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Advanced Pharmacology > Arrhythmia Pharmacology > Flashcards

Arrhythmia Pharmacology Flashcards

1
Q

What are the two main components of heart function?

A

-Electrical
-Mechanical

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2
Q

Someone can have failure of the mechanical pump with normal rhythm; this would be seen in conditions like…

A

-Heart failure
-Ischemia
-Hypertension

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3
Q

When the electrical component falters, _____ can develop that compromise effective pumping

A

Arrhythmias

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4
Q

When the conduction system falters, ___ ___ and ____ ____ ___ can develop

A

AV blocks and bundle branch blocks

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5
Q

The resting membrane potential of a NA node cell is approximately ____ mV, while that of a ventricular muscle cell is ____ mV

A

55; 86

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6
Q

The ventricular action potential has a much _____ plateau phase; this ensures that ventricular myocytes have adequate time to contract before the onset of the next action potential

A

Longer

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7
Q

The depolarization of ventricular myocytes stimulated by ____ ____

A

Pacemaker cells

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8
Q

What are the five phases of depolarization?

A

-Phase 4: resting membrane potential
-Phase 0: rapid depolarization
-Phase 1: early depolarization
-Phase 2: plateau
-Phase 3: late repolarization

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9
Q

The rate of pacemaker discharge can be affected by what 3 factors?

A

-As spontaneous depolarization increases (phase 4), so does the rate of firing
-As the threshold becomes more negative, the rate of firing increases
-As resting membrane potential becomes more positive, the rate of firing increases

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10
Q

The ____ node has the fastest intrinsic firing rate or 60-100 bpm, there is the native pacemaker for the heart

A

SA

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11
Q

The SA node suppresses the intrinsic rhythm of the other pacemakers, known as ____ ____

A

Overdrive suppression

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12
Q

The VA node is about 40-40 bpm, and is known as the ____ ____

A

Latent pacemaker

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13
Q

_____ rhythm may result from slowing of the SA node

A

Junctional

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14
Q

The ____ measures the body surface potentials induced by cardiac electrical activity

A

EKG

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15
Q

The ____ wave reflects atrial depolarization

A

P

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16
Q

The ____ complex represents ventricular depolarization

A

QRS

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17
Q

The ____ wave indicates ventricular repolarization

A

T

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18
Q

____ are defects in impulse formation that stem from the SA node

A

Arrhythmias

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19
Q

Arrhythmias cause altered _____; this can be a normal physiological response

A

Automaticity

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20
Q

The sympathetic nervous system can cause altered automaticity by increasing ____ by increasing beta-1 stimulation

A

Catecholamines

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21
Q

The sympathetic nervous system can also increase heart rate by increasing _____ channels

A

Calcium

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22
Q

The parasympathetic nervous system can impact automaticity by releasing ____

A

Acetylcholine

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23
Q

What effects can the parasympathetic nervous system have on automaticity?

A

-Reduced pacemaker current-> decrease channel opening
-Threshold more positive-> decrease calcium channel openings
-RMP more negative-> increasing potassium channel openings

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24
Q

The latent pacemaker cells take over the SA node’s role when the SA node is ____; this is known as an escape beat or escape rhythm

A

Slowed

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25
Q

Latent pacemaker cells fire at a rate ____ than normal SA node rate (ectopic beat or rhythm)

A

Faster

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26
Q

What can lead to a series of ectopic beats or an ectopic rhythm?

A

-Ischemia
-Electrolyte imbalances
-Increases sympathetic tone

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27
Q

Tissue damage disrupts cellular ____

A

Membranes

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28
Q

____ is when a normal action potential stimulates extra abnormal depolarizations

A

Afterdepolarization

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29
Q

What are the two types of afterdepolarization?

A

-Early
-Delayed

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30
Q

Early afterdepolarizations usually occur during phase ___ or ____

A

2 or 3

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31
Q

Early afterdepolarizations are often due to the flow of ____

A

Ions

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32
Q

If early afterdepolarization are sustained, it leads to ____ ____ ____

A

Torsades de Pointes

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33
Q

Torsades de Pointes cause ____ ____ of varying amplitude and direction

A

QRS complexes

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34
Q

Torsades de Pointes is a medical emergency that requires ____ or ____ for treatment

A

Magnesium or defibrillation

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35
Q

Early afterdepolarization generally occurs during the _____ phase of the action potential, although they can also occur during the plateau phase

A

Repolarization

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36
Q

Repetitive afterdepolarizations can trigger an ____

A

Arrhythmia

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37
Q

Delayed afterdepolarizations occur just after the completion of _____

A

Repolarization

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38
Q

Delayed afterdepolarizations have an _____ mechanism, but it appears that intracellular Ca2+ accumulation activates the Na+/Ca2+ exchanger, and the resulting electrogenic influx of 3 Na+ for each extruded Ca2+ depolarizes the cell

A

Unknown

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39
Q

Another defect of impulse conduction is re-entry which is a self-sustaining electrical impulse of the _____

A

Myocardium

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40
Q

What two conditions are needed for re-entry?

A

-Unidirectional block
-Slowed retrograde conduction velocity

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41
Q

______ result from re-entry

A

Tachyarrhythmias

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42
Q

A ____ block is when an impulse fails to propagate normally through the conduction system

A

Conduction

43
Q

With a conduction block, the tissue is still ____, and this leads to tissue damage

A

Refractory

44
Q

What are the results of a conduction block?

A

-Heart rate decreases
-Bradycardia results
-Subsidiary pacemakers may fire (e.g. junction or ventricles)

45
Q

An accessory tract pathway is an electrical pathway that bypasses the ____ node

A

AV

46
Q

Accessory tract pathways are also known as the Bundle of ____, which sends impulses directly from the atria to ventricles

A

Kent

47
Q

With accessory tract pathways, impulses can travel down ____ and ____ pathways

A

Normal, accessory

48
Q

Accessory tract pathways result in ____-____ of the ventricles

A

Pre-excitation

49
Q

Accessory tract pathways are seen as short PR intervals and slurring of the QRS complexes, called ____ waves

A

Delta

50
Q

Accessory tract pathways also create favorable conditions for ____ and ____

A

Re-entry and tachyarrhythmias

51
Q

The bundle of kent is an accessory electrical pathway that conducts impulses directly from the atria to the ventricles, bypassing the ____ node

A

AV

52
Q

What are the general mechanisms of antiarrhythmic agents?

A

-Alter max diastolic potential in pacemaker cells
-Alter rate of phase 4 depolarization
-Alter threshold potential
-Alter action potential duration

53
Q

Ion channels can switch ____, much like we talked about with the histamine receptor

A

Conformation

54
Q

When ion channels switch conformations, this changes the cellular _____

A

Permeability

55
Q

Drugs can have different affinities for different conformations; this is known as ____-____ binding

A

State-dependent

56
Q

Sodium channel blockers have what 3 conformational states?

A

-Open: upstroke
-Closed: resting
-Inactivated: plateau phase

57
Q

Most sodium channel blockers bind preferentially to the ____ and ____

A

Open and inactivated

58
Q

Sodium channel blockers dissociate from sodium channels during ____

A

Diastole

59
Q

Sodium channel blockers depress more sodium conduction in ______ tissue than in normal tissue

A

Ischemic

60
Q

In ischemic tissue, cardiac myocytes take longer to be ____

A

Depolarized

61
Q

Sodium channel blockers prolong the _____ state of sodium channel ions which makes the channels accessible to sodium blockers for longer

A

Inactivation

62
Q

Sodium channel blockers allow for the selectivity of ____ tissue to address possible arrhythmic potential

A

Ischemic

63
Q

Complications of the use of antiarrhythmic agents:

A

-In many cases, agents can cause arrhythmias
-If you can’t completely stop the impulse, it may go somewhere else
-Common problem with re-entry arrhythmias

64
Q

Antiarrhtymic drugs can have _____ effects that usually occur early in treatment

A

Proarrhythmic

65
Q

What type of arrhythmias can antiarrhythmic drugs cause?

A

-VT
-VF
-Torsade de Pointes

66
Q

Torsade de Pointes is a polymorphic ____ preceded by a prolonged ____ interval

A

VT; QT

67
Q

The exact mechanism of how antiarrhythmic drugs cause arrhythmias is ____

A

Unknown

68
Q

What are risk factors for proarrhythmia?

A

-History of significant ventricular arrhythmias
-CAD or valvular heart disease
-Electrolyte imbalances
-History of long QT syndrome
-Drugs that prolong the QT interval

69
Q

What are the 4 classes of antiarrhythmic agents?

A

-Class I: Na+ channel blockers
-Class II: Beta-adrenergic receptor blockers
-Class III: K+ channel blockers
-Class IV: Ca++ channel blockers

70
Q

Sodium channel blockers shift the threshold to more ____ potential

A

Positive

71
Q

Sodium channel blockers decrease the slope of phase 4 _____

A

Depolarization

72
Q

Sodium channel blockers also act on ventricular myocytes, meaning they decrease the upstroke velocity of phase ____

A

0

73
Q

Some class 1A antiarrhythmic agents prolong _____

A

Repolarization

74
Q

Sodium channel blockers decrease the likelihood of re-entry and prevent arrhythmia by…

A

-Decreasing conduction velocity
-Increasing the refractory period of ventricular myocytes

75
Q

There are 3 subclasses of sodium channel blockers with similar effects on action potentials of SA node, but different effects on ____ action potentials

A

Ventricular

76
Q

Class IA antiarrhythmic agents ____ block sodium channels

A

Moderately

77
Q

Class IA antiarrhythmic agents prolong the repolarization of SA and ventricular cells in order to…

A

-Decrease conduction velocity
-Increase effective refractory period

78
Q

The net result of class IA antiarrhythmic agents is decreased _____

A

Re-entry

79
Q

Class IA antiarrhythmic agents can prolong the ____ interval

A

QT

80
Q

Quinadine is a class IA antiarrhythmic agent that blocks transmitter release from the ____ nerve

A

Vagus

81
Q

Quinidine also has _____ effects

A

Anticholinergic

82
Q

Quinidine can _____ conduction through the AV node; this can be bad, especially in patients with atrial flutter

A

Increase

83
Q

Quinidine, a class IA antiarrhythmic agent, is used less now because of ___ ___

A

Side effects

84
Q

Adverse effects of Quinidine (class IA antiarrhythmic agent):

A

-Diarrhea
-Nausea
-Light-headedness
-Headache

85
Q

Quinidine (Class IA antiarrhythmic agent) would be contraindicated in patients with…

A

-QT prolongation (torsades de pointes)
-Conduction blocks
-Myasthenia gravis
-Sick sinus syndrome
-Liver failure

86
Q

Quinidine is metabolized by ____

A

CYP450

87
Q

Quinidine increases plasma levels of _____

A

Digoxin

88
Q

What are the symptoms of digoxin toxity?

A

-Hypokalemia

89
Q

What effects would hypokalemia have on Quinidine?

A

-Decreases Quinidine efficacy
-Exacerbates QT prolongation
-Increases risk for torsades de pointes

90
Q

Class IA agents are used much less now in favor of class ___ agents

A

III

91
Q

Procainamide is another class IA antiarrhythmic that is effective for ____ and ____ arrhythmias

A

Supraventricular and ventricular

92
Q

Procainamide is used for the conversion of new-onset ____ to ____

A

A-fib to NSR

93
Q

In acute MI, Procainamide (class IA antiarrhythmic agent) can be used to decrease the likelihood of ___-___ arrhythmias

A

Re-entry

94
Q

Procainamide can be used for ____ ____, but is not the preferred drug

A

Ventricular tachycardia

95
Q

Adverse effects of Procainamide (class IA antiarrhythmic):

A

-Peripheral vasodilation (SNS block)
-Chronic therapy: Lupus-like syndrome/positive antinuclear antibodies-> discontinue drug

96
Q

Procainamide is metabolized in the liver to _____

A

NAPA

97
Q

NAPA is an active metabolite that produces pure class ____ antiarrhythmic effects

A

III

98
Q

What are the clinical effects of NAPA?

A

-Prolongs the refractory period
-Lengthens the QT interval

99
Q

NAPA does not appear to cause the ____-___ side effects of Procainamide

A

Lupus-like

100
Q

Disopyramide is another class IA antiarrhythmic agent that has similar effects as Quinidine in its ____ and ____ effects, but different side effects

A

Electrophysiologic and antiarrhythmic

101
Q

Disopyramide (class IA antiarrhythmic) causes fewer GI problems but has even more profound _____ effects vs Quinidine

A

Anticholinergic

102
Q

What anticholinergic effects does Disopyramide have?

A

-Urinary retention
-Dry mouth

103
Q

Disopyramide would be contraindicated in patients with…

A

-Uncompensated heart failure
-Obstructive uropathy or glaucoma
-Conduction block between the atria and ventricles
-Sinus-node dysfunction

Advanced Pharmacology (10 decks)

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