide - treatmetn of acute Afib (IV ONLY, duration 6h)

Dofetilide - treatment/prophylaxis of Afib (Oral, duration 7h)

36
Q

What is the major toxicity of Group 3

A

Torsades de pointes

37
Q

What is Amiodarone?

A

Classified under Group 3 and is useful in most types of arrhythmias and is considered the MOST EFFICACIOUS of all antiarrhythmic drugs.

38
Q

MOA of Amiodarone

A

Broad Spectrum! Blocks sodium, calcium, and potassium channels and B adrenoreceptors.

39
Q

Clinical Applications of Amiodarone

A

Becuase of its toxicities, approved for use mainly in arrhythmias that are resistant to other drugs. Used very extensively, off label, in a wide variety of arrhythmias because of its superior efficacy

40
Q

What is the PK of Amiodarone

A

Oral, parenteral.

Half-life and duration of action: 1-10w

41
Q

What are the toxicities of Amiodarone

A

Thyroid abnormalities, deposits in skin and cornea, pulmonary fibrosis, optic neuritis
Torsades is RARE with amiodarone

42
Q

What is Dornedarone

A

Amiodarone analog that may be less toxic. Also acts on sodium, potassium, and calcium channels but is only approved for treatment of AFib or flutter

43
Q

What is Sotalol and what is its MOA, clinical applications, PK, and toxicities?

A

I(K) block and B-adrenoceptor block
Ventricular arrhthmias and Afib
Oral admin (duration 7h)
Dose-related torsades de pointes and cardiac depression

44
Q

What are the prototypes drugs of Group 4

A

Verapamil and Diltiazem (CCBs)

45
Q

Are DHPs useful as antiarrhythmics?

A

NO! They decrease arterial pressure enough to evoke a compensatory sympathetic discharge to the heart which FACILITATES arrhythmias

46
Q

MOA of Group 4

A

Effective in arrhythmias that must traverse calcium-dependent cardiac tissue such as the AV node. These agents cause a state- and use-dependent selective depression of calcium current. Reduce inward calcium current during the AP and during phase 4. As a result, conduction is slowed in the AV node and refractoriness is prolonged. Pacemarker depolarization during phase 4 is also slowed by excessive calcium current.

AV conduction velocity is decreased and ERP and PR interval are increased.

47
Q

What are the clinical applications and PK of Group 4 drugs

A

Verapamil - AV nodal re-entry (nodal tachycardia) especially in prophylaxis (oral, parenteral; duration 7h)

Diltiazem - rate control in Afib (oral, parenteral; duration 6h)

48
Q

What are the toxicities of Group 4

A

Depression of cardiac contractility, AV conduction, and BP

Constipation

49
Q

What are the miscellaneous antiarrhythmic drugs

A

Adenosine
Potassium ion
Magnesium ion

50
Q

MOA of Adenosine

A

Normal component of the body, but when given in high doses as an IV bolus, the drug slows or completely blocks conduction in the AV node.

Causes increase in diastolic I(K) of AV node that causes marked hyperpolarization and conduction block. Reduced I(Ca).

51
Q

What is the clinical application of Adenosine

A

EXTREMELY effective in abolishing AV nodal arrhythmia, and because of its very low toxicity it has become the drug of choice for this arrhythmia.

52
Q

What is the PK and Toxicities of Adenosine

A

Extremely short duration of action (15s)
Toxicity includes flushing and hypotension, but because of their short duration these effects do not limit the use of the drug. Transient chest pain and dyspnea (probably due to bronchoconstriction) may also occur.

53
Q

Potassium Ion MOA, Use, PK, and Toxicities

A

Increase in all K currents, decreased automaticity, decreased digitalis toxicity. Depresses ectopic pacemakers.
Oral or IV
Toxicities include both hypokalemia and hyperkalemia, which are associated with arrhythmogenesis. Severe hyperkalemia causes cardiac arrest.

54
Q

Magnesium Ion MOA, Use, PK, and Toxicities

A

Poorly understood MOA, possible increase in Na/K ATPase activity.
Use in digitalis arrhythmias and other arrhythmias if serum Mg is low.
IV administration
Toxicities include muscle weakness and severe hypermagnesemia which can cause respiratory paralysis

55
Q

Sympatholytic Definition

A

Blocks sympathetic stimulation –> BB would be considered to be a sympatholytic agent!

Cardio Block (6 decks)

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