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Pharm EXAM 2 > Chapter 27- dysrhythmias > Flashcards

Chapter 27- dysrhythmias Flashcards

1
Q

what are the four intervals in the heart

A

-stimulation for the electrical impulse
-transmission to adjacent tissue
-contraction of atria then ventricles
-relaxation of atria then ventricles

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2
Q

what does automaticity mean

A

ability for the heart to generate electrical impulses

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3
Q

what does conductivity mean

A

ability of tissues to transmit electrical impulses

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4
Q

what is the pacemaker of the heart

A

SA node

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5
Q

what is an action potential

A

contraction of myocytes, controlled by voltage

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6
Q

what do sarcomeres, troponin, and Ca part of

A

neurons will stimulate muscle cells, which stimulate contraction

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7
Q

what is a sarcomere

A

contraction unit

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8
Q

what is troponin

A

binds to calcium, opening sites and causing contraction

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9
Q

what does calcium do

A

react to troponin

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10
Q

what electrolytes is the SA node dependent on

A

Na and K

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11
Q

what is automaticity

A

allows any part of the conduction system to start an impulse

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12
Q

what is the absolute refractory period

A

the cells can not respond to a new stimulus

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13
Q

what causes arrhythmias

A

irregular electrical impulse and or conduction

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14
Q

ectopic focus/ectopic beat and causes

A

impulse started by something other than SA
-hypoxia, ischemia, hypokalemia

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15
Q

what is an atria flutter

A

the atria is beating faster than the ventricles
-lub, lub, lub

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16
Q

what is atria fibrillation?

A

AV cannot keep up with SA – no p wave

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17
Q

what is a heart block

A

signal between atria and ventricles is messed up or blocked, emergency intervention is needed

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18
Q

the main concern when starting antidysrthmias

A

making the dysrhythmia worse or creating a new one

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19
Q

what is cardioversion

A

shock to the heart

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20
Q

what is defibrillation

A

emergency situation, VTAC and VFIB can be shocked

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21
Q

pacemaker

A

for tachy and brady arrhythmias to keep heart pace WNL
-some can do both if needed

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21
Q

what is ablation

A

Burnout problem areas

22
Q

MOA of antidysrhythmic drugs

A

-reduce automaticity
-slow conduction impulses
-prolong the refractory period

23
Q

when are antidysrhythmic drugs used

A

-treatment of atrial fibrillation or flutter
-maintaining NSR after ablation
-suppressing fast/irregular ventricle rate – isn’t filling with enough blood
-dysrhythmias that could be fatal — A fib causing clots

24
Q

how do sodium channel blockers work

A

blocks the opening of sodium channels

25
Q

what can sodium channel blockers treat

A

atrial dysthymia, supraventricular tachycardia – bursts of high rapid HR which are normally idiopathic

26
Q

side effects of sodium channel blockers

A

arrhythmias, bradycardia, hypotension
-respiratory depression, dizziness, syncope, drowsiness, fatigue, confusion, anticholinergic

27
Q

nursing concern for sodium channel blockers

A

interacts with anticoagulants and A fib pts need them

28
Q

common sodium channel blockers

A

quinidine, lidocaine

29
Q

how do beta blockers work

A

decrease conduction through the SA/AV node
-decreases cardiac excitability, workload, and oxygen consumption

30
Q

what are beta blockers used to treat

A

-dysrhythmia from SNS stimulation, a fib, and flutter, post-MI and CHF to prevent v-fib

31
Q

side effects of beta blockers

A

BRADYCARDIA, HYPOTENSION, DIZZY, SYNCOPE
-Av block, bronchospasm, dyspnea, drowsiness, fatigue, ED

32
Q

nursing considerations of beta blockers

A

-taper off
-when taken with Ca blocker can increase risk of heart block

33
Q

common beta blockers

A

METOPEROL and ETGENELOL
-propranolol, acebutolol, esmolo

34
Q

what does potassium do for the heart

A

control contractility

35
Q

what should potassium levels be

A

3.5-5

36
Q

hypokalemia signs

A

ventricular dysrhythmias, muscle weakness, decreased deep tendon reflexes, weak peripheral pulses

37
Q

issues with IV potassium

A

can burn, should be given in a Central line

38
Q

hyperkalemia signs

A

dysrhythmias, v-fib, HB, cardiac arrest, muscle twitching, numbness in hands, feet and mouth

39
Q

what can quickly bring down potassium levels

A

insulin/dextrose

40
Q

how do potassium channel blockers work

A

prolongs action potential, slows repolarization, and prolongs the refractory period

41
Q

when are potassium channel blockers used

A

given IV for life-threatening tacy dysrhythmias
given PO for tachycardia, V/A fib, and A flutter

42
Q

side effects of potassium channel blockers

A

bradycardia, hypotension, weakness, dizziness, worsened/new dysrhythmias, PULMONARY TOXICITY, HEPATOTOXICITY, blurred vision

43
Q

who should not take potassium channel blockers

A

AV block, shock, hypotension, respiratory depression, and renal/hepatic impairment

44
Q

common potassium channel blockers

A

AMIODARONE
-dofetilide, ibutilide, sotalol

45
Q

how do calcium channel blockers work

A

reduce automaticity of SA node and slow conduction of AV node

46
Q

what can calcium channel blockers treat

A

supraventricular dysrhythmias (SA and AV) and tachycardia
-emergency for A-fib, SVT

47
Q

side effects of calcium channel blockers

A

BRADYCARDIA, HYPOTENSION,
-flushed skin, MI, hepatotoxicity, peripheral edema

48
Q

who shouldn’t take calcium channel blockers

A

HB, sick sinus, HF, hypotension, renal/hepatic, PREGNANCY

49
Q

nursing considerations with calcium channel blockers

A

grapefruit, monitor with beta-blockers and digoxin

50
Q

what is sick sinus

A

irregular heart rhythm

51
Q

how does adenosine work and when is it used

A

depression of conduction at the AV node, causing NSR
-EMERGENCY MED

52
Q

can digoxin treat dysrthmias

A

YES

Pharm EXAM 2 (8 decks)

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