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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
--- is a class IB antiarrhythmic
lidocaine
26
ventricular arrhythmias can be treated with --- antiarr
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
why do class I anti-arrhy not cause bradycardia
effects the non-nodal tissues by blocking Na channels does not cause change in nodal cells (sinus or AV node) ## Footnote class I good for ventricular arrhythmias
28
what class of drug does this
class I- antiarrhythmic Na channel blocker (lidocaine class Ib)
29
lidocaine is what class of drug and is used for
Class 1b antiarrhythmic can only be given **IV** used for Vtach can cause depression, seizures (cats) vomiting can cause transient hypotension under GA
30
side effects of lidocaine
Depression, seizures (cats are more sensitive), vomiting transient hypotension noticed under GA ## Footnote Class Ib anti-arrhythmic - Na channel blocker used for Vtach
31
what drug
lidocaine treat Vtach ## Footnote Class Ib anti-arrhythmic - Na channel blocker used for Vtach
32
how does class II anti-arrhythmic work
beta blocker blocks sympathic tone to the heart **reduces HR by slowing sinus node**
33
beta blockers are --- drugs
class II antiarrhythmics
34
--- is a 2nd gen class II antiarrhythmic
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
what are some side effects of Class II anti-arrhythmics
beta blockers **negative inotrope**: can cause reduced myocardial contractility and cardiac output can **worsen CHF and cause hypotension** ## Footnote atenolol is a 2nd gen class II AA
36
how to treat
atrial tachycardia give beta blocker (IV esmolol) will slow HR by slowing conduction through AV node → can cause AV block (P wave no QRS) ## Footnote atenolol and esmolol (2nd gen class II beta blockers)
37
how does class III AA drug work
potassium channel blocker prolongs repolarization: makes the AP all the same length (widens) does not effect the conduction velocity used for **ventricular arrhythmias** ## Footnote L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization)
38
--- is a class III AA
L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization) used for ventricular arrhythmias
39
how does class III AA effect reentry
## Footnote L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization): prevents ventricular arrhythmias
40
sotalol is ---
L-sotalol: class III AA: K channel blocker causes widened AP (prolongs repolarization): prevents ventricular arrhythmias
41
what will sotalol do
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
--- class of AA will slow AV nodal conduction
IV calcium channel blocker
43
--- is a class IV AA
diltiazem calcium channel blocker: will slow AV nodal conduction will **slow Afib**, will stop supraventricular reentry arrhythmias in the AV node
44
diltiazem is used to slow conduction through ---
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
will diltiazem effect Vtach?
no class IV calcium channel blocker will slow supraventricular arrhythmias such as Afib, by slowing conduction through the AV node
46
--- is a calcium channel blocker used to relax vascular smooth muscle
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
digoxin is used for
slows ventricular response rate in **Afib** will slow AV nodal conduction parasympathomimetic effect
48
--- are parasymptholytics that stop bradycardia
Atropine, Glycopyrrolate
49
rapid Afib should be teated with
**digoxin**: acts as parasympathomimetic, slows AV nodal conduction **diltiazem**: class IV calcium channel blocker, will slow conduction through the AV node
50
how to treat Vtach
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 ## Footnote 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
V fib! must shock back to rhythm
52
how to treat 3rd degree AV block
****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
how would you treat
pacemaker sick sinus syndrome bradycardia with long pause and escape beat
54
how to place pacemaker
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
how to treat bradycardia
56
how to treat SVT other then Afib
57
how to treat AFib
58
how to treat Ventricular arrhythmias | graph
59
how to treat Vfib | graph
60
--- class cause Reduce slope of phase 0 and peak of AP
class I na channel blockers ## Footnote lidocaine
61
--- class will cause Small reduction in phase 0, shortens APD, decreases ERP, increases post-repolarization refractoriness
class I na channel blocker IB: lidocaine
62
--- class of AA will Slows rate of spontaneous depolarization and conduction velocity in SA and AVN
type II beta blocker atenolol, esmolol
63
--- class of AA will cause Markedly prolongs repolarization (phase 3), lengthen ERP and APD
class III: K channel blockers Amiodarone Sotalol
64
--- class of AA will cause Slows rate of spontaneous depolarization and conduction velocity in SA and AVN
class IV: Ca channel blockers Diltiazem Verapamil

23 spring: med surg (60 decks)

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