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Pharm 1 > drug therapy for dysrhythmias > Flashcards

drug therapy for dysrhythmias Flashcards

1
Q

describe how the heart is an electrical pump

A

-electricity resides in specialized tissues that generate and conduct electrical impulses (contractlu tissue)
-activities result in effective cardiac contraction and blood distribution throughout the body

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2
Q

what is the path of electricity in the heart

_______ -> _________ -> __________ …

A

SA node -> AV node -> bundle of His -> right and left bundle branches -> purkinje fibers

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3
Q

the heart oumps in regular intervals with four events, what are they?

A

1) stimulation from electrical impulse
2) transmission to adjacent tissue
3) contraction of atria, then ventricles
4) relaxation of atria, then ventricles

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4
Q

cardiac conduction relies on…

two things

A

automaticity and conductivity

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5
Q

describe…

automaticity

A

ability of the heart to generate an electrical impulse

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6
Q

describe…

conductivity

A

ability of cardiac tissue to transmit electrical impulses

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7
Q

what are the cells of muscle contraction in the heart

A

myocytes

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8
Q

contraction of myocytes is initiated by electril impulses, known as…

A

action potentials

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9
Q

action potential releases internal stores of ____ into the muscle cells and triggers contraction

A

Ca+

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10
Q

what is the contracting unit of muscle cells that contains actin and myosin?

A

sarcomere

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11
Q

describe troponin

A

Ca+ sensitive complex in muscle cells

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12
Q

what part of the conduction system can start an impulse?

A

-any part may start an impulse
-but SA node has the fastest rate of automaticity (pacemaker)

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13
Q

initiation of an impulse is dependent on…

A

Na and K ion movement

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14
Q

electrical stimulus must reach specific ____ to cause contraction

A

threshold

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15
Q

what happens after contraction?

A

-period of decreased excitability
-cells cannot respond to new stimulus (absolute refractory period)

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16
Q

describe the process of conductivity

A

-impulses originate in SA node
-transmitted though intermodal pathways to AV node
-impulse is delayed for a period of time
-impulse then travels predictable route

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17
Q

look at this pic for a minute

A
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18
Q

describe dysrhythmias

(arrthuthmias)

A

-abnormalities in cardiac rate or rhythm
-can originate in any part in conduction system

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19
Q

what does dyrhythmia result from?

A

irregular electrical impulse formation, conduction, or both

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20
Q

what allows cells other than SA node to initiate electrical impulse that reach the highest level in contraction

SA nose failure or slow depolarization

A

automaticity

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21
Q

what is it called when an impulse originates somewhere other than SA node

A

ectopic focus (more commonly called ectoptic beat)

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22
Q

ectopic beat is activated by…

A

-hypoxia (low O2)
-ischemia (low blood flow to tissue)
-hypokalemia (low K+)

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23
Q

what does ectopic beat indicate?

A

indicates myocardial irritability

potentially serious cardiac function impairment

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24
Q

what part of an EKG will atrial function show up on?

A

P wave

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25
Q

describe…

atrial tachycardia

A

HR in atria is faster than normal

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26
Q

describe…

atrial flutter

A

-atria beat regularly but faster than normal and more often than ventricles do
-narrow QRS

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27
Q

describe…

atrial fibrillation

A

-atrai beat irregularly
-SA node firing so fast, AV node cant keep up with the signals
-no P wave on EKG

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28
Q

what are some different atrial dysrhythmias

A

-tachycardia
-flutter
-fibrillation
-PACs (premature atrial contraction)

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29
Q

what are some different ventricular dysrhythmias

A

-tachycardia
-flutter
-fibrillation
-PVCs (premature ventricular contraction)

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30
Q

describe…

ventricular tachycardia

A

-rapid contraction of ventricles
-idiopathic
-leads to cardiac arrest

this is a shockable rhythm

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31
Q

describe…

ventricular fibrillation

A

-quick, rapid ventricle contraction
-widens out to vtach then to asystole

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32
Q

what part of EKG readings indicate ventricular function

A

QRS complex

33
Q

describe…

sinus bradycardia

A

-normal rhythm but slow
-HR <59bpm

34
Q

describe…

sinus tachycardia

A

-normal rhythm, but fast
-HR >100bpm

35
Q

describe…

heart block

A

-medical emergency
-signal between atria and ventricular pathway is interrupted either totally or partially

36
Q

describe the prior goal of pahrmacotherapy for dysrhythmias

A

-ppl went straight to meds
-supressing dysrhythmias with meds resulted in higher mortality rate among pts receiving antidysrhythmic drug therapy than those who were not

37
Q

what is the newest goal of therapy for dysrhythmias

A

-prevent, relieve symptoms, and prolong survival
-increase in nonpharmacologic stretgies for dysrhythmia management

38
Q

what are some nonpharmacologic stretegies for dysrhythmia management?

and describe them just a little

A

-cardioversion (shock heart)
-defibrillation (used in emergency medicine, used for vtach and vfib)
-radiofrequency catheter ablation (uses catheter to send radiofrequency to stop dysrhythmias)
-pacemakers (implanted, used for brady arrythmias and sinus bradycardia)
-implantable cardioverter defibrillators (ICD) (used for tachy arrythmias)

39
Q

the mechanisms of action of anidysrythmic drugs are grouped into 3 possibilities, what are they?

A

-reduce automaticity
-slow conduction of impulses through the heart
-prolong refractory period

40
Q

antidysrhymic drugs are classified according to…

A

mechanism of action and conduction system effect

41
Q

what are some indications of use of antidysrhythmic drugs?

A

-conversion of atrial fibrillation or flutter to NSR (normal sinus rhythm)
-maintaining NSR postconversion
-suppresion of fast or irregular ventricular rate that alters cardiac output
-presence of dangerous dysrhythmias that are potentially fatal

42
Q

anyone with afib is going to be taking…

A

anticoagulants

43
Q

describe…

sodium channel blockers

A

-now rarely used
-can cause/worsen dysrhythmias
-binds to and blocks the opening of sodium channels
-MOA depends on which class (IA, IB, IC) the med is in

44
Q

what are sodium channel blockers used in the treatment of

A

atrial dysrythmia, supreventricular tachycardia (bursts of high rapid HR)

45
Q

what are some side effects of sodium channel blockers

A

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

46
Q

what are some examples of sodium channel blockers

A

-quinidine
-lidocane (used for ventricular dysrhythmias)

47
Q

what are some nursing concerns associated with sodium channel blockers

A

interferes with anticoagulants and respiratory issues

48
Q

describe the action of beta adrenergic blockers

A

reduce activation of beta receptors = decrease conduction through SA/AV nodes = decrease automaticity = slower HR

decreases cardiac excitability, cardiac workload, and oxygen consumption

49
Q

what are beta adrenergic blockers used in the treatment of?

A

-management of dysrhythmia from excessive SNS stimulation, afib, and a-flutter (thought to slow ventricular rate)
-post MI/CHF (though to prevent vfib)

50
Q

what are some side effects of beta-adrenergic blockers?

A

-bradycardia
-AV block
-hypotension
-dizziness, syncope
-bronchospasm
-dyspnea
-drowsiness
-fatigue
-erectile dysfunction

51
Q

what are some nursing concerns/pt teaching associated with beta adrenergic blockers?

A

-rebound hypertension/tachycardia/dysrhythmias with abrupt withdrawal: must taper off over two weeks
-caution with PMH of asthma/respiratory disease

-use with verapamil (ca+ blocker) can increase risk of heart block, as well as bradycardia and hypotension

52
Q

what are some examples of beta adrenergic blockers

A

-propanolol
-acebutolol
-esmolol

53
Q

describe potassium

A

-main intracellular ion
-involved with cardiac rhythm (contractility of the myocardium)

54
Q

what is the normal value of K+

A

3.5 to 5.0 mEq/L

55
Q

describe hypokalemia

whats the lab value

A

less than 3.5mEq/L

56
Q

what are the signs and symptoms of hypokalemia

A

-ventricular dysrhythmias
-muscle weakness/decreased DTRs
-weak peripheral pulses

57
Q

describe treatment of hypokalemia

A

-increase dietary K+ rich foods
-oral meds (preferred)
-peripheral IV meds

58
Q

describe oral administration of K+

A

-no more than 20 mEq/hr
-give with meals/assess swallowing
-pills can be split
-availabe in liquid or pill form

59
Q

describe peripheral IV administration of K+

A

-20-40 mEq/hr
-do not exceed 20 mEq/hr (can do 40 mEq/2hrs)
-burnsssss
-if burning occurs, stop and assess site

60
Q

describe hyperkalemia

whats the lab value

A

greater than 5.0 mEq/L

61
Q

what are the signs and symptoms of hyperkalemia

A

-dysrhythmias
-vfib
-heart block
-cardiac arrest
-muscle twitching
-numbness in hands, feet, and mouth

62
Q

describe the tx of hyperkalemia

A

-restrict dietary K+ rich foods
-sodium polystyrene (binds to K+ and causes diarrhea)
-IV administration of insulin/dextrose shift K+ back into cells

63
Q

how do potassium channel blockers work?

A

-inhibit adrenergic stimulation
-block K+ channels = prolong duration of action potential = slow repolarization = prolong refreactory period

64
Q

what are K+ channel blockers used to treat?

A

-IV for life threatening tachydysrhythmias (not first line r/t fisk for pulmonary toxicity)
-PO for recurrent tachycardia, V&A fibrillation and A flutter

65
Q

what are some side effects of K+ channel blockers

A

-bradycardia
-hypotension (weakness and dizziness)
-worsen or new dysrhythmias
-pulmonary toxicity (IV)
-hepatotoxicity
-blurred vision/photosensitivity

CAUTION with AV block, shock, hypotension, respiratory depression, renal/hepatic impairment

66
Q

what are some examples of potassium channel blockers?

A

-amiodarone (IV)
-dofetilide
-ibutilide
-sotalol

67
Q

what are some nursing concerns associated with K+ channel blockers?

A

-monitor HR, BP, and ALT/AST levels
-ausculate and evaluate lung sounds

68
Q

describe how calcium channel blockers work

A

block calcium ion channels = reduce automaticity in SA node and slow conduction through AV node = slow HR = prolong refractory period

69
Q

what are calcium channel blockers used to treat?

A

-supraventricular dyrhythmias (@ SA and AV nodes)
-tachycardia
-can be emergency med for Afib, SVT requiring IV administration

70
Q

what are some side effects of calcium channel blockers

A

-bradycardia
-hypotension (HA, dizziness, lightheadedness)
-flushed skin
-MI
-hepatotoxicity
-peripheral edema

caution with heartblock, sick sinus syndrome, heart failure, hypotension, hepatic/renal insufficiency, pragnancy

71
Q

what are some examples of calcium channel blockers

A

-diltiazem
-verapamil

72
Q

what are some nursing concerns asociated with calcium channel blockers

A

-avoid grapefruit and grapefruit juice
-monitor when beta blockers and digoxin
-monitor for peripheral edema

73
Q

name two unclassified antiarrhythmic drugs

A

adenosine and digoxin

74
Q

describe adenosine

A

-emergency med, used for SVT when a vagal meneuver doesnt work
-naturally occurring component of all body cells

75
Q

how does adenosine work

A

depresses conduction @ AV node = resotre NSR in SVT pts

76
Q

how is adenosine administered

A

-rapid bolus administration r/t rapid metabolism out of the system
-given slowly, wont reach cardiac tissue

77
Q

what are some vagal maneuvers

(actions to stop SVT)

A

-hold breath and bear down for 20 secs
-stick face in ice water

78
Q

describe components of pharmacologic therapy of dysrhythmias

A

-requires accurate ID of dysrhythmia
-understand mechanisms of dysrhythmia
-monitoring is imperitive: observing hemodynamic and ECG effects of dysrhythmia
-knowledge of pharmacologic actions of specific meds
-therapeutic effects outwaugh potential adverse effects

Pharm 1 (29 decks)

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