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Challenges > Cardiac rhythm drugs: antidysrhythmic drugs > Flashcards

Cardiac rhythm drugs: antidysrhythmic drugs Flashcards

1
Q

______: have unique characteristics that allow them to regulate the heart rate and rhythm

A

Cardiac cells

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2
Q

Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse

A

Automaticity

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3
Q

Automaticity

A

Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse

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4
Q

Pacemaker cells usually only exist in the _____________

A

SA Node, AV junction, and Purkinje fibers

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5
Q

Other cells can have ______ (initiate electrical impulses) after MI, electrolyte imbalances, hypoxia, and drug toxicity, leading to ______

A

automaticity, dysrhythmias

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6
Q

______-includes all cardiac cells

A

Excitability

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7
Q

Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli

A

excitability

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8
Q

excitability

A

Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli

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9
Q

Mechanical, chemical, or electrical impulses can cause a response to any cardiac cell because of their ______

A

excitability

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10
Q

The ability of cardiac cells to transmit the electrical impulse to adjacent heart cells

A

Conductivity

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11
Q

Conductivity

A

The ability of cardiac cells to transmit the electrical impulse to adjacent heart cells

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12
Q

conductivity: The impulse travels to the cells and ______ in rapid succession creates deflections seen on ECG.

A

depolarization

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13
Q

If impulses travel too fast or to slow, through blocked pathways, or through abnormal pathways, a ______exists

A

dysrhythmia

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14
Q

The ability of cardiac cells to shorten in response to electrical stimulation

A

Contractility

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15
Q

Contractility

A

The ability of cardiac cells to shorten in response to electrical stimulation

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16
Q

Is a mechanical event, not electrical

A

contractility

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17
Q

contractility: ______ starts the contraction, causing the heart to squeeze blood out to the body

A

Depolarization

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18
Q

Conductivity withOUT contraction is called ______

A

PEA

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19
Q

______ withOUT contraction is called PEA

A

Conductivity

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20
Q

Is enhanced by drugs like digoxin, dopamine, and epinephrine

A

contractility

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21
Q

what drugs enhance contractility?

A

Is enhanced by drugs like digoxin, dopamine, and epinephrine

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22
Q

_____ slows and strengthens the contractions

A

digoxin

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23
Q

______ increases HR, and contractility and BP

A

dopamine and epinephrine

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24
Q

_______ vasoconstricts peripherally, it doesn’t increase ________,

A

levophed (norepinephrine) , HR (in lower doses)

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25
Q

levophed is not ______

A

inotropic

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26
Q

______ –increases contractility and increases HR and BP

A

epinephrine, dopamine

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27
Q

is not given for septic/feverish patients (can send septic patients into SVT)

A

dopamine

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28
Q

_______ is a side effect of epinephrine

A

pulmonary edema (pink frothy stuff)

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29
Q

pulmonary edema is a side effect of which drug?

A

epinephrine

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30
Q

how do you treat PEA?

A

like asystole, with epi and compressions

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31
Q

With EVERY rhythm, we should ask: ______________

A

“Does it have a pulse?”

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32
Q

The change in electrical charge inside the cardiac cell when it is stimulated

A

Cardiac Action Potential

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33
Q

Cardiac Action Potential

A

The change in electrical charge inside the cardiac cell when it is stimulated

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34
Q

What does cardiac action potential cause?

A

Polarization, Depolarization, Repolarization

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35
Q

the change in electrical potential associated with the passage of an impulse along the membrane of a muscle cell or nerve cell.

A

action potential

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36
Q

action potential

A

the change in electrical potential associated with the passage of an impulse along the membrane of a muscle cell or nerve cell.

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37
Q

The electrical state that exists at the cardiac cell membrane when the cell is at rest

A

polarization

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38
Q

polarization, what is it? what electrical activity is occuring? where is it in the EKG strip?

A

The electrical state that exists at the cardiac cell membrane when the cell is at rest

NO electrical activity is occurring

ECG displays an iso-electric line “baseline”

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39
Q

The electrical event that results in a contraction of the cardiac muscle

A

Depolarization

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40
Q

Depolarization

A

The electrical event that results in a contraction of the cardiac muscle

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41
Q

when does atrial depolarization occur, as in what wave is it?

A

p wave

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42
Q

what wave represents ventricular depolarization?

A

QRS

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43
Q

a period immediately following stimulation during which a nerve or muscle is unresponsive to further stimulation.

A

refractory period

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44
Q

Resistance of the cell membrane to a stimulus

A

refractory period

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45
Q

what are the three kinds of refractory period?

A

Absolute refractory period
Relative refractory period
Supernormal refractory period

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46
Q

Brief period during depolarization when the cells WILL NOT respond to further stimulation, no matter how strong the stimulus

A

absolute refractory period

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47
Q

when is the absolute refractory period?

A

In the cardiac rhythm, this is from the beginning of the QRS to the peak of the T wave

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48
Q

This means that nothing can interfere with a cardiac contraction once it has started

A

absolute refractory period

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49
Q

Some of the cells have repolarized

These cells may respond if there is a ______ stimulus during the relative refractory period or “vulnerable period”

A

“stronger than normal”

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50
Q

A stronger than normal stimulus during the relative refractory period may result in ________ which can turn into ________ an d eventually ____

A

R on T, torsades, v fib

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51
Q

______ occurs when a stimulus that causes QRS depolarization lands on the last half of the T wave. (Remember absolute refractory period only goes through the first half of the T wave)

A

R on T Phenomenon

52
Q

R on T may lead to _________

A

ventricular fibrillation

53
Q

Comes after relative refractory period
A weaker-than-normal stimulus can cause cells to depolarize
This period corresponds to the end of the T wave

A

supernormal period

54
Q

know that we only ______ for patients that have a heartbeat

A

synchronize cardiovert

55
Q

know that we only synchronize cardiovert for patients that ______

A

have a heartbeat

56
Q

what is done for patients who dont have a pulse in V tach or fib?

A

defibrilation

57
Q

Give the pathway of the Cardiac conduction system

A

SA node
AV node
Bundle of his
Bundle branches
Perkinje fibers

58
Q

Cardiac Rhythm Drugs:

______
______
______
Can reduce myocardial excitability
Can lengthen the refractory period
Can stimulate the autonomic nervous system

A

Alter cardiac electrophysiologic function to treat/prevent dysrhythmias
Can affect the AV node, increasing or reducing conduction speed
Can alter ectopic pacemakers and the SA node

59
Q

Cardiac rhythm drugs:

Alter cardiac electrophysiologic function to treat/prevent dysrhythmias
Can affect the AV node, increasing or reducing conduction speed
Can alter ectopic pacemakers and the SA node
______
______
______

A

Can reduce myocardial excitability
Can lengthen the refractory period
Can stimulate the autonomic nervous system

60
Q

What are the different anti dysrhythmic drug groups?

A

Sodium Channel Blockers
Beta-Adrenergic Blockers
Potassium Channel Blockers
Calcium Channel Blockers

61
Q

What is the MAJOR CONCERN WITH ALL ANTI-DYSRHYTHMIC DRUG GROUPS? WHAT IS THE RESULT OF THE POTENTIAL EFFECT?

A

TOXICITY. TOXICITY CAN CAUSE DYSRHYTHMIAS.

62
Q

What are the 1a sodium channel blockers?

A

Procainamide, quinidine, disopyramide

63
Q

What are class 1a sodium channel blockers used to treat?

A

***Used for SVT, V-tach, Atrial Flutter, Atrial Fibrillation

64
Q

What are the class 1b sodium channel blockers?

A

lidocaine, mexiletine, phenytoin

65
Q

What are class 1b sodium channel blockers used to treat?

A

Used only short-term for ventricular dysrhythmias

66
Q

What are the class 1c sodium channel blockers?

A

Propafenone, flecainide

67
Q

What are 1c sodium channel blockers used to treat?

A

used to treat SVT

68
Q

These drugs are designed to SLOW cardiac conduction velocity

A

sodium channel blockers

69
Q

phenytoin is used for __________ and required _____

A

seizures and dysrhythmias , filter tubing

70
Q

What are the main complications of sodium channel blockers 1a

A

Lupus
CBC -neutropenia, thrombocytopenia, agranulocytosis
cardio toxicity
hypotension

71
Q

Sodium channel blockers 1a:

Systemic Lupus Syndrome
monitor for ______
give NSAIDS PRN
discontinue for rising ANA titer

A

butterfly rash

72
Q

Sodium channel blockers 1a:

Systemic Lupus Syndrome
monitor for butterfly rash
give ______ PRN
discontinue for rising ANA titer

A

NSAIDS

73
Q

Sodium channel blockers 1a:

Systemic Lupus Syndrome
monitor for butterfly rash
give NSAIDS PRN
discontinue for ______

A

rising ANA titer

74
Q

Sodium channel blockers 1a:

______

CBC weekly for 12 weeks, then periodically

watch for infection/bleeding

STOP with bone marrow suppression

A

Neutropenia, thrombocytopenia, agranulocytosis

75
Q

Sodium channel blockers 1a:

Neutropenia, thrombocytopenia, agranulocytosis

CBC weekly for ______, then periodically

watch for infection/bleeding

STOP with bone marrow suppression

A

12 weeks

76
Q

Sodium channel blockers 1a:

Neutropenia, thrombocytopenia, agranulocytosis

CBC weekly for 12 weeks, then periodically

watch for ______

STOP with bone marrow suppression

A

infection/bleeding

77
Q

Sodium channel blockers 1a:

Neutropenia, thrombocytopenia, agranulocytosis

CBC weekly for 12 weeks, then periodically

watch for infection/bleeding

STOP with ______

A

bone marrow suppression

78
Q

Sodium channel blockers 1a:

Cardio toxicity

monitor for ______

procainamide level should be 4-10mcg/ml

toxicity presents as confusion, drowsiness, vomiting

A

dysrhythmias (widened QRS)

79
Q

Sodium channel blockers 1a:

Cardio toxicity

monitor for dysrhythmias (widened QRS)

procainamide level should be ______

toxicity presents as confusion, drowsiness, vomiting

A

4-10mcg/ml

80
Q

Sodium channel blockers 1a:

Cardio toxicity

monitor for dysrhythmias (widened QRS)

procainamide level should be 4-10mcg/ml

toxicity presents as ______

A

confusion, drowsiness, vomiting

81
Q

Sodium channel blockers 1a:

hold med if patient is ______

A

hypotensive

82
Q

What are the major complications of sodium channel blockers class 1 b?

A

CNS effects
Respiratory Arrest

83
Q

Sodium channel blockers 1b:

CNS Effects

things slow down
blood flow is decreased to brain bc
_______

A

perfusion is decreased (low bp)

84
Q

What are sodium channel blocker complications with class 1c?

______, ______, ______, weakness, hypotension, bronchospasm

A

Bradycardia, heart failure, dizziness

85
Q

What are sodium channel blocker complications with class 1c?

Bradycardia, heart failure dizziness, ______, ______, ______

A

weakness, hypotension, bronchospasm

86
Q

What are the Class II antidysrhythmics?

A

Beta blockers

87
Q

Give examples of Beta blockers, what do they end in?

A

Propranolol, esmolol, acebutolol. Beta blockers typically end in lol.

88
Q

What affects do beta blockers have on the circulatory system?

A

lower heart rate and blood pressure

89
Q

Work by preventing sympathetic nervous system stimulation of the heart

A

beta blockers

90
Q

beta blockers work by preventing ______ stimulation of the heart

A

sympathetic nervous system

91
Q

Beta blockers

Therapeutic uses:

________________
________________
________________
________________
angina,
PVCs,
severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia

A

afib,
aflutter,
paroxysmal SVT,
hypertension,

92
Q

Beta blocker:

Therapeutic uses:

afib,
aflutter,
paroxysmal SVT,
hypertension,
________________
________________
________________
________________
________________

A

angina,
PVCs,
severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia

93
Q

Beta blocker complications

Propranolol:

________________
________________
________________
dizziness,
hypotension,
bronchospasm

A

bradycardia,
weakness,
heart failure,

94
Q

Beta blocker complications

Propranolol:

________________
________________
________________
bradycardia,
weakness,
heart failure,

A

dizziness,
hypotension,
bronchospasm

95
Q

______ can be given to bring heart rate up

A

atropine

96
Q

beta blockers if patient is experiencing side effects:

for the most part –if patients are perfusing their organs (MAP__________) we usually let them __________, maybe give __________

A

over 65, ride it out, fluid bolus

97
Q

____________ can be a good short term fix for poor central perfusion. hypotension can be caused by beta blockers.

A

Trendelenburg

98
Q

What are Class III anti dysrhythmics called?

A

Potassium channel blockers

99
Q

What are the Class III antidysrhythmics or potassium channel blockers?

A

Amiodarone, sotalol, ibutilide, dofetilide, dronedarone

100
Q

how do potassium channel blockers work?

A

Work by prolonging the action potential and refractory period of the cardiac cycle

Delays repolarization

Dilates blood vessels

101
Q

What cardiac conditions do potassium channel blockers work for?

A

Afib ,Vfib, vtach really need to know that amiodarone is used for vfib and vtach

102
Q

What is amiodarone used for?

A

vfib and vtach

103
Q

amiodarone –v fib and v tach -__________ for no pulse, ____________ for pulse

A

300 mg, 150 mg

104
Q

Complications of potassium channel blockers (amiodarone):

________________
________________
________________
Other effects
Phlebitis with administration
Hypotension, bradycardia, AV block

A

Pulmonary Toxicity -breathing troubles
Sinus Brady and AV block
Visual disturbances

105
Q

Complications of potassium channel blockers (amiodarone):

Pulmonary Toxicity -breathing troubles
Sinus Brady and AV block
Visual disturbances
________________
________________
________________

A

Other effects
Phlebitis with administration
Hypotension, bradycardia, AV block

106
Q

____________ is the drug of choice for v fib and v tach, know how fast we give it on drips, know how fast we give it IV push

A

Amiodarone

107
Q

Amiodarone is the drug of choice for ____________________, know how fast we give it on drips, know how fast we give it IV push

A

v fib and v tach

108
Q

Decreases electrical conduction through the AV node and decreases automaticity in the SA node

A

adenosine

109
Q

What conditions is adenosine used for?

A

Used for SVT or Wolff-Parkinson-white syndrome (WPW)

110
Q

Complications from adenosine:
________________
________________
________________
________________

A

sinus brady,
hypotension,
dyspnea with bronchoconstriction, flushed face from vasodilation

111
Q

for SVT –want an IV close to ____________, ___________ , want a ____________ (adenosine, flush immediately)

A

the heart, large bore, three way stop cock

112
Q

adenosine:

may see ________ for a few seconds, warn them that they might feel like theyre going to _____ for a few seconds, have _________ nearby in case you need it

A

asystole, die, crash cart

113
Q

What to do for adenosine administration? Monitor the _____. Effects usually last _________, have IV ______ prepared

A

ECG, 1 min or less, bolus

114
Q

Adenosine administration:

Dose 1: _____ rapid IVP followed by 20 ml rapid saline bolus

Dose 2: ______ rapid IVP followed by 20 ml rapid saline bolus

Dose 3: ______ rapid IVP followed by 20 ml rapid saline bolus

A

6mg, 12 mg, 12 mg

115
Q

adenosine: Give at site ______ to heart

A

closest

116
Q

Digoxin:

Decreases electrical ______ through _____ node

Decreases ______ in ______ node

______ myocardial contraction

A

conduction, AV

automaticity, SA

INCREASES

117
Q

What cardiac conditions does digoxin treat?

A

Treats: heart failure, Afib, A-flutter, SVT

118
Q

What are side effects of digoxin?

A

Can result in bradycardia, hypotension, cardiotoxicity, GI disturbances, fatigue, visual disturbances

119
Q

With digoxin, monitor HR for ____ minute, and hold dose if hr less than ____

A

1 minute, less than 60

120
Q

What is the therapeutic level of digoxin?

A

0.5-2.0 ng/mL

121
Q

What is digoxins relationship with potassium ?

A

inverse

122
Q

What lab do you need to monitor with digoxin?

A

potassium

123
Q

______ increases risk of toxicity with digoxin

A

Hypokalemia

124
Q

Educate patients taking digoxin to eat ____________ diet

A

high potassium

125
Q

What is seen in high doses with digoxin?

A

halos

126
Q

increases in mycardial contractions is called what affect?

A

inotropic effect

127
Q

Digoxin:

___________HR, _________myocardial contractions (inatropic effects),

A

decrease , increases

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