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hlsc 222- midterm 2 > Antidysrhymic Drugs > Flashcards

Antidysrhymic Drugs Flashcards

1
Q

Dysrhythmia

A

abnormaility in rhythm of heartbeat

  • if severe can disable heart so NO BLOOD PUMPs
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2
Q

2 types of dysrhythmia

A

Tachydysrhythmias- increased HR
Brady dysthrhythmias-
decreased HR

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3
Q

what is important to know before prescribing antidysthmias drugs

A
  • can cause dysrhythmias
  • increased risk of death
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4
Q

what is replacing antidysrhythic drugs

A

Implantable defibrillators

Arrhythmia radio frequency ablation- destroys cells that cause dysrhythmias

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5
Q

What do dysrhythmias result from?

A

alternation of cardiac electrical impulses

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6
Q

SA node

A

heart PACEMAKER
- spont. depolariztion
- atria contracts in unison

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7
Q

AV node

A

impulse delayed
- allows complete atrial contraction

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8
Q

His-Purkinjie System

A

spreads impulse rapidly to all parts of ventricles
- ventricles contract in unison

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9
Q

2 kinds of cardiac action potentials

A

1) fast potentials
- contractile cardiac tissue

2) Slow potentials
- self-excitable cardiac tissue

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10
Q

Fast Potentials- what happens

A

0: depolarization
- influx of Na+
- drugs that block Na+ channels slow ventricle depolarization

  1. Rapid, partial repolariztation
    - no effects of drugs
  2. Prolonged plateau
    - drugs that reduce calcium influx reduce myocardial contractility
  3. Rapid depolarization due to efflux K+
    - K+ channel blockers delay polarization
    = prolonged time between 2 heartbeats
  4. Under pathological conditions depolarization may occur in all cardiac cells
    - dysrhythmia
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11
Q

Slow potential Pathway
Draw it too :)

A
  1. depolarization by slow influx of Ca2+
    - drugs that suppress Ca2+ influx slow/stop AV node contraction

2 and 3. repolarization
- NO effect of drugs here

  1. SA node and AV node cells begin next depolarization
    - beta blockers and calcium channel blockers suppress here = decrease SA node activity
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12
Q

ECG measures

A

electrical activity of Fast Potentials
-CONTRACTILE CELLS

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13
Q

DRAW ecg normal

A

P wave
Q, R, S
T wave

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14
Q

PR interval

A

lengthening
- conduction delayed through AV node
- several drugs increase PR interva

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15
Q

QRS will widen if

A

conduction through ventricles is slowed

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15
Q

QT interval is prolonged by

A

prolonged by drugs that delay ventricular repolarization

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16
Q

ST segment
what drug depresses it

A

end of QRS to beginning of T

Digoxin depresses ST segment

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17
Q

2 causes of Dysrhythmias

A

1) Disturbances of impulse formation (automaticity)

2) Disturbances of impulse conduction

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18
Q

Causes of Dysrhythmias
(6)

A

hypoxia
electrolyte imbalance
cardiac surgery
reduced coronary blood flow,
myocardial infarction (MI)
antidysrhythmic drugs

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19
Q

disturbance of impulse formation

A

occur in cells capable of automaticity, but can occur in others that don’t express automaticity (contractile cells)

increased Purkinje fiber automaticity
- Common cause of dysrhythmias

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20
Q

Disturbances of impulse conduction

A

first degree block: impulse is delayed but NOT blocked

second degree block: some impulses go through but not others

Third degree block: all traffic through AV node stops

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21
Q

Re-entry (recirculating Activation)

A

mechanism that produces dysrhythmias

started by a self-sustaining circuit of repetitive cardiac stimulation

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22
Q

Re-entrant Activation

A

one-way conduction block

impulses can’t travel downward in Branch 1
BUT can travel upward in branch 1 (because muscle impulses are very strong)

Results: impulse travels up Branch 1, and then back down Branch 2

Process continues to repeat itself
= repetitive ectopic beats

23
Q

Drug Effect I and II

A

I: eliminates block in branch 1

2: drug converts one-way block to a two-way block

24
Q

4 groups of Antidysrhythmic Drugs

A

Class I: sodium channel blockers

class II: beta blockers

class III: potassium channel blockers

class iv: calcium channel blockers

25
Q

class I drug function

A

sodium channel blockers

slows impulse conduction in atria, ventricles and His-Purkinje system

26
Q

Class II function

A

Beta blockers

reduce calcium entry
= SA (reduce automaticity), AV (slow conduction), atria/ ventricle, reduces contractility

27
Q

Class III function

A

Potassium Channel Blockers

delay repolarization
- prolong action potential and refractory period

28
Q

Class IV function

A

calcium channel blockers

Verapamil/diltiazem/ same effects as Class II
–> reduce calcium entry

29
Q

2 groups of dysrhythmias

A

1) Supraventricular (above ventricle)

2) Ventricular (more dangerous)

30
Q

2 phases of treatment for dysrhythmias

A

1) dysrhythmia termination
- electrical countershock, drugs, or both)

followed by

2) long-term suppression with drugs

can also be treated with
-ICD: fxns as pacemaker and defibrillator
- destroying small areas of cardiac cells

31
Q

Treatment for Supraventricular Dysrhythmias (SA)
arise in SA and AV node

A

only dangerous if results in increased rate of ventricular contraction
= ventricle filling imcomplete and CO reduced

Treatment: block impulse through AV node
- not by eliminating dysthymia itself

Drug Class II, Class IV, adenosine and digoxin

32
Q

Treatment for Atrial Fibrillation

A

most common sustained dysrhythmia
- rapid random firing of atrial ectopic foci
- high risk of stroke (potential clot formation)

Treatment: beta blocker = restore normal rhythm or slow ventricular rate
Warfarin to prevent stroke

33
Q

Sustained Supraventricular Tachycardia

A

due to AV node Re-entrant activation
= HR 200 bpm

Treatment: IV beta blocker or calcium channel blocker

34
Q

Ventricular Dysrhythmias

A

LIFE threating emergency

Cause:
multiple ventricular ectopic foci firing
localized twitching takes place all over the ventricle
= coordinated contraction IMPOSSIBLE

Result:
loss of consciousness and tissue become CYANOTIC/ DEATH soon follows

Treatment:
Immediate defibrillation
Amiodarone

35
Q

Ventricular Tachycardia

A

Arise from SINGLE rapid firing ectopic focus
- generally location of an old infarction

Long-term Treatment:
ICD
Amiodarone

36
Q

Torsades de Pointes

A

potentially fatal dysrhythmia due to PROLONGATION OF QT INTERVAL

Treatment
Class I or III drugs

37
Q

Class I : Sodium Channel Blockers drug name

A

Quinidine

source: natural source from bark of Cichona Tree

38
Q

Mechanism of Class 1: Sodium Channel Blockers

A

Blocking Na+ channels
= widening of QRS by slowing ventricle depolarization and increase QT (delays repolarization

39
Q

Class I Adverse Effects

A

Diarrhea: immediate and intense
- can result in treatment being discontinued

Cardiotoxicity:
high conc. of quinidine = disrupt ventricle contractions

40
Q

Class I Drug Interactions

A

Quinidine can double Digoxin levels

41
Q

Class II Drug Interactions

A

Propranolol

42
Q

Class II mech of action

A

beta blockers act on calcium channels

blocks beta1 (heart) and beta2 receptors (lungs)

decreases SA node automaticity
Decreased AV node conduction

Decreases myocardial contractility

Prolongs PR interval

43
Q

Class II Therapeutic Use

A

treating dysrhythmias caused by excessive Sympathetic NS stimulation

44
Q

Adverse Effects

A

Heart: cause heart failure, AV block

Lungs: asthma pts can cause bronchospasm

45
Q

Class III drug name

A

Amiodarone

46
Q

Class III mechanism

A

delay repolarization in fast potentials (SA, AV)

Prolonged action potential duration and QT interval

47
Q

Class III therapeutic Use

A

effective against atrial and ventricle dysrhytmias
-serious toxicities

PO and IV

48
Q

Class III Adverse Effects

A

Lung damage main concern in high-dose, long-term patients, visual impairment
still frequently used

49
Q

Class IV drug name

A

Verapamil and Diltiazem

50
Q

Class IV mechanism of action

A

Slow ventricular rate in atrial fibrillation patients

IV: effects in minutes

51
Q

Class IV adverse effects

A

bradycardia
av block
heart failure

52
Q

Class IV drug interactions

A

Elevate Digoxin levels
- digoxin toxicity

53
Q

Other antidysrhythmic drugs

A

Adenosine

Digoxin

54
Q

Adenosine

A

drug choice for Supraventricular Dysrhythmias (SRV)

Mechanism
inhibition of cAMP-induced calcium influx
= decreased automaticity in SA node and slows conduction through AV node

IV

55
Q

Digoxin

A

Primary indication is heart failure

suppresses dysrhythmias by decreasing automaticity of AV node and conduction through AV node

adverse effects: dysrhythmias

hlsc 222- midterm 2 (9 decks)

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