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CPR Week 2 > 3.2.2. Antiarrythmic Drugs I and II > Flashcards

3.2.2. Antiarrythmic Drugs I and II Flashcards

1
Q

What are Class I drugs?

A

Na+ channel blockers

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2
Q

What are class II drugs?

A

Beta Blockers

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3
Q

What are class III drugs?

A

K+ channel blockers

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4
Q

What are class IV drugs?

A

Ca2+ channel blockers

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5
Q

What do the subtypes of Class I do?

A

IA - ↓ ventricular conduction (↑ QRS interval); prolong ventricular AP (↑ QT interval)

IB - slow conduction and ↑ threshold for firing of abnormal cells

IC - ↓ ventricular conduction (↑ QRS interval)

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6
Q

When do we use each of the subtypes of class I drugs?

A

IA - Atrial and ventricular arrhythmias IB - Acute ventricular arrhythmias IC - Ventricular arrhythmias

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7
Q

Examples of Class IA drugs

A

Quinidine, procainamide, disopyramide

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8
Q

Example of Class IB drugs

A

Lidocaine

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9
Q

Examples of Class IC drugs

A

Flecainide, propafenone

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10
Q

Side effects of Class IA drugs

A

Quinidine: cinchonism (headache, tinnitus) and torsades de pointes (polymorphic ventricular tachycardia due to ↑ QT interval);

procainamide: drug-induced lupus like symptoms

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11
Q

Side effects of Class IB drugs

A

CV and CNS depression w/ overdose

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12
Q

Side effects of Class IC drugs

A

Can cause arrhythmias (especially in post-MI patients)

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13
Q

How do Beta blockers work?

A

↓ AV nodal conduction (↑ PR interval)

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14
Q

When do we use beta blockers?

A

Ventricular and supraventricular arrhythmias

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15
Q

Side effects of Beta Blockers?

A

Bradycardia, AV block

Propanolol - Can cause bronchoconstriction

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16
Q

Examples of Beta Blockers

A

Esmolol (IV, rapid acting), metroprolol, propranolol

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17
Q

How do class III drugs work?

A

Prolong ventricular AP (↑ QT interval)

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18
Q

When do we use Class III drugs?

A

Treatment and prevention of ventricular arrhythmias

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19
Q

Examples of Class III drugs?

A

Amiodarone, sotalol, Ibutilide, Dofetilide (AIDS)

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20
Q

Side effects of class III drugs?

A

Amiodarone: pulmonary fibrosis, hepatotoxicity, thyroid disease

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21
Q

How do class IV drugs work?

A

↓ AV nodal conduction

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22
Q

When do we use class IV drugs?

A

Supraventricular arrhythmias

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23
Q

Examples of Class IV drugs?

A

Verapamil, diltiazem

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24
Q

Side effects of class IV drugs

A

Constipation, bradycardia, AV block

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25
How does Adenosine work and when do we use it?
↓ AV nodal conduction Supraventricular arrhythmias
26
Side effects of Adenosine
Flushing, hypotension, chest pain
27
How does Magnesium work and when do we use it?
We don't know how it works... Use it for Torsades de pointes
28
Side effects of using Mg2+
Respiratory depression
29
What is our "superstar" drug?
Amiodarone!
30
What liver functions can Amioderone afffect and what results from it?
Potent inhibitor of hepatic CYP3A4, CYP2C9; p-glycoprotein (inhibits renal flow)
31
What is automaticity?
In heart physiology, autorhythmicity (also called automacity) is the ability of cardiac cells to depolarize spontaneously, i.e. without external electrical stimulation from the nervous system.
32
What are 3 mechanisms that can cause a Sinus Rhythm to speed up?
Beta-1 stimulation, Hypokalemia, or mechanical stretch
33
What are 3 mechanisms that can cause a Sinus Rhythm to slow down?
ACh, INa blockers (Inward Sodium current), or Adenosine (Ca 2+ blocker)
34
What does Digoxin do and what do we use it for?
Digoxin - used to lower resting potential used to treat arrhythmias complicated by Heart Failure
35
Describe what is meant by slow response cells
Sino-Atrial Node cells (slow response cells) - Phase 0 (upswing/depolarization) is driven by Ca channels - Phase 3 is K channel these cells are ONLY time dependent
36
Describe what is meant by fast response cells
Atrial & Ventricular Muscle Cells (fast response cells) - Phase 0 is driven by INa - Phase 1& 2 (plateau) (2 = absolute refractory period) is driven by Ca channels (ICaL (long), ICaT (transient)) - Phase 3 (relative refractory) is K channel (IK, IK1) These cells are time AND voltage dependent
37
Effect of INa blockers on fast response cells
with INa blockers (Class I), these cells become ONLY time dependent
38
Effect of IK blockers on fast response cells
with IK blockers (Class III), these cells become ONLY voltage dependent
39
What is happening during the p wave?
P wave = SA depolarization
40
What is occurring between P and S
P through QRS = atrial (SA node) depolarization and complete repolarization
41
What is the QRS wave?
QRS = depolarization of the ventricles
42
What is happening with the T wave?
T wave = repolarization of the ventricles
43
What is happening with the QT interval?
QT Interval = complete ventricular depolarization and repolarization
44
many drugs can prolong the time in the QT interval and predispose people to \_\_\_\_\_.
many drugs can prolong the time in this interval and predispose people to arrhythmias
45
How does the Na channel work?
Opens for a VERY short amount of time and gets inactivated via the “ball and chain” mechanism Goes from closed → Open → inactivated → Closed (and repeat)
46
What activates and deactivates the Na Channel?
phosphorylation = inactivation dephosphorylation = activation
47
In the process of the Na channel Goes from closed → Open → inactivated → Closed (and repeat) What portion is slow? Fast?
Closed → Open = fast Inactivated → Closed = slow
48
What part of the Na channel pathway do Na channel blockers act?
Inactivated → Closed = slow this is when Na channel blockers act.
49
What type of channel positions do Na Channel blockers act?
some bind to open some bind to inactivated does not bind to closed state
50
How do Na Channel blockers work?
Na channel blockers decrease the potential at which Na channels can recover
51
What does this show? How do you know? ![](https://lh4.googleusercontent.com/-KZ28ivGSEklAVpKB24oiMuup8rnEzBRwCZz1mGIHVh5qnxhJEfxkG4p8TOTiXHCq9bY6FbyBZ2SeDJi_SkTmk-InKnzRQYaQyEQb-2faX7VBYpf6vhUBtBjHtu-inXE9Q)
Sinus tachycardia (A); arrows = P waves
52
What does this show? How do you know? ![](https://lh3.googleusercontent.com/IyUqg5KMJWgNIBH8FpKAQLJ-72yBy_rIU2hyBDdbIKSJbdJwXr5fkSReVUfjJF_8RN-tXQpkAxqwJyxtiwTOBv7arNWhT_7Qf-OvvjEkex6gD96iBy3SvJ4C4c3g6MoCNQ)
Sinus bradycardia (B); arrows = QRS complex (P wave = tiny)
53
What does this show? ![](https://lh6.googleusercontent.com/1iZdiU5TkwOH4kpTD8wT0Qiw_umsOO_Z4r_ruByfctx5xLD3XJewdSKVjwECh6cI0E_N1Pb4HTbTNGPnajX1SMmVGdqLU9LIyp73gdefABWR8PstVmxO_KX-4FNmH6fJFg)
Irregular Arrhythmia
54
Arrhythmias due to conduction issues are treated how? What is happening in these cases?
If Vagal input becomes too high, you can get P waves without associated QRS complexes, because the AP cannot get passed the AV node No drugs to treat this, we just use pacemakers
55
Effect of Class Ia, b, and c drugs on the ventricular action potential:
![](https://lh4.googleusercontent.com/Xo2oIQifj0iN5UpoRKgQMi1a_DjUZHoH8zEI9c7NG4MdDfPoSRmsHX6xmmQXPcnc2PZdfAF8jyW7qmy4pNIZyZfTs4lmP-uJwnwzngWRmcDwO_UJnVx2M5TyVZvw1wDFEw)
56
Clinically, what do we use for supraventricular tachycardia?
IV adenosine and Verapamil
57
Clinically what do we use for Atrial Fibrillation with heart failure?
Digoxin
58
Clinically, what do we use for non-life threatening tachycardia?
Beta blockers
59
Clinically, what do we use for Ventricular tachcardia?
IV Amiodarone, Lidocaine, Sotalol, Procainamide
60
What is the first and most important therapeutic principle of antiarrhythmic drugs?
Identify and remove the precipitating factors (Hypoxia, ischemia, electrolyte disturbances, diseases, etc)
61
There are two main mechanisms that generate arrhythmias, what are they?
1. reduce automaticity 2. increase refractoriness
62
How can we reduce automaticity?
decrease phase 4 slope increase threshold increase maximum diastolic potential increase AP duration
63
How can we increase refractoriness?
blockade of Na channels prolong action potential (K channels)
64
Where does Atropine do its thing?
M2 neurotransmitter receptor
65
Where does Digoxin do its thing?
Na/K ATPase pump
66
Compare the Cardiac EKG phases of a pacemaker vs. standard ventricular contraction
![](https://lh6.googleusercontent.com/3grWlzuQyokRo2sOVDtzu2LhQqB3jZU0NQfoZCKIlHcbTEHpXK7Hu8_yvgNHHmUBOQ0vyf9s-EW1rT0qqilsa8EZosJkDZxOMuOaejudIFTx2cfFflwebS5Zepmw0vQdjA)
67
What type of pattern is this? ![](https://lh5.googleusercontent.com/JfWmUnmN6jF8Hs_u8weJ2w7OAUSkgVs0a60ADb5g5r6HeAphChj53qUFF3NWscfJCS7TZxLj83k-GkLsJbDfvCuYQ4Xgf1mUR4ci22U0XSSblDYGnlGLv3BQ1mq7susu_A)
Paroxysmal Super Ventricular Tachy
68
What is PSVT? How do we treat it?
![](https://lh5.googleusercontent.com/a3-csE9gS3yLLtF_sD95GULpr_VAoR9yW6FkBIooASYf-1JoBz7BiitE4QD7RRivcjaHduOSPJeHzcrUDsQerM2EvwssK9MUztr9ca_WPZAbpa97dNQYuTiRSg35GDjfBw)
69
Describe Torsades de Pointes and what it looks like on an ECG
![](https://lh6.googleusercontent.com/IZRQGOWHrub7rC3CxPg-n5zgzz6c3oCxBNhZ-6tw9xNVZb3SeTeiBYdMdCsuCmH7aYDEi_PGB-9-AO2muBnh0rthN1oxqnF4RsPEQHJptGgrf3gutogQGajC6eLvN6SnDw)
70
Explain triggered arrhythmias and the two types
![](https://lh3.googleusercontent.com/crQ64vHbC5mPMQT62Cri796vbg58WNZLrCfaIgqDcXvou1YQPpOdFOiEFGvZFYvOemmyzFdt8zki0TVcRwmW5E0bjq-geJFyH1RjHqDPlWVGEa7EtItBCKSDPr4PZAXDSg)

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