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23 spring: med surg > Test 1: lecture 8 arrhythmias > Flashcards

Test 1: lecture 8 arrhythmias Flashcards

1
Q

antiarrhythmic drugs have no guarantee to —

A

prevent sudden death

can help decrease signs: syncope, weakness and CHF

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2
Q

3 major causes of arrhythmias

A

abnormal impulse generation
triggered activity
abnormal impulse conduction

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3
Q

altered automaticity of sinus node will cause

A

increased= too fast= sinus tach= increased sympathetic tone

decreased= too slow= sinus bradycardia = increased vagal tone

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4
Q
A

ventricular premature contractions

wierd and wide QRS

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5
Q

abnormal automaticity in myocardium leads to

A

ectopic beats

can be atrial or ventricular premature beats or tachycardia

caused by disease myocardium sending off signals when it should not

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6
Q

early afterdepolarization

A

EAD

arrhythmia caused by early impulse
is AP duration is prolonged
can be genetic defect in german sheperds
can be drug toxicity

leads to Vtach

goal is to shorten action potenial to skip these extra beats

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7
Q

delayed afterdepolarization

A

is calcium overload
can be from digoxin toxicity
leads to Vtach

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8
Q

if conduction velocity is too fast leads to

A

atrial or ventricular tachycardia

want to slow conduction to allow for normal HR

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9
Q

what can cause too low conduction velocity in the heart

A

AV block

leads to bradycardia

P waves do not lead to QRS, only ventricular contraction from escaped PVCs

need to fix through pacemaker

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10
Q

how does reentry cause arrhythmia

A

impulse hits obstacle

new impulse comes quickly and one lead unable to depolarize in time, allows impulse to loop around itself

Cardiac impulse is not completing the normal conduction pathway due to a block, but following an alternative circuit around the blocked area and looping back upon itself

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11
Q

what is needed for reentry to occur

A

premature beats

variable conduction velocity (block or damage that delays depolarization)

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12
Q

how to treat arrhythmias due to reentry

A

slow spontaneous depolarization
and conduction velocity

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13
Q

what are some common arrhythmias caused by reentry

A

Afib
AV reentry trachycardia
Vtach or Vfib

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14
Q
A

A fib

no P wave- wiggly baseline
R-R interval irregular

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15
Q
A

Vtach/ V fib

wierd and wide QRS
very fast
can’t see P waves

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16
Q

fast depolarization of Purkinje fibers, atrial / ventricular myocardial cells is by

A

sodium (Na) channels

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17
Q

repolarization of Purkinje fibers, atrial / ventricular myocardial cells is by

A

potassium (K)
leaving cell

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18
Q

slow depolarization of sinus node and AV cells is by

A

calcium

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19
Q

slow spontaneous depolarization of sinus node and AV cells is by

A

sodium (funny channels→slow leak)
calcium

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20
Q

class I antiarrhythmic

A

Na channel blockers

(prevents Na into cell, slows down depolarization of myocardial cells)

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21
Q

class II antiarrhythmic

A

beta-adrenergic blocker

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22
Q

class III antiarrhythmic

A

potassium channel blocker

prevents K from leaving cell, causes slower repolarization, leads to longer space between beats

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23
Q

class IV antiarrhythmic

A

calcium channel blockers

prevents depolarization of nodal cells

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24
Q

class I antiarrhythmic will work by — conduction velocity and suppress abnormal —

A

na channel blocker

slows conduction velocity of myocardial cells
→cause decrease in slope and disrupts reentry circuits

suppress abnormal automaticity in sick non-nodal tissues
→will slow down phase 4
→non-nodal tissues should not have automaticity (drug will stop them from beating on their own)

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25
Q

— is a class IB antiarrhythmic

A

lidocaine

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26
Q

ventricular arrhythmias can be treated with — antiarr

A

class I: Na channel blockers
ex: lidocaine (class 1B)

class III: K channel blockers
ex. sotalol

a little by class II Beta blockers (—olol), but they mostly decrease SYM to SA node cause decreased HR

27
Q

why do class I anti-arrhy not cause bradycardia

A

effects the non-nodal tissues by blocking Na channels

does not cause change in nodal cells (sinus or AV node)

class I good for ventricular arrhythmias

28
Q

what class of drug does this

A

class I- antiarrhythmic

Na channel blocker (lidocaine class Ib)

29
Q

lidocaine is what class of drug and is used for

A

Class 1b antiarrhythmic

can only be given IV

used for Vtach

can cause depression, seizures (cats) vomiting
can cause transient hypotension under GA

30
Q

side effects of lidocaine

A

Depression, seizures (cats are more sensitive), vomiting
transient hypotension noticed under GA

Class Ib anti-arrhythmic - Na channel blocker used for Vtach

31
Q

what drug

A

lidocaine

treat Vtach

Class Ib anti-arrhythmic - Na channel blocker used for Vtach

32
Q

how does class II anti-arrhythmic work

A

beta blocker

blocks sympathic tone to the heart

reduces HR by slowing sinus node

33
Q

beta blockers are — drugs

A

class II antiarrhythmics

34
Q

— is a 2nd gen class II antiarrhythmic

A

atenolol- selective for β1 receptors

beta blocker: slows down HR by slowing down impulse of sinus node

used for supraventricular arrhythmias: Afib, or tachycardia (feline hyperthyroidism)

35
Q

what are some side effects of Class II anti-arrhythmics

A

beta blockers

negative inotrope: can cause reduced myocardial contractility and cardiac output

can worsen CHF and cause hypotension

atenolol is a 2nd gen class II AA

36
Q

how to treat

A

atrial tachycardia

give beta blocker (IV esmolol)

will slow HR by slowing conduction through AV node → can cause AV block (P wave no QRS)

atenolol and esmolol (2nd gen class II beta blockers)

37
Q

how does class III AA drug work

A

potassium channel blocker

prolongs repolarization: makes the AP all the same length (widens)

does not effect the conduction velocity

used for ventricular arrhythmias

L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization)

38
Q

— is a class III AA

A

L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization)

used for ventricular arrhythmias

39
Q

how does class III AA effect reentry

A

L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization): prevents ventricular arrhythmias

40
Q

sotalol is —

A

L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization): prevents ventricular arrhythmias

41
Q

what will sotalol do

A

L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization): prevents ventricular arrhythmias

before had sustained Vtach now has sinus rhythm with occasional VPCs

42
Q

— class of AA will slow AV nodal conduction

A

IV

calcium channel blocker

43
Q

— is a class IV AA

A

diltiazem

calcium channel blocker: will slow AV nodal conduction

will slow Afib, will stop supraventricular reentry arrhythmias in the AV node

44
Q

diltiazem is used to slow conduction through —

A

AV node

class IV: calcium channel blocker

used to stop/slow supraventricular arrhythmias such as Afib

will also stop reentry through the AV node

45
Q

will diltiazem effect Vtach?

A

no

class IV calcium channel blocker
will slow supraventricular arrhythmias such as Afib, by slowing conduction through the AV node

46
Q

— is a calcium channel blocker used to relax vascular smooth muscle

A

will cause hypotension

amlodipine

calcium channel blocker= class IV AA

DOES NOT effect HR like other class IV AA diltiazem which slows conduction through AV node to stop AFib

47
Q

digoxin is used for

A

slows ventricular response rate in Afib

will slow AV nodal conduction
parasympathomimetic effect

48
Q

— are parasymptholytics that stop bradycardia

A

Atropine, Glycopyrrolate

49
Q

rapid Afib should be teated with

A

digoxin: acts as parasympathomimetic, slows AV nodal conduction

diltiazem: class IV calcium channel blocker, will slow conduction through the AV node

50
Q

how to treat Vtach

A

If VT rate is rapid over several seconds: can cause
weakness or collapse (poor cardiac output)

  • If very rapid Þ If R on T phenomenon: VT can
    degenerate into ventricular fibrillation (VF) Þ sudden
    death!
  • Class I or class III antiarrhythmic drugs

class I: Na channel blocker: slowss conduction, suppresses abnormal automaticity from non-nodal tissue: lodocaine Ib

class III:K channel blocker: makes long repolarization: sotalol

51
Q
A

V fib!

must shock back to rhythm

52
Q

how to treat 3rd degree AV block

A

**no conduction through AV node

atria beating according to SA node

ventricles beating according to ventricle pacing/escape beat (very slow)

need to place pacemaker

53
Q

how would you treat

A

pacemaker

sick sinus syndrome
bradycardia with long pause and escape beat

54
Q

how to place pacemaker

A

through jugular vein

Lead tip is advanced in RV apex

Pacemaker generator in
subcutaneous pouch in neck

After 2 months the tip is fully scarred into the chamber wall

55
Q

how to treat bradycardia

56
Q

how to treat SVT other then Afib

57
Q

how to treat AFib

58
Q

how to treat Ventricular arrhythmias

graph

59
Q

how to treat Vfib

graph

60
Q

— class cause Reduce slope of phase 0 and peak of AP

A

class I
na channel blockers

lidocaine

61
Q

— class will cause Small reduction in phase 0, shortens APD, decreases ERP, increases post-repolarization refractoriness

A

class I
na channel blocker
IB: lidocaine

62
Q

— class of AA will Slows rate of spontaneous depolarization and conduction velocity in SA and AVN

A

type II beta blocker

atenolol, esmolol

63
Q

— class of AA will cause Markedly prolongs repolarization (phase 3), lengthen ERP and APD

A

class III: K channel blockers

Amiodarone
Sotalol

64
Q

— class of AA will cause Slows rate of spontaneous depolarization and conduction velocity in SA and AVN

A

class IV: Ca channel blockers

Diltiazem
Verapamil

23 spring: med surg (60 decks)

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