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FA - Cardiovascular > Cardio - Pharm (Part 3: Cardiac glycosides & Antiarrhythmics) > Flashcards

Cardio - Pharm (Part 3: Cardiac glycosides & Antiarrhythmics) Flashcards

Pg. 301-304 in First Aid 2014 Pg. 282-284 in First Aid 2013 Sections include: -Cardiac glycosides -Antiarrythmics - Na+ channel blockers (class I) -Antiarrythmics - Beta-blockers (class II) -Antiarrythmics - K+ channel blockers (class III) -Antiarrythmics - Ca2+ channel blockers (class IV) -Other antiarrythmics

1
Q

What is a prominent example of a cardiac glycoside? What is its % bioavailability, % protein bound, and half-life?

A

Digoxin - 75% bioavailabiity, 20-40% protein bound, t1/2 = 40 hours

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2
Q

How is digoxin cleared from the body?

A

Urinary excretion

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3
Q

What is the mechanism by which cardiac glycosides/digoxin work? What are the 2 major effects that this has?

A

Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. (1) Increased intracellular [Ca2+] –> positive inotropy. (2) Stimulates vagus nerve –> decrease HR.

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4
Q

For what 2 conditions are cardiac glycosides/digoxin used clinically, and why?

A

(1) CHF (increase contractility) (2) Atrial fibrillation (Decrease conduction at AV node & depression of SA node)

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5
Q

What 3 major toxicities are associated with cardiac glycosides/digoxin? Describe each.

A

(1) Cholinergic- nausea, vomiting, diarrhea, blurry yellow vision (Think: “Van Gogh”) (2) ECG - Increased PR, Decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block (3) Can lead to hyperkalemia, a poor prognostic indicator

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6
Q

What findings can cardiac glycosides cause on an ECG?

A

Increased PR, Decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block

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7
Q

What are 3 factors predisposing patients to cardiac glycoside/digoxin toxicity, and why?

A

(1) Renal failure (decreased excretion) (2) Hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase) (3) Verapamil, Amiodarone, Quinidine (Decreases digoxin clearance, displaces digoxin from tissue-binding sites)

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8
Q

What is/are the antidote(s) for cardiac glycosides/digoxin?

A

Slowly normalize K+, lidocaine, cardiac pacer, anti-digoxin Fab fragments, Mg2+

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9
Q

What class are Antiarrhythmics that act as Na+ channel blockers? What are the subdivisions of this class? Give at least 2 examples of drugs that fall under each subdivision.

A

Class I; Class IA - Quinidine, Procainamide, Disopyramide; Class IB - Lidocaine, Mexiletine; Class IC - Flecainide, Propafenone

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10
Q

What 3 mechanistic effects do Class IA antiarrhythmics have?

A

(1) Increase AP duration, (2) Increase effective refractory period (ERP), (3) Increase QT interval.

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11
Q

For what kinds of arrhythmias do Class IA antiarrhythmics work?

A

Both atrial and ventricular arrhythmias, especially re-entrant and ectopic supraventricular (SVT) and ventricular (VT) tachycardia

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12
Q

Name 3 Class IA antiarrhythmics.

A

(1) Quinidine (2) Procainamide (3) Disopyramide

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13
Q

What are 5 toxicities are associated with Class IA antiarrhythmics? Specify which toxicities apply to only certain drugs in this class.

A

(1) Cinchonism (headache, tinnitus with quinidine) (2) Reversible SLE-like syndrome (procainamide) (3) Heart failure (disopyramide) (4) Thrombocytopenia (5) Torsades de pointes due to increased QT interval

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14
Q

Name 2 Class IB antiarrhythmics. What other drug can fall into this category?

A

(1) Lidocaine (2) Mexiletine; Phenytoin can also fall into the IB category.

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15
Q

What is the mechanism of Class IB antiarrhythmics? What do Class IB antiarrhythmics preferentially affect?

A

Decrease AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue

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16
Q

For what kinds of arrhythmias are Class IB antiarrhythmics used?

A

Acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias. Think: “IB is Best post-MI”

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17
Q

What are 2 toxicities associated with Class IB antiarrhythmics?

A

(1) CNS stimulation/depression (2) Cardiovascular depression

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18
Q

Name 2 Class IC antiarrhythmics.

A

(1) Flecainide (2) Propafenone; Think: “class iC Flecainide Propafenone = Can I have Fries, Please.”

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19
Q

What is the mechanism of Class IC antiarrhythmics? How does it differ from Class IA/IB antiarrhythmics?

A

Significantly prolongs refractory period in AV node. Minimal effect on AP duration.

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20
Q

For what kind of arrhythmias are Class IC antiarrhythmics used clinically?

A

SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

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21
Q

What is a toxicity of Class IC antiarrhythmics? In what condition(s) are they contraindicated?

A

Proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.

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22
Q

What effect do Class I Antiarrhythmics (Na+ channel blockers) have on each of the following: (1) Conduction (2) Phase 0 depolarization (3) Threshold for firing in abnormal pacemaker cells.

A

(1) Slow or block (decrease) conduction (especially in depolarized cells) (2) Decrease slope of phase 0 depolarization and (3) Increase threshold for firing in abnormal pacemaker cells.

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23
Q

Are Class I antiarrhythmics (Na+ channel blockers) state dependent or independent? Why or why not?

A

Are state dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia])

24
Q

What metabolic condition causes increased toxicity for all class I antiarrhythmics?

A

Hyperkalemia causes increased toxicity for all class I drugs.

25
Q

Graph the Na current of ventricular depolarization, depicting changes in slope of phase 0 caused by each of the following Class I antiarrhythmics: (1) Class IA (2) Class IB (3) Class IC.

A

See p. 302 in First Aid 2014 for the 3 graphs on the right hand side. Note: Class IC decreases slope the most, then Class IA, then Class IB

26
Q

What kind of drugs make up Class II antiarrhythmics? What are 6 examples of such drugs?

A

Antiarrhythmics - Beta blockers (Class II); (1) Metoprolol (2) Propanolol (3) Esmolol (4) Atenolol (5) Timolol (6) Carvedilol

27
Q

What is the mechanism of Class II Antiarrhythmics (Beta-blockers)? What is particularly sensitive to their effects, and what results?

A

Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4. Av node particularly sensitive - increase PR interval.

28
Q

Which Class II antiarrhythmic (Beta-blocker) is very short acting?

A

Esmolol very short acting

29
Q

What is/are the major clinical use(s) for Class II anti-arrhythmics (beta-blockers)?

A

SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

30
Q

What are 4 toxicities associated with all Class II Antiarrhythmics (beta-blockers)?

A

(1) Impotence, (2) Exacerbation of COPD and asthma, (3) Cardiovascular effects (bradycardia, AV block, CHF), (4) CNS effects (sedation, sleep alterations).

31
Q

What condition may Class II antiarrhythmic (beta-blocker) drugs mask?

A

May mask the signs of hypoglycemia.

32
Q

What class of antiarrhythmic is Metoprolol? What particular toxicity does it cause?

A

Class II antiarrhythmics (Beta-blockers); Metoprolol can cause dyslipidemia

33
Q

What class of antiarrhythmic is Propanolol? What particular toxicity does it cause?

A

Class II antiarrhythmics (Beta-blockers); Propanolol can exacerbate vasospasm in Prinzmetal angina.

34
Q

In what patient population are Class II (Beta-blocker) antiarrhythmics contraindicated, and why?

A

Contraindicated in cocaine users (risk of unopposed alpha-adrenergic receptor agonist activity)

35
Q

What is used to treat an overdose of Class II (Beta-blocker) antiarrhythmics?

A

Treat overdose with glucagon.

36
Q

Graph pacemaker cell potential (x) versus membrane potential (y), indicating the effect of Class II (beta-blocker) antiarrhythmics on slope of phase 4 depolarization and AV node.

A

See p. 303 in First Aid 2014 for visual near top/middle of page

37
Q

What are 4 examples of Class III (K+ channel blockers) antiarrhythmics?

A

(1) Amiodarone (2) Ibutilide (3) Dofetilide (4) Sotalol; Think: “AIDS”

38
Q

What is the mechanism of Class III (K+ channel blockers) antiarrhythmics? In what context are they used?

A

Increase AP duration, Increase ERP. Used when other antiarrhythmics fail. Increase QT interval.

39
Q

What are 3 conditions for which Class III (K+ channel blocker) antiarrhythmics are used clinically? Which of these conditions is only treated by 2 particular drugs, and what are those 2 drugs?

A

(1) Atrial fibrillation, (2) Atril flutter; (3) Ventricular tachycardia (amiodarone, sotalol)

40
Q

What class of antiarrhythmics is Sotalol? What are 2 toxicities associated with it?

A

Class III (K+ channel blocker) antiarrhythmic; (1) Torsades de pointes (2) Excessive Beta blockade

41
Q

What class of antiarrhythmics is Ibutilide? What toxicity is associated with it?

A

Class III (K+ channel blocker) antiarrhythmic; Torsades de pointes

42
Q

What class of antiarrhythmics is Amiodarone? What are 8 toxicities associated with it?

A

Class III (K+ channel blocker) antiarrhthmic; (1) Pulmonary fibrosis (2) Hepatotoxicity (3) Hypothyroidism/Hyperthyroidism (amiodarone is 40% iodine by weight) (4) Corneal deposits (5) Skin deposits (blue/gray) resulting in photodermatitis (6) Neurologic effects (7) Constipation (8) Cardiovascular effects (bradycardia, heart block, CHF)

43
Q

What are 3 things that should be checked for clinically when giving a patient amiodarone?

A

Remember to check PFTs, LFTs, and TFTs when using amiodarone

44
Q

Although Amiodarone is technically a Class III (K+ channel blocker) antiarrhythmic, what is important to know about its actual effects?

A

Amiodarone has class I, II, III, and IV effects and alters the lipid membrane.

45
Q

Graph the effect of Class III antiarrhythmics on cell action potential, labeling their effect on K+ current.

A

See p. 303 in First Aid 2014 for graph at bottom of page

46
Q

What type of drugs are Class IV (Ca2+ channel blocker) antiarrhythmics? Give 2 examples.

A

Class IV (Ca2+ channel blocker) antiarrhythmics; (1) Verapamil (2) Diltiazem

47
Q

What is the mechanism of Class IV (Ca2+ channel blocker) antiarrhythmics?

A

Decrease conduction velocity, Increase ERP, Increase PR interval.

48
Q

What are 2 clinical uses for Class IV (Ca2+ channel blocker) antiarrhythmics?

A

(1) Prevention of nodal arrhythmias (e.g., SVT) (2) Rate control in atrial fibrillation

49
Q

What are 4 toxicities associated with Class IV (Ca2+ channel blocker) antiarrhythmics?

A

(1) Constipation (2) Flushing (3) Edema (4) CV effects (CHF, AV block, sinus node depression)

50
Q

Graph the effects of Class IV (Ca2+ channel blocker) on membrane potential, indicating its effects on action potential and AV node.

A

See p. 304 in First Aid 2014 for graph at top of page

51
Q

What are 2 examples of antiarrhythmics other than Class I-IV antiarrhythmics?

A

(1) Adenosine (2) Mg2+

52
Q

What is the mechanism of Adenosine as an antiarrhythmic?

A

Increase K+ out of cells => hyperpolarizing the cell and decrease Ca current.

53
Q

For what clinical use is Adenosine the drug of choice?

A

Drug of choice in diagnosing/abolishing supraventricular tachycardia.

54
Q

Describe the length of action of Adenosine.

A

Very short acting (~15 sec).

55
Q

What are 3 adverse effects of Adenosine?

A

Adverse effects include (1) flushing, (2) hypotension, (3) chest pain.

56
Q

What 2 drugs/substances block the effects of adenosine?

A

Effects blocked by theophylline and caffeine.

57
Q

In what 2 conditions is Mg2+ effective?

A

Effective in Torsades de pointes and Digoxin toxicity.

FA - Cardiovascular (18 decks)

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