Cardiac rhythm drugs: antidysrhythmic drugs Flashcards
1
Q
______: have unique characteristics that allow them to regulate the heart rate and rhythm
A
Cardiac cells
2
Q
Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse
A
Automaticity
3
Q
Automaticity
A
Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse
4
Q
Pacemaker cells usually only exist in the _____________
A
SA Node, AV junction, and Purkinje fibers
5
Q
Other cells can have ______ (initiate electrical impulses) after MI, electrolyte imbalances, hypoxia, and drug toxicity, leading to ______
A
automaticity, dysrhythmias
6
Q
______-includes all cardiac cells
A
Excitability
7
Q
Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli
A
excitability
8
Q
excitability
A
Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli
9
Q
Mechanical, chemical, or electrical impulses can cause a response to any cardiac cell because of their ______
A
excitability
10
Q
The ability of cardiac cells to transmit the electrical impulse to adjacent heart cells
A
Conductivity
11
Q
Conductivity
A
The ability of cardiac cells to transmit the electrical impulse to adjacent heart cells
12
Q
conductivity: The impulse travels to the cells and ______ in rapid succession creates deflections seen on ECG.
A
depolarization
13
Q
If impulses travel too fast or to slow, through blocked pathways, or through abnormal pathways, a ______exists
A
dysrhythmia
14
Q
The ability of cardiac cells to shorten in response to electrical stimulation
A
Contractility
15
Q
Contractility
A
The ability of cardiac cells to shorten in response to electrical stimulation
16
Q
Is a mechanical event, not electrical
A
contractility
17
Q
contractility: ______ starts the contraction, causing the heart to squeeze blood out to the body
A
Depolarization
18
Q
Conductivity withOUT contraction is called ______
A
PEA
19
Q
______ withOUT contraction is called PEA
A
Conductivity
20
Q
Is enhanced by drugs like digoxin, dopamine, and epinephrine
A
contractility
21
Q
what drugs enhance contractility?
A
Is enhanced by drugs like digoxin, dopamine, and epinephrine
22
Q
_____ slows and strengthens the contractions
A
digoxin
23
Q
______ increases HR, and contractility and BP
A
dopamine and epinephrine
24
Q
_______ vasoconstricts peripherally, it doesn’t increase ________,
A
levophed (norepinephrine) , HR (in lower doses)
25
levophed is not ______
inotropic
26
______ –increases contractility and increases HR and BP
epinephrine, dopamine
27
is not given for septic/feverish patients (can send septic patients into SVT)
dopamine
28
_______ is a side effect of epinephrine
pulmonary edema (pink frothy stuff)
29
pulmonary edema is a side effect of which drug?
epinephrine
30
how do you treat PEA?
like asystole, with epi and compressions
31
With EVERY rhythm, we should ask: ______________
“Does it have a pulse?”
32
The change in electrical charge inside the cardiac cell when it is stimulated
Cardiac Action Potential
33
Cardiac Action Potential
The change in electrical charge inside the cardiac cell when it is stimulated
34
What does cardiac action potential cause?
Polarization, Depolarization, Repolarization
35
the change in electrical potential associated with the passage of an impulse along the membrane of a muscle cell or nerve cell.
action potential
36
action potential
the change in electrical potential associated with the passage of an impulse along the membrane of a muscle cell or nerve cell.
37
The electrical state that exists at the cardiac cell membrane when the cell is at rest
polarization
38
polarization, what is it? what electrical activity is occuring? where is it in the EKG strip?
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”
39
The electrical event that results in a contraction of the cardiac muscle
Depolarization
40
Depolarization
The electrical event that results in a contraction of the cardiac muscle
41
when does atrial depolarization occur, as in what wave is it?
p wave
42
what wave represents ventricular depolarization?
QRS
43
a period immediately following stimulation during which a nerve or muscle is unresponsive to further stimulation.
refractory period
44
Resistance of the cell membrane to a stimulus
refractory period
45
what are the three kinds of refractory period?
Absolute refractory period
Relative refractory period
Supernormal refractory period
46
Brief period during depolarization when the cells WILL NOT respond to further stimulation, no matter how strong the stimulus
absolute refractory period
47
when is the absolute refractory period?
In the cardiac rhythm, this is from the beginning of the QRS to the peak of the T wave
48
This means that nothing can interfere with a cardiac contraction once it has started
absolute refractory period
49
Some of the cells have repolarized
These cells may respond if there is a ______ stimulus during the relative refractory period or "vulnerable period"
“stronger than normal”
50
A stronger than normal stimulus during the relative refractory period may result in ________ which can turn into ________ an d eventually ____
R on T, torsades, v fib
51
______ 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)
R on T Phenomenon
52
R on T may lead to _________
ventricular fibrillation
53
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
supernormal period
54
know that we only ______ for patients that have a heartbeat
synchronize cardiovert
55
know that we only synchronize cardiovert for patients that ______
have a heartbeat
56
what is done for patients who dont have a pulse in V tach or fib?
defibrilation
57
Give the pathway of the Cardiac conduction system
SA node
AV node
Bundle of his
Bundle branches
Perkinje fibers
58
Cardiac Rhythm Drugs:
______
______
______
Can reduce myocardial excitability
Can lengthen the refractory period
Can stimulate the autonomic nervous system
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
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
______
______
______
Can reduce myocardial excitability
Can lengthen the refractory period
Can stimulate the autonomic nervous system
60
What are the different anti dysrhythmic drug groups?
Sodium Channel Blockers
Beta-Adrenergic Blockers
Potassium Channel Blockers
Calcium Channel Blockers
61
What is the MAJOR CONCERN WITH ALL ANTI-DYSRHYTHMIC DRUG GROUPS? WHAT IS THE RESULT OF THE POTENTIAL EFFECT?
TOXICITY. TOXICITY CAN CAUSE DYSRHYTHMIAS.
62
What are the 1a sodium channel blockers?
Procainamide, quinidine, disopyramide
63
What are class 1a sodium channel blockers used to treat?
***Used for SVT, V-tach, Atrial Flutter, Atrial Fibrillation
64
What are the class 1b sodium channel blockers?
lidocaine, mexiletine, phenytoin
65
What are class 1b sodium channel blockers used to treat?
Used only short-term for ventricular dysrhythmias
66
What are the class 1c sodium channel blockers?
Propafenone, flecainide
67
What are 1c sodium channel blockers used to treat?
used to treat SVT
68
These drugs are designed to SLOW cardiac conduction velocity
sodium channel blockers
69
phenytoin is used for __________ and required _____
seizures and dysrhythmias , filter tubing
70
What are the main complications of sodium channel blockers 1a
Lupus
CBC -neutropenia, thrombocytopenia, agranulocytosis
cardio toxicity
hypotension
71
Sodium channel blockers 1a:
Systemic Lupus Syndrome
monitor for ______
give NSAIDS PRN
discontinue for rising ANA titer
butterfly rash
72
Sodium channel blockers 1a:
Systemic Lupus Syndrome
monitor for butterfly rash
give ______ PRN
discontinue for rising ANA titer
NSAIDS
73
Sodium channel blockers 1a:
Systemic Lupus Syndrome
monitor for butterfly rash
give NSAIDS PRN
discontinue for ______
rising ANA titer
74
Sodium channel blockers 1a:
______
CBC weekly for 12 weeks, then periodically
watch for infection/bleeding
STOP with bone marrow suppression
Neutropenia, thrombocytopenia, agranulocytosis
75
Sodium channel blockers 1a:
Neutropenia, thrombocytopenia, agranulocytosis
CBC weekly for ______, then periodically
watch for infection/bleeding
STOP with bone marrow suppression
12 weeks
76
Sodium channel blockers 1a:
Neutropenia, thrombocytopenia, agranulocytosis
CBC weekly for 12 weeks, then periodically
watch for ______
STOP with bone marrow suppression
infection/bleeding
77
Sodium channel blockers 1a:
Neutropenia, thrombocytopenia, agranulocytosis
CBC weekly for 12 weeks, then periodically
watch for infection/bleeding
STOP with ______
bone marrow suppression
78
Sodium channel blockers 1a:
Cardio toxicity
monitor for ______
procainamide level should be 4-10mcg/ml
toxicity presents as confusion, drowsiness, vomiting
dysrhythmias (widened QRS)
79
Sodium channel blockers 1a:
Cardio toxicity
monitor for dysrhythmias (widened QRS)
procainamide level should be ______
toxicity presents as confusion, drowsiness, vomiting
4-10mcg/ml
80
Sodium channel blockers 1a:
Cardio toxicity
monitor for dysrhythmias (widened QRS)
procainamide level should be 4-10mcg/ml
toxicity presents as ______
confusion, drowsiness, vomiting
81
Sodium channel blockers 1a:
hold med if patient is ______
hypotensive
82
What are the major complications of sodium channel blockers class 1 b?
CNS effects
Respiratory Arrest
83
Sodium channel blockers 1b:
CNS Effects
things slow down
blood flow is decreased to brain bc
_______
perfusion is decreased (low bp)
84
What are sodium channel blocker complications with class 1c?
______, ______, ______, weakness, hypotension, bronchospasm
Bradycardia, heart failure, dizziness
85
What are sodium channel blocker complications with class 1c?
Bradycardia, heart failure dizziness, ______, ______, ______
weakness, hypotension, bronchospasm
86
What are the Class II antidysrhythmics?
Beta blockers
87
Give examples of Beta blockers, what do they end in?
Propranolol, esmolol, acebutolol. Beta blockers typically end in lol.
88
What affects do beta blockers have on the circulatory system?
lower heart rate and blood pressure
89
Work by preventing sympathetic nervous system stimulation of the heart
beta blockers
90
beta blockers work by preventing ______ stimulation of the heart
sympathetic nervous system
91
Beta blockers
Therapeutic uses:
________________
________________
________________
________________
angina,
PVCs,
severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia
afib,
aflutter,
paroxysmal SVT,
hypertension,
92
Beta blocker:
Therapeutic uses:
afib,
aflutter,
paroxysmal SVT,
hypertension,
________________
________________
________________
________________
________________
angina,
PVCs,
severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia
93
Beta blocker complications
Propranolol:
________________
________________
________________
dizziness,
hypotension,
bronchospasm
bradycardia,
weakness,
heart failure,
94
Beta blocker complications
Propranolol:
________________
________________
________________
bradycardia,
weakness,
heart failure,
dizziness,
hypotension,
bronchospasm
95
______ can be given to bring heart rate up
atropine
96
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 __________
over 65, ride it out, fluid bolus
97
____________ can be a good short term fix for poor central perfusion. hypotension can be caused by beta blockers.
Trendelenburg
98
What are Class III anti dysrhythmics called?
Potassium channel blockers
99
What are the Class III antidysrhythmics or potassium channel blockers?
Amiodarone, sotalol, ibutilide, dofetilide, dronedarone
100
how do potassium channel blockers work?
Work by prolonging the action potential and refractory period of the cardiac cycle
Delays repolarization
Dilates blood vessels
101
What cardiac conditions do potassium channel blockers work for?
Afib ,Vfib, vtach really need to know that amiodarone is used for vfib and vtach
102
What is amiodarone used for?
vfib and vtach
103
amiodarone –v fib and v tach -__________ for no pulse, ____________ for pulse
300 mg, 150 mg
104
Complications of potassium channel blockers (amiodarone):
________________
________________
________________
Other effects
Phlebitis with administration
Hypotension, bradycardia, AV block
Pulmonary Toxicity -breathing troubles
Sinus Brady and AV block
Visual disturbances
105
Complications of potassium channel blockers (amiodarone):
Pulmonary Toxicity -breathing troubles
Sinus Brady and AV block
Visual disturbances
________________
________________
________________
Other effects
Phlebitis with administration
Hypotension, bradycardia, AV block
106
____________ 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
Amiodarone
107
Amiodarone is the drug of choice for ____________________, know how fast we give it on drips, know how fast we give it IV push
v fib and v tach
108
Decreases electrical conduction through the AV node and decreases automaticity in the SA node
adenosine
109
What conditions is adenosine used for?
Used for SVT or Wolff-Parkinson-white syndrome (WPW)
110
Complications from adenosine:
________________
________________
________________
________________
sinus brady,
hypotension,
dyspnea with bronchoconstriction, flushed face from vasodilation
111
for SVT –want an IV close to ____________, ___________ , want a ____________ (adenosine, flush immediately)
the heart, large bore, three way stop cock
112
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
asystole, die, crash cart
113
What to do for adenosine administration? Monitor the _____. Effects usually last _________, have IV ______ prepared
ECG, 1 min or less, bolus
114
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
6mg, 12 mg, 12 mg
115
adenosine: Give at site ______ to heart
closest
116
Digoxin:
Decreases electrical ______ through _____ node
Decreases ______ in ______ node
______ myocardial contraction
conduction, AV
automaticity, SA
INCREASES
117
What cardiac conditions does digoxin treat?
Treats: heart failure, Afib, A-flutter, SVT
118
What are side effects of digoxin?
Can result in bradycardia, hypotension, cardiotoxicity, GI disturbances, fatigue, visual disturbances
119
With digoxin, monitor HR for ____ minute, and hold dose if hr less than ____
1 minute, less than 60
120
What is the therapeutic level of digoxin?
0.5-2.0 ng/mL
121
What is digoxins relationship with potassium ?
inverse
122
What lab do you need to monitor with digoxin?
potassium
123
______ increases risk of toxicity with digoxin
Hypokalemia
124
Educate patients taking digoxin to eat ____________ diet
high potassium
125
What is seen in high doses with digoxin?
halos
126
increases in mycardial contractions is called what affect?
inotropic effect
127
Digoxin:
___________HR, _________myocardial contractions (inatropic effects),
decrease , increases
