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CPR Exam 3 > CPR 7.16 Pharmacology: Anti-arrhythmics > Flashcards

CPR 7.16 Pharmacology: Anti-arrhythmics Flashcards

1
Q

Describe the MOA for Class I anti-arrhythmic drugs. What phase do they act on?

A

Na+ Channel block: conduction velocity by blocking fast sodium channels. (Phase 0) Affect the upstroke of AP in non-nodal tissues and thus slow or abolish abnormal pacemakers.

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2
Q

Describe the MOA for Class II anti-arrhythmic drugs. What phase do they act on? What area of the heart is especially sensitive to B blockers?

A

Beta Blockade: Block Beta-1 adrenoreceptors to inhibit sympathetic effects on the heart. beta-blockers can attenuate these sympathetic effects and thereby decrease sinus rate, decrease conduction velocity (which can block reentry mechanisms), and inhibit aberrant pacemaker activity.
-AV node is sensitive.

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3
Q

Describe the MOA for Class III anti-arrhythmic drugs. What phase do they act on?

A

Action Potential Prolongation: Increase effective refractory period (AP duration) and repolarization (Phase 3) by blocking potassium channels.

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4
Q

Describe the MOA for Class IV anti-arrhythmic drugs. What phase do they act on?

A

Ca++ Channel Block: These block slow inward calcium channels and thus reduce pacemaker firing rate by slowing the rate of rise of depolarizing pacemaker potentials (phase 4 depolarization). These drugs also reduce conduction velocity at the AV node, because those cells, like SA nodal cells, depend on the inward movement of calcium ions to depolarize.

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5
Q

Describe the MOA of Adenosine as an anti-arrytmic.

A

Activates Cardiac A1 adenosine receptors. Reduces SA firing and AV conduction.

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6
Q

Name the Class I-A anti-arrhythmics and describe their effects.

A

(a) Fxn: Na+ and K+ blocking, thus slows conduction velocity (though less than IC drugs) and prolongs ERP.
(b) Ex: Procainamide, Quinidine, Disopyramide

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7
Q

What are the indications for Class I-A anti-arrhythmics?

A

atrial fibrillation/flutter; supraventricular & ventricular tachyarrhythmias

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8
Q

Quinidine is associated with what unique side effects?

A

Syncope and torsade de pointes

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9
Q

Procainamide is associated with what unique side effects and how do these occur?

A
  • Procainamide is converted to NAPA which can accumulate wth chronic therapy or renal dysfunction and cause QT prolongation.
  • Lupus like syndrome with procainamide.
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10
Q

Name some common Class I-B anti-arrhythmics and describe their effects.

A

(a) Fxn: Most selective for Na+ channels. No change in conduction velocity and small decrease in ERP. Selectively binds depolarized and ischemic cells. Have Fastest recovery time.
(b) Ex: Lidocaine, Mexiletine, Phenytoin

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11
Q

How must Class I-B anti-arrhythmics be administered and why?

A

must be administered IV (high first pass metabolism)

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12
Q

Name common indications and side effects of Class I-B anti-arrhytmics.

A

V-tachycarrythmias, especially related to ischemia.

Least cardiotoxic of the anti-arrhythmics. Hypotension at large doses. CNS effects.

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13
Q

Name some common Class 1-C anti-arrhythmics and describe their effects.

A

Na+ and K+ Blocking. Greates decrease in conduction velocity, medium increase in ERP.
(b) Ex: Flecainide, Propafenone

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14
Q

What are the main indications and contraindication for Class 1-C Anti-arrhythmics?

A

(c) Indications: life-threatening supraventricular tachyarrhythmias (SVT) and ventricular tachyarrhythmias (VT)
(d) Contraindications: post-MI

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15
Q

What are some common side effects of Class 1-C anti-arrhythmics?

A

(1) Cardiac: Proarrhythmia in patients with ischemic heart disease. Beta-blocking effect can cause 1st or 2nd degree AVN block (propafenone).
(2) Non-Cardiac: bronchospasm (Propafenone).

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16
Q

(1) Inactivation Gate: H (open at rest).
(2) Activation Gate: M gate: determines assage of ions.
Drugs bind to what state?

A

(3) Na+ Channels bind to Open or Inactivated states, not Resting channel.

17
Q

Explain how Class I drugs have enhanced effects in ischemic tissues?

A

(1) Decreased resting MP causes more channels to be in inactivated state. Drug administration in this state results in even Slower conduction velocity and prolonged AP.

18
Q

What are the 4 (5) categories of Beta blockers used for anti-arrhytmias?

A

Non-selective, B1 selective, Partional agonist, Combined A1 and Beta blockers, Esmolol

19
Q

Name the most common Non-selective beta-1 and beta-1 blocker

A

Propanolol.

20
Q

Name some common B1 selective blockers

A

Metorpolol and Atenolol

21
Q

Name some Partial Agonist B blockers

A

Pindolol, Acebutolol, Penbutolol.

22
Q

Name 2 combined alpha1 and Beta blocker drugs

A

Carvedilol, Labetolol.

23
Q

How does esmolol work as an anti-arrhythmic?

How is it administered?

A

(B-antagonist): short acting, 10 minute half life. Given IV.

24
Q

List the major side effects of B-blockers

A

Bradycardia, Hypotension, AVN block, Bronchospasm.

25
Q

List the major indications/contraindications of B blockers

A
  1. Indications: Atrial arrhythmias and prevention of recurrent infarct and death.
  2. Contraindications: sinus bradycardia and partial AV block. Non-selectives contraindicated in Asthma/COPD.
26
Q

What are 3 examples of common Class III anti-arrhythmics?

A

Amiodarone and Dronedarone, Dofetilide.

27
Q

Describe the range and efficacy of Amiodarone

A

(a) Most efficacious of all anti-arrhythmic drugs. Broad spectrum of action (Blocks Sodium, Calcium, Potassium, and Beta adrenoreceptors). Longest half life (1 week). Low incidence of torsades de pointes despite QT prolongation.

28
Q

What are some side effects of amiodarone?

A

Interstitial lung disease, Pulmonary fibrosis, Corneal microdeposits, Thyroid abnormalities, Cutaneous photosensitivity

29
Q

Describe the composition of Dronedarone and its side effects

A

(a) Derivative of amiodarone, lacks iodine and is less efficacious.
(b) Side Effects: Fewer. Contraindicated in NYHA Class IV HF. Liver toxicity.

30
Q

What is a unique detrimental side effect of Class III Anti-arrhythmics?

A

: Reverse Use Dependence (channels More inhibited at Lower HR, increased change of early afterdepolarization) and QT prolongation (most)

31
Q

What are the indications for Class III anti-arrhytmic drugs

A

Serious ventricular arrhythmias and supraventricular arrhythmias

32
Q

What are the Class IV anti-arrhythmic drugs?

Where/how do they work?

A

Diltiazem and Verapamil\

Depress SA and AV nodes

33
Q

How does adenosine work as an anti-arrhythmic?

A

Activates Cardiac A1 adenosine receptors. Reduces SA firing and AV conduction.

34
Q

What are the unique indications and pharmacokinetics of adenosine?

A

Paroxysmal SVT.

IV only.

CPR Exam 3 (11 decks)

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