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pharm exam 2 > drug therapy for dysrhythmias > Flashcards

drug therapy for dysrhythmias Flashcards

1
Q

the heart is an

A

electrical pump

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2
Q

regular intervals with four events

A

stimulation from electrical impulse -> transmission to adjacent tissue -> contraction of atria, then ventricles -> relaxation of atria, then ventricles

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3
Q

cardiac conduction: automaticity

A

ability of the heart to generate an electrical impulse

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4
Q

cardiac conduction: conductivity

A

ability of cardiac tissue to transmit electrical impulses

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5
Q

what is unique about the cardiac automaticity conduction

A

any part of conduction system can start an impulse, SA node has the fastest rate of automaticity (pacemaker), initiation of impulse dependent on Na and K ion movement

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6
Q

in automaticity, what happens after contraction

A

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

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7
Q

what is unique about the cardiac conductivity conduction

A

impulses originate in the SA node to AV node, impulse then travels predictable route

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8
Q

cardiac dysrrhythmias(arrhythmias)

A

abnormalities in cardiac rate or rhythm

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9
Q

dysrhythmias originate in

A

any part of the conduction system

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10
Q

dysrhythmias result from

A

electrical impulse formation, conduction or both

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11
Q

in dysrhythmias, the cardiac automaticity allows

A

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

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12
Q

if impulse originates in other than the SA node in dysrhythmias, then it is referred to as

A

ectopic focus or ectopic beat

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13
Q

result of ectopic beat is

A

hypoxia, ischemia, hypokalemia

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14
Q

hypoxia is

A

low O2 in the blood

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15
Q

ischemia is

A

no blood to the tissue

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16
Q

ectopic beats indiciate

A

myocardial irritability; potentially serious cardiac function impairment

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17
Q

atrial tachycardia

A

heart rate in the atria are beating faster than normal

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18
Q

atrial flutter

A

narrow QRS; when the atria beats regularly but faster than normal and more often than the ventricles; ratio of 4 to 1; atria could contract 4 times before ventricles: should be 1 to 1

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19
Q

atrial fibrillation

A

when the atria beats irregularly; SA node is firing so fast that the AV node can’t keep up; no P wave because of how fast SA is firing

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20
Q

ventricular tachycardia

A
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21
Q

ventricular flutter

A
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22
Q

ventricular fibrillation

A
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23
Q

antidysrhythmic nonpharmacologic therapy goal

A

prevent, relieve symptoms, and prolong survival; increase use of nonpharmacologic strategies for dysrhythmia management

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24
Q

prior goal of pharmacotherapy

A

suppress dysrhythmias resulted in higher mortality rate among patients receiving antidysrhythmic drug therapy than those who were not

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25
Q

nonpharmacologic strategy: cardioversion

A

pads on front of chest and on back(anteriorly & posteriorly) can shock the heart

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26
Q

nonpharmacologic strategy: defibrillation

A

put pads on, check rhythms of the heart (Vtach and Vfib)

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27
Q

nonpharmacologic strategy: radiofrequency catheter ablation

A

procedure dr. uses catheter to send radio frequency energy, makes circular scars around cells around heart

28
Q

pace makers

A

implantable cardioverter defibrillation; for low HR (30-40), will shock patient if HR goes below 60 to set the pace of the heart

29
Q

antidysrhythmic drug therapy: MOA

A

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

30
Q

antidysrhythmic drug therapy: indications for use

A

conversion of atrial fibrillation or fatter to NSR, maintaining NSR postconversion, suppression of fast or irregular ventricular rate that alters cardiac output, presence of dangerous dysrhythmias that are potentially fatal

31
Q

antiarrhyrthmic agents

A

sodium channel blockers, beta-adrenergic blockers, potassium channel blockers, calcium channel blockers

32
Q

sodium channel blockers

A

can cause/ worsen dysrhythmias, block the opening of sodium channels, rarely used

33
Q

sodium channel blockers treat

A

atrial dysrhythmias, supraventricular tachycardia (bursts of high rapid heart rates)

34
Q

side effects of sodium channel blockers

A

arrhythmias, bradycardai, hypotension, respiratory depression, dizziness, syncope, drowsiness, fatigue, confusion, anticholinergic

35
Q

nursing concern when using sodium channel blockers

A

interfere with anticoagulants

36
Q

beta-adrenergic blockers do what

A

reduce activation of beta receptors = decrease conduction through SA/ AV node = decrease automaticity = slow HR; decreases cardiac excitability, cardiac workload and oxygen consumption

37
Q

beta-adrenergic blockers treat

A

management of dysrhythmias from excessive SNS stimulation, a-fibrillation, and a-flutter(though to slow ventricular rate), post MI/CHF (thought to prevent v-fib)

38
Q

side effects of beta-adrenergic blockers

A

bradycardia, AV block, hypotension, dizziness, syncope, bronchospasm, dyspnea, drowsiness, fatigue

39
Q

what rebound side effect will happen with beta-adrenergic blockers if NOT tapered off

A

hypertension/ tachycardia/ dysrhythmias with abrupt withdrawal

40
Q

nursing concerns when using beta-adrenergic blockers

A

the use with verapamil (Ca2+ blocker) can increase renal failure and heart block; so check if there are on verapamil before administering

41
Q

examples of beta-adrenergic blockers

A

propranolol, acebutolol, esmolol

42
Q

potassium

A

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

43
Q

normal K+ levels

A

3.5-5.0 mEg/L

44
Q

hypokalemia, s/sx

A

less than 3.5; ventricular dysrhythmias, muscle weakness/ decreased DTR’s, weak peripheral pulses

45
Q

treat hypokalemia

A

increase dietary K+ rich foods, oral (no more than 20mEg/hr with meals, pills can be spilt), peripheral IV(20-40mEg/L; do not exceed 20/hr; mixed with other solution)(IV not recommended)

46
Q

hyperkalemia, s/sx

A

greater than 5.0; dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands feet and mouth

47
Q

hyperkalemia, s/sx

A

greater than 5.0; dysrhythmias, V-fib, HB, cardiac arrest, muscle twitching, numbness in hands feet and mouth

48
Q

treat hyperkalemia

A

restrict dietary K+ rich foods, give sodium polystyrene(kayexalate): binds K+ and causes diarrhea, IV administration of insulin with dextrose shifts K+ back into cells

49
Q

potassium channel blockers: inhibits adrenergic stimulation

A

blocks potassium channels= prolong duration of action potential = slow depolarization = prolong refractory period

50
Q

potassium channel blockers treat

A

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

51
Q

side effects of potassium channel blockers

A

Brady cardia. hypotension (weakness, dizziness), worsen or new dysrhythmias, pulmonary toxicity (IV), hepatotoxicity, blurred vision/ photosensitivity

52
Q

contraindications for potassium channel blockers

A

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

53
Q

examples of potassium channel blockers

A

amiodarone, dofetilide (tikosyn), ibutilide, sotalol

54
Q

calcium channel blockers

A

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

55
Q

calcium channel blockers treat

A

supraventricular dysrhythmias (at SA & AV nodes), tachycardia; can be emergency medication for A-fub, SVT requiring IV administration

56
Q

side effects of calcium channel blockers

A

Bradycardia, hypotension(HA, dizziness, lightheaded), flushed skin, MI, hepatotoxicity, peripheral edema

57
Q

contraindications with calcium channel blockers

A

HB, sick sinus, HF, hypotension, hepatic/renal insufficiency, pregnancy

58
Q

examples of calcium channel blockers

A

diltiazem, verapamil

59
Q

nursing concerns with calcium channel blockers

A

avoid grapefruit/ grapefruit juice, monitor with beta blockers and digoxin

60
Q

class I acts on what blocker

A

sodium channel blocker

61
Q

class II acts on what blocker

A

beta-adrenergic blocker

62
Q

class III acts on what blockers

A

potassium channel blocker

63
Q

class IV acts on what blocker

A

calcium channel blocker

64
Q

unclassified anti arrhythmic

A

adenosine, digoxin

65
Q

adenosine is used when

A

emergency medication; used for SVT when a vagal maneuver doesn’t work; natural occurring component of all body cells; depressed conduction at AV node = restore NSR in SVT patients; given as a rapid bolus administration r/t rapid metabolism out of the system (if you give slow It won’t reach the cardiac tissue)

66
Q

pharmacologic therapy of dysrhythmias

A

understanding mechanisms of dysrhythmias, requires accurate ID of dysrhythmia, monitoring imperative(observing hemodynamic and ECG effects of dysrhythmia), knowledge of pharmacologic actions of specific medications, therapeutic effects outweigh potential adverse effects

pharm exam 2 (8 decks)

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