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hlsc 220- midterm 2 > Antidysrhymic Drugs > Flashcards

Antidysrhymic Drugs Flashcards

(56 cards)

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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

Study These Flashcards
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

Study These Flashcards
A

I: eliminates block in branch 1

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

24
4 groups of Antidysrhythmic Drugs
Class I: sodium channel blockers class II: beta blockers class III: potassium channel blockers class iv: calcium channel blockers
25
class I drug function
sodium channel blockers slows impulse conduction in atria, ventricles and His-Purkinje system
26
Class II function
Beta blockers reduce calcium entry = SA (reduce automaticity), AV (slow conduction), atria/ ventricle, reduces contractility
27
Class III function
Potassium Channel Blockers delay repolarization - prolong action potential and refractory period
28
Class IV function
calcium channel blockers Verapamil/diltiazem/ same effects as Class II --> reduce calcium entry
29
2 groups of dysrhythmias
1) Supraventricular (above ventricle) 2) Ventricular (more dangerous)
30
2 phases of treatment for dysrhythmias
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
Treatment for Supraventricular Dysrhythmias (SA) arise in SA and AV node
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
Treatment for Atrial Fibrillation
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
Sustained Supraventricular Tachycardia
due to AV node Re-entrant activation = HR 200 bpm Treatment: IV beta blocker or calcium channel blocker
34
Ventricular Dysrhythmias
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
Ventricular Tachycardia
Arise from SINGLE rapid firing ectopic focus - generally location of an old infarction Long-term Treatment: ICD Amiodarone
36
Torsades de Pointes
potentially fatal dysrhythmia due to PROLONGATION OF QT INTERVAL Treatment Class I or III drugs
37
Class I : Sodium Channel Blockers drug name
Quinidine source: natural source from bark of Cichona Tree
38
Mechanism of Class 1: Sodium Channel Blockers
Blocking Na+ channels = widening of QRS by slowing ventricle depolarization and increase QT (delays repolarization
39
Class I Adverse Effects
Diarrhea: immediate and intense - can result in treatment being discontinued Cardiotoxicity: high conc. of quinidine = disrupt ventricle contractions
40
Class I Drug Interactions
Quinidine can double Digoxin levels
41
Class II Drug Interactions
Propranolol
42
Class II mech of action
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
Class II Therapeutic Use
treating dysrhythmias caused by excessive Sympathetic NS stimulation
44
Adverse Effects
Heart: cause heart failure, AV block Lungs: asthma pts can cause bronchospasm
45
Class III drug name
Amiodarone
46
Class III mechanism
delay repolarization in fast potentials (SA, AV) Prolonged action potential duration and QT interval
47
Class III therapeutic Use
effective against atrial and ventricle dysrhytmias -serious toxicities PO and IV
48
Class III Adverse Effects
Lung damage main concern in high-dose, long-term patients, visual impairment still frequently used
49
Class IV drug name
Verapamil and Diltiazem
50
Class IV mechanism of action
Slow ventricular rate in atrial fibrillation patients IV: effects in minutes
51
Class IV adverse effects
bradycardia av block heart failure
52
Class IV drug interactions
Elevate Digoxin levels - digoxin toxicity
53
Other antidysrhythmic drugs
Adenosine Digoxin
54
Adenosine
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
Digoxin
Primary indication is heart failure suppresses dysrhythmias by decreasing automaticity of AV node and conduction through AV node adverse effects: dysrhythmias

hlsc 220- midterm 2 (9 decks)

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