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Final Test: Dynamics II > Anti-arrhythymic drugs > Flashcards

Anti-arrhythymic drugs Flashcards

1
Q

What are the effects of sodium channel blockade?

A

-decreased excitability and automaticity -decrease conduction velocity to fast response cells -increase refractoriness

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2
Q

What are the type IB drugs and what is their action?

A

sodium channel blockers Names: lidocaine phenytoin tocainamid mexiletine

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3
Q

What is the half life of procainamide?

A

1

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4
Q

What is the metabolite of procainamide? and what is its effect on various channels?

A

1

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5
Q

How is the metabolite of procainamide eliminated?

A

1

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6
Q

What are the side effects of procainamide?

A

1

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7
Q

What is the effect of lidocaine and what does it do?

A

blocks open and inactivated sodium channels

its an amide local anesthetic

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8
Q

What is the main use of lidocaine? and when is it not useful?

A
  1. treats ventricular tachycardia or fibrillation thru IV
  2. lowers incidence of VF in patients with acute MI
  3. used for ventricular arrhythmias during cardiac manipulations, like surgery
  4. DONT use to treat arrhthmias
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9
Q

How can lidocaine not be given and why is this?

A

not give orally because first pass;

also b/c need rapid action to treat VF and VT

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10
Q

What are the side effects of lidocaine?

A
  1. seizures
  2. other CNS side effects if large dose is given rapidly
  3. malignant hypetermia produced
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11
Q

Which drugs are analogs of lidocaine?

A

mexiletine

tocainide

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12
Q

What is the use of phenytoin?

A
  1. anticonvulsant drug (grand mal or psychomotor seizures)
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13
Q

How does phenytoin work?

A

binds to INACTIVE sodium channels–has a rapid recovery from block

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14
Q

What is the phenytoin route in the body and because of this what must be done?

A

undergoes extensive first pass metabolism, saturable

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15
Q

Describe the toxicity of phenytoin?

Side effects?

A

small increases in doses can create large amount in plasma blood= toxic

correct plasma levels based on albumin

CNS side effects:

  1. ataxia (incoordination)
  2. nistagmus
  3. mental cofusion
  4. slurred speech
  5. gingival hyperplasia
  6. rash or fever

Hematologic:

  1. bone marrow depression
  2. low WBC counts
  3. low platelets
  4. macrocytosis
  5. megaloblastic anemia (sensitive to folic acid)
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16
Q

What are the type IC drugs?

A

they are sodium channel blocker w/ potassium channel blocker activity

Names:

flecainade

-propafenone

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17
Q

What is the action of flecainide?

A

binds sodium channel when OPEN, long recovery time

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18
Q

What are the indications/uses for flecainide?

A

ONLY for life-threatening refractory arrhythmias

if it is used for atrial flutter or fibrillation- use beta blockers or digoxin

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19
Q

What is the action of propafenone?

A

same as flecanide but has beta adrenergic blocking activity;

will under go extensive first pass metabolism and has zero order kinetics

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20
Q

What are the indications for propafenone?

A
  1. dangerous because has strong proarrhythmic action
  2. used to treat ventricular arrhythmias (sustained ventricular tachycardia)
  3. used to maintain supraventricular tachycaridas, including atrial fibrillation
  4. watch ANA titers
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21
Q

How is propafenone broken down?

A

extensive first pass

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22
Q

What must be monitored while taking propafenone?

A

ANA titers

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23
Q

What are the type II antiarrhythmic drugs? Name some examples.

A

they are beta blockers

Names:

propranolol

sotalol

acetobutolol

esmolol

metoprolol

nadolol

atenolol

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24
Q

How do type II anti-arrhythmics work?

A
  • inhibit SNS stimulation on the heart
  • reduce automaticity
  • prolong AV conduction time
  • decrease myocardial contractility

but they do prevent epinephrine induced hypokalemia

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25
What is an important action of type II anti-arrhythmic drugs?
increase threshold to reach ventricular fibrillation, less death after myocaridal infaraction
26
What are the important uses of type II anti-arrhythmic drugs?
1. control the ventricular response with atrial fibrillation and flutter used with caution if function is depressed
27
What are the side effects for type II anti-arrhythmic drugs? What can happen if they are abruptly stopped?
Same as those for beta blockers can get rebound symptoms if stopped abruptly such as increase in blood pressure, angina pectoris, and arrhymias have a membrane stablizing effect
28
Why would type II anti-arrhythmic drugs have a membrane stabilizing effect?
due to inhibition of sodium channels
29
What is sotalol?
non selective beta blocker but also block potassium current
30
What effect does sotalol have on the QT interval on ECG?
prolongs action potential duration and QT interval
31
What are the actions of sotalol?
1. blocking beta receptors + potassium current: drug decreases automaticity, slows AV conducation, and prolong refractoriness
32
What are some of the uses of sotalol?
management of ventricular arrhythmias
33
What are some side effects of sotalol?
increases incidence of Torsades de pointses, esp. if hypokalemia is present
34
What is esmolol?
a cardioselective drug,
35
What is the course of esmolol in the body: waht is the half life, how is it broken down, etc?
has a very short half life of 9 minutes metabolized within central compartment---\> esterases present in red blood cells
36
What are type III anti-arrhythmics? Give examples.
potassium channel blockers; prolong phase 3, AP, and prolong QT Names: bretylium amiodarine sotalol dronedarone ibutilide dibutilide
37
What is the function of type III anti-arrhythmics?
potassium channel blockers
38
What is the action of bretylium?
* prolongs AP * reduces heterogeneity of repolarization times * induce transient hypertension from NE release
39
What are some side effects of bretylium?
* decrease norepinephrine release * hypotension
40
What are some good features about bretylium (see molecular structure)?
doesn't get into brain because of quaternary ammonium compound
41
What is the amiodarone?
classified as a type III but as all effects Type 1B: blocks inactive sodium channels, revocery from block rapid Type IV: decreases Ca++ current Type III: decreases K+ currents Type II: noncompetitive beta blockers anti-thyroid action
42
Classify the effects of amoidarone? Type IB Type IV Type II Type II thyroid
1
43
On an ECG, what effect would amoidarone have?
see cards
44
What are the current indications for amoidarone?
IV: treats ventricular fib. and unstable ventricular tachycardia oral therapy: VT and VF resistant to other drugs
45
What are the molecular features of amoidarone?
highly lipophilic concentrated in tissues, slowly accumulates( loading regimen), slowly eliminated
46
What is it metabolized into?
metabolized to desethyl-amiodarine---\> pharmacological activity of parent drug potent inhibitor of hepatic metabolism and renal elimination of many drugs
47
What are amoidarone drug interactions?
potent inhibitor or hepatic metabolism and or renal eliminati of many drugs increases effects * digoxin * quinidine * procainamid * fentayl * warfarin * dextromethophan * cyclosporin * cholestriamine and phenytonin---\> may decrease amoidarone levels * beta blockers used with care-----\> both have beta blocking activity * additive effects (verapamil and diltiazem)----\> AV block-----\> bradycardia and depressed myocardial contractility
48
What serious adverse events have been reported with chronic treatment of amoidarone?
pulmonary fibrosis: doses greater than 100mg/day hepatic dysfunction or hypo or hyperthyrodism, neuromuscular symptoms corneal micodeposits
49
When is IV amiodarone contraindicated? What are the side effects?
* cardiogenic shock * marked sinus bradycardia * second or thrid degree AV block * Side effects * hypotension * bradycardia * arrhythmia
50
What are type IV antiarrhythmics? Give examples.
Calcium channel blockers Names: - verapamil - diltiazem - bepridil (type III effects- blocks K+ channels ) - adenosine - magnesisum
51
What are the most common type of IV antiarrhythmics and how do they affect the body?
most common: verapamil, diltiazem, and bepridil major effects in SA nodes and AV nodes * AV conduction velocity decreases and refractoriness increases: explains efficacy in supra-ventricular tacycardia, reentrant arrthmias whose circuit involves the AV node * reduce ventricular rate in atrial flutter and fibrillation * can induce bradycardia * reduced cardiac contractility and BP (effects of drugs) *
52
What are the indications and uses for type IV anti-arrhythmics?
1
53
What is bepridil and what is its action?
* in addition to CCB action * increases AP duration (type III)---\> antiarrythmic and pro-arrhythmic effects
54
When are CCB's contraindicated?
don't give with patient on concomitant beta blocker---can induce severe bradycardia, AV node blockage, hypotension, depression of cardiac contracitlity-CHF
55
Name some other anti-arrhythmics?
adenosine
56
What are the actions of adenosine?
specific adensoine receptors; activates potassium currents in the atrium, SA, and AV nodes increase in potassium current hyperpolarizes, inhibits automaticity, and shortens AP duration
57
What are overall effects of adenosine?
inhibits automaticity, hyperpolarizes and shortens AP duration
58
What is the effect of adenosine and the AV node?
slows down conduction time in the AV node (AV node block) may produce a transient asystole less than 5 sev
59
What is the use of IV bolus of adenosine?
1. acute termination of reentrant supraventricular arrhythmias
60
What can happen when a large doses of adenosine?
induces hypotension and flushing due to peripheral vasodilation
61
What is adenosine's course of action in the body, how is it metabolized, what is its half life?
half life is secondsl immediately carrier mediated uptake into most cells where it is metabolized must be give rapid IV bolus through large central IV line

Final Test: Dynamics II (11 decks)

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