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Pharmacology > Pharm 11- Antiarrhythmics > Flashcards

Pharm 11- Antiarrhythmics Flashcards

1
Q

Arrythmia

A

abnormalities in the electrical impulse generation of conduction through the heart

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2
Q

What percent of anesthetized patients have arrythmias?

A

> 50%

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3
Q

What percent of patinets with MIs have arrhythmias?

A

80%

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4
Q

How do virutally all antiarrythmics work?

A

Altering the ionic transmembrnae balance (Na+ Ca++, K+) or the sympathetic tone to the heart; which alters the shape of the action potential

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5
Q

What is the name of the classification system that classifies 4 types of antiarrhythmics?

A

The Vaughan Williams Classification

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6
Q

What classes are Na+ channel blockers?

A

1A, 1B, 1C

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7
Q

What class is B-Blockers?

A

2

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8
Q

WHat class is K+ blocker?

A

3

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9
Q

What class is Ca++ channel blocker?

A

4

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10
Q

How does class IA work on the action potential?

A

Slows phase 0 depolarization in ventricular muscle fibers

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11
Q

How does class IB work on the action potential?

A

Shortens Phase 3 repolarization in ventricular muscle fibers

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12
Q

How does class IC work on the action potential?

A

Markely slows phase 0 depolarization in ventricular muscle fibers

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13
Q

How does class II work on the action potnetial?

A

Inhibits phase 4 depolarization in SA and AV nodes

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14
Q

How does class III work on the action potential?

A

Prolongs phase 3 repolarization in ventricular muscle fibers

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15
Q

How does class IV work on the action potential?

A

Inhibits action potential in SA and AV nodes

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16
Q

How do Class I: Na+ Channel Blockers work?

A

Preferentially bind to open Na+ channels rather than to fully repolarization Na+ channels; preferentially block conduction in tssues that are depolarizing more frequently (use-dependence blockade)

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17
Q

Use-Dependence Blockade

A

preferentially blocking conduction in tissues that are depolarizing more frequently; used in Class I: Na + channel blockers

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18
Q

How are the 3 subclasses of Class I antiarrythmics differentiated?

A

Ia: Shorten the AP and affect QRS
Ib: Shortern the AP w/o affecting QRS
Ic: Does not shorten the AP

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19
Q

Which Class is nicknamed “Membrane stabilizers?”

A

Class Ia: Na+ Channel Blockers

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20
Q

How do Class Ia: Na+ Channel Blockers shift the action potential?

A

Shift to the right by slowing Phase 0 depolarization; hence their nickname “membrane stabilizers”; also inhibits some K+ channels (class III activitY) which widens the AP causing prolonged QT intervals

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21
Q

How do Class Ia: Na+ Channel Blockers widen the AP causing prolonged QT intervals?

A

They inhibit some K+ channels (class III activitY)

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22
Q

What is the pneumonia to remember Ia drugs?

A

Double Quarter Pounder

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23
Q

What are the three Class Ia drugs?

Double Quarter Pounder

A

Disopyramide (Norpace)
Quinidine (Quinidex)
Procainamide (Pronestryl, Procan)

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24
Q

Quinidine (Quinidex)

A

Administered Orally

Various tachyarrhythmias, but rarely used due to toxic side effects: Cinchonism/Torsades de Pointes

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25
Q

Cinchonism

A

poisoning due to excessive ingestion of cinchona alkaloids; unclear vision red skin vomiting vertigo diarrhea

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26
Q

Torsades de Pointes

A

Polymorphic Ventricular Tachycardia

usually resolves spontaneously; may devolve in to V-fib

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27
Q

Dispyramide (Norpace)

A

More negative inotropic effects and increase SVR than Quinidine (Quinidex); could precipitate HF
3-4th line antiarrythmic

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28
Q

What is the most widely used Ia: Na+ channel blocker?

A

Procainamide (Pronestryl, Procan)

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29
Q

Procainamide (Pronestryl, Procan)

A

most widely used Ia
Derived from procaine (anesthetic)
Given orally IV, IM
Adverse effects similar to Quinidine (although less severe) but may cause reversible lupus erythematosus

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30
Q

Reversible Lupus Erythematosus

A

Autoimmune disease; Neurologic manifestations are among the features of systemic lupus erythematosus (SLE), a multisystem autoimmune connective tissue disorder with various clinical presentations. SLE affects many organ systems, including the central and peripheral nervous systems and muscles

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31
Q

How do Class Ib: Na+ Channel Blockers shift the action potential?

A

Shift the AP to the left by shortening Phase 3 repolarization.

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32
Q

Where do class Ib : Na+ Channel Blockers have their greatest effect?

A

Heart cells with long action potentials like Purkinje fibers and ventricular myocytes

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33
Q

What is the pneumonic for remember Class Ib: Na+ channel blockers?

A

Lettuce, Mayo and Tomato

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34
Q

What are some examples of Class Ib: Na+ Channel Blockers

A

Lidocaine (Xylocaine)
Mexiletine (Mextil)
Tocainide (Tonocard)

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35
Q

Lidocaine (Xylocaine)

A

Local anesthetic
Only given parenterally
Wide therapeutic index
Extends refractory period further into diastole in depressed cardiomyocytes than healthy ones (sick heart cells have a longer refractory period so they cant fire as fast)

36
Q

What is the major toxic side effect of Lidocaine (Xylocaine) at high doses?

A

Cardiac depression

37
Q

What is the drug of choice for ventricular arrhythmias particularly those associated with “sick hearts’ with arrhythmias like post MI?

A

Lidocaine (Xylocaine)

*or post XC removal

38
Q

Why is Lidocaine (Xylocaine) a common component of cardioplegia?

A

To stop arrhythmias; minimizes instances of ventricular arrhythmias Ex. used for PVCs

39
Q

If choosing between EKGs which patient should receive lidocaine (xylocaine) what do you look for?

A

Ventricular anomalies such as PVCs; ventricular arrhythmias

40
Q

Mexiletine (Mextil)

A

Like an oral lidocaine (xylocaine)

used in the treatment of ventricular tachyarrythmias

41
Q

Tocainide (Tonocard)

A 
Like lidocaine (xylocaine)
Given orally
used in patients resistance to and or sensitive to lidocaine (xylocaine) /mexiletine (mextil)
42
Q

What is Tocainide (Tonocard) a second or third line treatment and not a first?

A

Pulmonary toxicity fairly common; can cause pulmonary fibrosis rendering i a 2nd or 3rd line treatment; can be as fatal as ventricular arrhythmias

43
Q

What are the effects of giving Class Ic: Na+ Channel Blockers?

A

Does not shift the action potential.
Ic’s even have profound effects on normal hearts. Recent studies indicate some are very dangerous and are not used when better/safer alternatives are available (being phased out)

44
Q

What is the pneumonic for remember Class Ic: Na+ Channel Blockers?

A

Fries Please

45
Q

What are the two Class Ic: Na+ Channel Blockers? (fries please)

A

Flecainide (Tambocor)

Propafenone (Rhythmol)

46
Q

What is the effect of giving Flecainide (Tambocor)?

A

Given orally
Suppresses Phase 0 upstroke in Purkinje fibers and cardiomyocytes
Dramatically slows conduction and automaticitiy is decreased via an increase in the threshold potential
(more harm than good)

47
Q

What is Flecainide (Tambocor) used for?

A

Refractory ventricular arrhythmias (particularly PVCs)

48
Q

What effects of Flecainide (Tambocor) worsen CHF?

A

Negative inotropic effects

49
Q

Propafenone (Rhythmol)

A

Similar uses as quinidine; given orally

Considered to be a “broad spectrum” antiarrythmic but used mostly for supraventricular tachyarrhythmias

50
Q

How do Class II: B-Adrenoceptor Blockers work?

A

Work by diminishing Phase 4 depolarization= decreased automaticity, prolonged AV conduction, negative chronotrope, negative inotrope

51
Q

B1-blockers are selective for what?

A

Cardioselective, but many/most have other adrenergic blocker activity; some have partial adrenergic agonist activity

52
Q

What arrhythmias are B-Adrenoceptor Blockers used for?

A 
Atrial tachyarrhythmias 
Includes AV nodal re-entrant tachyarrythmias (most common type, particularly in women)
Ventricular arrhythmias (post MI)
53
Q

AV Nodal Re-entrant Tachyarrhythmias

A

Ectopic dischange during refractory period; cycle of circulating current is conducted

two tracts depolarizing at a different rate; two conducting tissues with different electrical properties; no abnormality on the EKG at rest

54
Q

What are some B-blockers used as antiarrhythmics?

A

Propranolol (inderal)
Metoprolol (Lopressor, Toprol- XL)
Esmolol (Brevibloc)

55
Q

Propranolol (Inderal)

A

Extenstively used for decades

Has been proven to decrease incidence of mortality within the first year of an MI

56
Q

The most commonly used B-blocker for treating cardiac arrythmias (less B2 than Inderal)

A

Metoprolol (Lopressor, Toprol-XL)

57
Q

Esmolol (Brevibloc)

A

Very short acting IV B-blocker commonly used during surgery and during emergencies

58
Q

How do Class III: K+ Channel Blockers work?

A

Block K+ channels with little effect on Na+ channels
Blocking the outward flow of K+ during repolarization they prolong the action potential without affecting Phase 0 (depolarization)

Increases refractory period and refractoriness; makes them less sensitive to arrhythmias

59
Q

How do Class III: K+ block re-entrant arrhythmias?

A

Prolonged AP with normal conduction velocity

60
Q

What are the negative side effects of Class III: K+ Channel Blockers?

A

Reverse use-dependence blockade; which can contribute to arrhythmias; generally prolong the QT

61
Q

What are the Class III: K+ Channel Blockers

A 
Amiodarone (Cordarone)
Drondarone (Multaq)
Sotalol (Betapace, Sorine)
Dofetilide (Tikosyn)
Ibutilide (Corvert)
62
Q

Amiodarone (Cordarone)

A

Iodinated Benzofuran, which means it looks a little like thyroxine; effects all cardiac tissues so it has a broad-spectrum of antiarrhythmic acitivty

2nd Line Rx for lots of refractory arrhythmias

63
Q

What is the drug of choice for A-fib?

A

Amiodarone (Cordarone)

64
Q

What is the half-life of amiodarone?

A

Very long half-life (20-100 days) combined with high ability to interact with other drugs and a boat-load of side-effects (particularly with long-term use) limits its use

65
Q

At what dosages do you get less toxicity?

A

100-200 mg/ day; but it takes weeks to months to get therapeutic levels because of the long half-life

66
Q

What high loading doses of amiodarone must you give?

A

800-1600 mg/day

67
Q

What are some side effects of amiodarone?

A

Sinus Bradycardia
Hypotension
ARDS and Pulmonary Fibrosis
and “a lot of other nasties”

68
Q

Dronedarone (Multaq)

A

Like amiodarone but w/o iodine (no thyroid dysfunction or blue skin)
Much shorter half-life (24 hours) than amiodarone
less effective than amiodarone for a-fib but has fewer of those side effects except risk of stroke and death

69
Q

Sotalol (Betapace, Sorine)

A

Non-selective B-blocker
Reduces post Mi mortality
Class III activity (lengthens the refractory period)
Reduces myocardial o2 consumption and acts as a powerful antiarrhthmic
Prevents fibrillation and makes defibrillating patients easier to its idea for post-MI patients

70
Q

What is the drug of choice for a-fib patients with HF or low ejection fractions?

A

Dofetilide (Tikosyn)

71
Q

What is the drug of choice for a fib?

A

Ibutilide (Corvert)

72
Q

Ibutilide (Corvert)

A

Class III and Ia antiarrhythmic properties

73
Q

What class if antiarrhtyhmics are more prone than others to cause arrhythmias?

A

Class III: K+ Channel blockers

74
Q

What is the effect of Class IV: Ca++ Channel Blockers?

A

Decrease the rate of Phase 4 spontaneous depolarization

Preferentially slow the rate of conduction in tissues dependent on calcium currents for depolarization

75
Q

What are examples of some Ca++ Channel Blockers?

A

Verapamil (calan, isoptin)
Cardizem (diltiazem)
Nifedipine (procardia)

76
Q

What is the order of preference of Ca++ Channel Blockers to use?

A

Verapamil > Cardizem > Nifedipine

77
Q

Verapamil/Cardizem for Arrhythmias

A

Interchangably for arrhtyhmias
Preferentially block the voltage sensitive channels
use-dependent (preferring to block channels on tissues depolarizing too fast) and block Ca++ channels most effectively on the AV and SA nodes

Tx Hypertension, angina, a flt

78
Q

Since Verapamil and Cardizem are both negative inotropes, so they should be avoided….

A

Patients with depressed EF, pateints with HF

79
Q

What are the classless antiarrhythmis?

A

Digoxin
Adenosine (Adenocard)
Magnesium Sulfate

80
Q

Digoxin

A

Shortens the refractory period in atrial and ventricular tissue while slowing conduction through the AV node; used to control ventricular response rates in a-fib and a-flut

81
Q

What is the drug of choice for abolishing SVT?

A

Adenosine (Adenocard)

82
Q

Adenosine

A

fast IV push on bypass; decresaes av node automaticity and cardiac conduction velocity and automaticity
Short half-life 10-15 sec

83
Q

Adenosine Dose

A

First dose: 6 mg fast IV push

If that doesn’t convert the SVT give 12 mg fast IV push

84
Q

What is the drug of choice for digoxin-induced arrhythmias?

A

Magnesium Sulfate

85
Q

Magnesium Sulfate

A

Slows rate of SA node impulse formation and the rate at which the impulse travels through myocardium
must be given iv to be effective as an antiarrhtyhmic

Pharmacology (23 decks)

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