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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
Latent pacemaker cells fire at a rate ____ than normal SA node rate (ectopic beat or rhythm)
Faster
26
What can lead to a series of ectopic beats or an ectopic rhythm?
-Ischemia -Electrolyte imbalances -Increases sympathetic tone
27
Tissue damage disrupts cellular ____
Membranes
28
____ is when a normal action potential stimulates extra abnormal depolarizations
Afterdepolarization
29
What are the two types of afterdepolarization?
-Early -Delayed
30
Early afterdepolarizations usually occur during phase ___ or ____
2 or 3
31
Early afterdepolarizations are often due to the flow of ____
Ions
32
If early afterdepolarization are sustained, it leads to ____ ____ ____
Torsades de Pointes
33
Torsades de Pointes cause ____ ____ of varying amplitude and direction
QRS complexes
34
Torsades de Pointes is a medical emergency that requires ____ or ____ for treatment
Magnesium or defibrillation
35
Early afterdepolarization generally occurs during the _____ phase of the action potential, although they can also occur during the plateau phase
Repolarization
36
Repetitive afterdepolarizations can trigger an ____
Arrhythmia
37
Delayed afterdepolarizations occur just after the completion of _____
Repolarization
38
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
Unknown
39
Another defect of impulse conduction is re-entry which is a self-sustaining electrical impulse of the _____
Myocardium
40
What two conditions are needed for re-entry?
-Unidirectional block -Slowed retrograde conduction velocity
41
______ result from re-entry
Tachyarrhythmias
42
A ____ block is when an impulse fails to propagate normally through the conduction system
Conduction
43
With a conduction block, the tissue is still ____, and this leads to tissue damage
Refractory
44
What are the results of a conduction block?
-Heart rate decreases -Bradycardia results -Subsidiary pacemakers may fire (e.g. junction or ventricles)
45
An accessory tract pathway is an electrical pathway that bypasses the ____ node
AV
46
Accessory tract pathways are also known as the Bundle of ____, which sends impulses directly from the atria to ventricles
Kent
47
With accessory tract pathways, impulses can travel down ____ and ____ pathways
Normal, accessory
48
Accessory tract pathways result in ____-____ of the ventricles
Pre-excitation
49
Accessory tract pathways are seen as short PR intervals and slurring of the QRS complexes, called ____ waves
Delta
50
Accessory tract pathways also create favorable conditions for ____ and ____
Re-entry and tachyarrhythmias
51
The bundle of kent is an accessory electrical pathway that conducts impulses directly from the atria to the ventricles, bypassing the ____ node
AV
52
What are the general mechanisms of antiarrhythmic agents?
-Alter max diastolic potential in pacemaker cells -Alter rate of phase 4 depolarization -Alter threshold potential -Alter action potential duration
53
Ion channels can switch ____, much like we talked about with the histamine receptor
Conformation
54
When ion channels switch conformations, this changes the cellular _____
Permeability
55
Drugs can have different affinities for different conformations; this is known as ____-____ binding
State-dependent
56
Sodium channel blockers have what 3 conformational states?
-Open: upstroke -Closed: resting -Inactivated: plateau phase
57
Most sodium channel blockers bind preferentially to the ____ and ____
Open and inactivated
58
Sodium channel blockers dissociate from sodium channels during ____
Diastole
59
Sodium channel blockers depress more sodium conduction in ______ tissue than in normal tissue
Ischemic
60
In ischemic tissue, cardiac myocytes take longer to be ____
Depolarized
61
Sodium channel blockers prolong the _____ state of sodium channel ions which makes the channels accessible to sodium blockers for longer
Inactivation
62
Sodium channel blockers allow for the selectivity of ____ tissue to address possible arrhythmic potential
Ischemic
63
Complications of the use of antiarrhythmic agents:
-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
Antiarrhtymic drugs can have _____ effects that usually occur early in treatment
Proarrhythmic
65
What type of arrhythmias can antiarrhythmic drugs cause?
-VT -VF -Torsade de Pointes
66
Torsade de Pointes is a polymorphic ____ preceded by a prolonged ____ interval
VT; QT
67
The exact mechanism of how antiarrhythmic drugs cause arrhythmias is ____
Unknown
68
What are risk factors for proarrhythmia?
-History of significant ventricular arrhythmias -CAD or valvular heart disease -Electrolyte imbalances -History of long QT syndrome -Drugs that prolong the QT interval
69
What are the 4 classes of antiarrhythmic agents?
-Class I: Na+ channel blockers -Class II: Beta-adrenergic receptor blockers -Class III: K+ channel blockers -Class IV: Ca++ channel blockers
70
Sodium channel blockers shift the threshold to more ____ potential
Positive
71
Sodium channel blockers decrease the slope of phase 4 _____
Depolarization
72
Sodium channel blockers also act on ventricular myocytes, meaning they decrease the upstroke velocity of phase ____
0
73
Some class 1A antiarrhythmic agents prolong _____
Repolarization
74
Sodium channel blockers decrease the likelihood of re-entry and prevent arrhythmia by...
-Decreasing conduction velocity -Increasing the refractory period of ventricular myocytes
75
There are 3 subclasses of sodium channel blockers with similar effects on action potentials of SA node, but different effects on ____ action potentials
Ventricular
76
Class IA antiarrhythmic agents ____ block sodium channels
Moderately
77
Class IA antiarrhythmic agents prolong the repolarization of SA and ventricular cells in order to...
-Decrease conduction velocity -Increase effective refractory period
78
The net result of class IA antiarrhythmic agents is decreased _____
Re-entry
79
Class IA antiarrhythmic agents can prolong the ____ interval
QT
80
Quinadine is a class IA antiarrhythmic agent that blocks transmitter release from the ____ nerve
Vagus
81
Quinidine also has _____ effects
Anticholinergic
82
Quinidine can _____ conduction through the AV node; this can be bad, especially in patients with atrial flutter
Increase
83
Quinidine, a class IA antiarrhythmic agent, is used less now because of ___ ___
Side effects
84
Adverse effects of Quinidine (class IA antiarrhythmic agent):
-Diarrhea -Nausea -Light-headedness -Headache
85
Quinidine (Class IA antiarrhythmic agent) would be contraindicated in patients with...
-QT prolongation (torsades de pointes) -Conduction blocks -Myasthenia gravis -Sick sinus syndrome -Liver failure
86
Quinidine is metabolized by ____
CYP450
87
Quinidine increases plasma levels of _____
Digoxin
88
What are the symptoms of digoxin toxity?
-Hypokalemia
89
What effects would hypokalemia have on Quinidine?
-Decreases Quinidine efficacy -Exacerbates QT prolongation -Increases risk for torsades de pointes
90
Class IA agents are used much less now in favor of class ___ agents
III
91
Procainamide is another class IA antiarrhythmic that is effective for ____ and ____ arrhythmias
Supraventricular and ventricular
92
Procainamide is used for the conversion of new-onset ____ to ____
A-fib to NSR
93
In acute MI, Procainamide (class IA antiarrhythmic agent) can be used to decrease the likelihood of ___-___ arrhythmias
Re-entry
94
Procainamide can be used for ____ ____, but is not the preferred drug
Ventricular tachycardia
95
Adverse effects of Procainamide (class IA antiarrhythmic):
-Peripheral vasodilation (SNS block) -Chronic therapy: Lupus-like syndrome/positive antinuclear antibodies-> discontinue drug
96
Procainamide is metabolized in the liver to _____
NAPA
97
NAPA is an active metabolite that produces pure class ____ antiarrhythmic effects
III
98
What are the clinical effects of NAPA?
-Prolongs the refractory period -Lengthens the QT interval
99
NAPA does not appear to cause the ____-___ side effects of Procainamide
Lupus-like
100
Disopyramide is another class IA antiarrhythmic agent that has similar effects as Quinidine in its ____ and ____ effects, but different side effects
Electrophysiologic and antiarrhythmic
101
Disopyramide (class IA antiarrhythmic) causes fewer GI problems but has even more profound _____ effects vs Quinidine
Anticholinergic
102
What anticholinergic effects does Disopyramide have?
-Urinary retention -Dry mouth
103
Disopyramide would be contraindicated in patients with...
-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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