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Last Exam Flashcards

1
Q

Causes of arrhythmias

A

coronary ischemia, tissue hypoxia, electrolyte disturbances, drugs, scarring or overstretching of heart fibers, overstimulation of sympathetic nervous system

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2
Q

Problems when conduction system goes wrong

A
  1. abnormal impulse conduction (SA stops firing, AV picks up and fires at slower rate)
  2. Abnormal impulse formation (early firing, leak of ions, causing everything to depolarize - speeds SA node up)
  3. Combo of both
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3
Q

Downside of anti-arrhythmias

A

All drugs that are used to treat arrhythmias can cause lethal arrhythmias

When you have normal tissues as well as abnormal tissue drugs can induce abnormal arrhythmias

A drug that was helpful when the heart was beating slowly becomes harmful when heart starts to beat fast.

Development of a myocardial infarction due to O2 depletion from suppressing abnormal rhythm

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4
Q

When to treat?

A

too fast, too slow, asynchronous beating

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5
Q

Class 1

A

Sodium Channel Blockade
Sodium channel-blocking drugs
subgroups 1A, 1B, 1C

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6
Q

Class 2

A

Blockade of Sympathetic Autonomic affects in heart-Beta Blockers

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7
Q

Class 3

A

Prolongation of the effective refractory period-Potassium channel blockers

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8
Q

Class 4

A

Calcium Channel Blockade

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9
Q

1A

A

prolong action potential and interact with sodium channel a medium length of time

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10
Q

1B

A

shorten action potential and interact with channel rapidly

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11
Q

1C

A

least effect on sodium channel and dissociate from sodium channel slowly

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12
Q

When do Class 1 work best?

A

Sodium channel blockers work better on cardiac tissue that is rapidly firing (tachycardia) because sodium channels spend more time in an open state

they suppress cardiac conduction more in a person with tachycardia versus a person with normal heart rate.

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13
Q

1A drugs

A

isopyramide (Norpace)
Quinidine (Quinidex)
Procainamide (Procan)

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14
Q

1B drugs

A

Lidocaine (Xylocaine)

Mexiletine (Mexitil)

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15
Q

1C drugs

A

Flecainide (Tambocor)

Propafenone (Rythmol)

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16
Q

MOA of 1A

A

Blocks sodium channel slowing upstroke of action potential, slowing conduction of electrical impulse

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17
Q

S/E of 1A procainamide

A

arrhythmias (torsade de pointes), SLE like syndrome, nausea, diarrhea, hypotension

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18
Q

Is 1A a first line option?

A

procainamide - no, short half life (q6) & bad side affects

quinidine - no, maintains normal sinus rhythm nicely, but increases mortality 2-fold

disopyramide - no, anticholinergic (occasionally used for ventricular arrhythmias)

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19
Q

S/E of quinidine (1A)

A

GI ( N,V,D) 33-50%, cinchonism (HA, dizziness and tinnitus), thrombocytopenia, prolongation of QT interval

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20
Q

drug interactions of quinidine?

A

warfarin & digoxin

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21
Q

S/E of disopyramide

A

Cause heart failure because it has negative inotropic actions (caution in elderly and those with HF), anticholinergic effects

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22
Q

Indications for 1A

A

Conversion/prevention of atrial fibrillation
Atrial flutter
Ventricular tachycardia
Prevention of ventricular fibrillation

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23
Q

1B MOA

A

blocks Na channels, more effect on cells with longer action potential like conduction and ventricular cells less effect on atrial cells

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24
Q

S/E of 1B lidocaine

A

hypotension, CNS (paresthesias, tremor, nervousness), nausea, light headed, slurred speech, seizures, drowsiness

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25
drug interactions of lidocaine (1B)
amiodarone (increased lidocaine levels)
26
How is 1B lidocaine given?
IV
27
when to use lidocaine (1B)?
Often first line to stop ventricular arrhythmias (ventricular tachycardia & prevent ventricular fibrillation) after cardio version or with an MI
28
when don't you use lidocaine 1B?
Should not be used as prophylaxis (to prevent) arrhythmias b/c that increases mortality
29
how is mexiletine given (1B)?
oral
30
S/E of mexiletine (1B)
tremor, gait disturbances blurred vision, lethargy and nausea
31
When is mexiletine used?
Used for long term suppression of ventricular arrhythmias | also helps chronic pain
32
1C MOA
Blocks sodium and potassium channels to a lesser extent and may cause more death than helps
33
Uses for 1C?
Conversion/prevention fo atrial fibrillation, atrial flutter, ventricular tachycardia, prevention of ventricular fibrillation
34
drug interactions for 1C?
digoxin (increases levels) warfarin (increases INR levels)
35
S/E of 1C?
ventricular arrhythmias, agranulocytosis, anemia, thrombocytopenia
36
class 2 uses?
Rate control for atrial fibrillation, atrial flutter, prevention of supraventricular tachycardia, with adjunctive ventricular antiarrhythmic therapy Beta blockers can prevent re-infarction and sudden death after an MI & Class 1s don’t. So they save lives.
37
class 2 agents?
Metoprolol, esmolol (IV), atenolol
38
Class 2 MOA?
Are beta blockers and reduce beta adrenergic activity in the heart. Elicit effect by: - Inhibit sympathetic activation of cardiac automaticity and conduction - Slowing heart rate, decreasing AV node conduction, and increasing AV node refractory period
39
Class 3 MOA?
Prolong the ventricular action potential by blocking rapid component of K+ channel
40
Uses for class 3?
These work best at slower heart rates, not at faster rates when needed most
41
Risk of class 3?
target AP puts pt at risk Slowing action potential at slower rates increases the risk of torsade de pointes
42
Class 3 drugs
``` Amiodarone (Cordarone)* Dronedarone (Multaq)* Sotalol (Betapace)+ Dofetilide (Tikosyn) Ibutilide (Corvert) ``` ``` *Amiodarone & dronedarone have Ib, II, and IV class activity in addition to class III actions +Sotalol has 50%/50% beta blocking properties and potassium blocking properties ```
43
MOA of Amiodarone
Prolong the action potential by blocking rapid component of K+ channel (primary) Also blocks sodium and calcium channels, & beta-adrenoceptors long half life (months) can cause problems due to that
44
Uses for Amiodarone?
- Approved for serious ventricular arrhythmias. - It is a first line drug for prevention of ventricular tachycardia - It does not increase death (like other anti-arrhythmics) - The treatment of first choice for ventricular arrhythmias & sudden death is an implantable defibrillator NOT drugs - If have an defibrillator & it is going off a lot use amiodarone to prevent uncomfortable discharges - Also used for atrial fibrillation. In low doses can keep someone in NSR
45
S/E of Amiodarone**
Cardiac: Bradycardia and heart block & can see prolonged QT on EKG Lung: Fatal pulmonary fibrosis Liver: Hepatitis Skin: Gray-blue skin discoloration Eye: Deposits pigment in retina- get halos; rarely optic neuritis & blindness Thyroid: Has iodine molecules and blocks conversion of thyroid hormone Can make hyperthyroid or hypothyroid*** Check thyroid function tests before start and when on it***
46
**Drug interactions of Amiodarone?
warfarin, digoxin, statins
47
How does dronedarone differ from amiodarone? (class 3)
Analog of amiodarone with a shorter ½ life (1 to 2 days vs. months) and the potential for less thyroid and pulmonary toxicity. Less effective in maintaining NSR than amiodarone
48
use of dronedarone? (class 3)
prevention of atrial fibrillation/flutter
49
S/E of dronedarone (class 3)
nausea, vomiting, diarrhea, abdominal pain, liver toxicities
50
MOA of sotalol? (class 3)
Beta blocker and action potential prolonging therapy by blocking potassium channels responsible for repolarization
51
uses for sotalol? (class 3)
for life threatening ventricular arrhythmias and maintenance of normal sinus rhythm (NSR) in atrial fibrillation
52
ADRs of sotalol? (class 3)
torsade de pointes, HF, bradycardia, AV block, wheezing, fatigue
53
Uses of Dofetilide? (class 3)
Conversion/prevention of atrial fibrillation/flutter
54
S/E of dofetilide? and special considerations? (class 3)
QT prolongation*, torsades de pointes, headache, dizziness Initial administration done in hospital under careful monitoring due to ADR
55
Uses for Ibutilide? (class 3)
IV, for rapid conversion fo recent onset of atrial fibrillation/flutter
56
S/E of ibutilide? (class 3)
torsades de pointes, hypotension, nausea
57
MOA of dofetilide and ibutilide? (Class 3)
target K channels
58
Class 4 MOA?
- Block the calcium channel - Do not work equally well in all cardiac cells. - These drugs work primarily in cardiac cells where the action potential upstroke is dependent on calcium i.e. SA and AV node
59
Class 4 drugs?
Diltiazem & verapamil
60
MOA of verpamil & diltiazem as antiarrhythmics?
Prolong conduction through the AV node & SA node
61
Uses of verapamil & diltiazem?***
- Supraventricular tachycardia (SVT; in other words non-ventricular tachycardia) - Reduce the rate in which the impulses go through the AV node. - Atria still beats fast but many of impulses get blocked at AV node so don’t send as many impulses to the ventricle which is the main pump
62
S/E of verapamil and diltiazem?
If give to someone with a misdiagnosed rhythm (think SVT and really is ventricular arrhythmia) can kill
63
Drugs that decrease conduction velocity?
1a, 1b, 1C**, class 4
64
drugs that increase refractory period
1a, class 2, class 3***, a little of class 4
65
drugs that decrease refractory period?
1b, some class 4
66
adenosine* MOA
activates K+ and inhibits influx of calcium in SA node, atrium and AV node. Works in AV node>>SA node
67
why do we like adenosine?
Half-life: 10 seconds
68
S/E of adenosine?
*flushing (20%), SOB and chest *burning (10%), less common HA, low BP, nausea and paresthesias, bronchospasm
69
Uses of adenosine?
- 1st choice for conversion of SVT to sinus rhythm because works and is gone fast - Slows conduction through AV node & increases AV node refractory period - In fact AV node conduction can be completely blocked for a few seconds, resulting in brief asystole
70
uses of magnesium?
- To treat digitalis induced ventricular arrhythmias - To suppress drug-induced torsades de pointes - To treat supraventricular arrhythmias associated with magnesium deficiency
71
MOA of magnesium?
IV, Magnesium is a very common intracellular cation with many roles in normal cardiac function
72
MOA potassium?
- Increasing potassium in the blood depresses ectopic pacemakers (tissue other than the conduction system depolarizing) and slows conduction - Too high or too low can increase arrhythmias, so need to normalize
73
principles of antiarrhythmics?
- Treatment of many arrhythmias are complicated & often handled by cardiologist - Not all arrhythmias need to be treated - If there is a risk of sudden death implantable defibrillator is the only thing to decrease mortality - Atrial fibrillation is a common arrhythmia often treated in primary care - Remember: Any drug that treats arrhythmias can cause one
74
What is A-fib?
Disorganized electrical impulses
75
options for a-fib?
BB or CCB

Pharm 5 (8 decks)

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