Cardiac Rhythm Drugs COPY Flashcards
Exam 1
1
Q
What is conductivity? simple
A
Ability to pass an impulse through
2
Q
What characteristic do cardiac cells have?
A
They have their own unique characteristics that allow them to regulate the heart rate and rhythm
3
Q
What are the properties of cardiac cells?
A
Automaticity, excitability, conductivity, contractility
4
Q
What is automaticity? simple
A
generates their own electric impulse
5
Q
What is excitability? simple
A
Ability to receive an impulse
6
Q
What is conductivity? applied
A
ability of cardiac cells to transmit the electrical impulse to adjacent heart cells
7
Q
What is contractility? simple
A
Ability to shrink and squeeze the movement of the heart
8
Q
Where do pacemaker cells usually exist?
A
SA Node, AV junction, Purkinje fibers
9
Q
What is automaticity? applied
A
Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse
10
Q
T/F You would choose to medicate a patient before shocking a patient during a code.
A
TRUE
11
Q
What is excitability? applied
A
Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli
12
Q
What can cause a excitability in any cardiac cell?
A
Mechanical, chemical, or electrical impulses
13
Q
What happens when impulses travel too fast or too slow?
A
Dysrhythmia occurs
14
Q
T/F Contractility is a electrical event, not mechanical?
A
False, contractility is a mechanical event
15
Q
What is contractility? applied
A
ability of cardiac cells to shorten in response to electrical stimulation
16
Q
Which event causes the heart to squeeze blood out to the body?
A
depolarization start the contraction, causing the heart to squeeze blood out to body
17
Q
What is PEA?
A
Conductivity without contraction
18
Q
Name three drugs that enhance contractility.
A
Digoxin, dopamine, and epinephrine
19
Q
How does Digoxin affect heart rate and contractility?
A
Slows HR and increase strength of contractility
20
Q
Why is Dopamine not the first choice for septic patients?
A
Increase HR, which may be already fast
21
Q
What is the effect of Epinephrine on conductivity and contractility?
A
Increase conductivity and contractility
22
Q
How does Levophed primarily work?
A
Vasoconstriction, then moves to the heart
23
Q
What does PEA stand for?
A
Pulseless electrical activity
24
Q
How do you treat PEA?
A
Like Asystole with Epinephrine
25
What does PEA look like?
Looks like a sinus rhythm, BUT patient has NO pulse
26
What is cardiac action potential?
Change in electrical charge inside cardiac cell when stimulated
27
What are the three events that occur during cardiac action potential?
Polarization, Depolarization, Repolarization
28
What is an action potential?
Change in electrical potential
29
Where does an action potential occur?
Along the membrane of a muscle cell or nerve cell
30
What is polarization?
Electrical state when cardia cell membrane is at rest
31
What is happening during polarization?
No electrical activity
32
What does an ECG display during polarization?
Iso-electric line baseline" "
33
What is depolarization?
Opposite of polarization – when the actual contraction occurs
34
What causes depolarization?
Reversal of electrical charges at the cell membrane
35
What is the significance of depolarization in the cardiac muscle?
Results in a contraction of the cardiac muscle
36
What does atrial depolarization represent?
P wave
37
What does ventricular depolarization represent?
QRS
38
What is the refractory period?
Unresponsiveness from nerve or muscle after stimulation
39
What is the resistance of the cell membrane to a stimulus called?
Refractory period
40
What are the three kinds of refractory period?
Absolute, relative, supernormal
41
What is the absolute refractory period?
Brief period when cells will not respond to further stimulation
42
When does the absolute refractory period occur in the cardiac rhythm?
From the beginning of the QRS to the peak of the T wave
43
What does the absolute refractory period mean for cardiac contractions?
Nothing can interfere with a cardiac contraction once it has started
44
What is the key requirement for administering a shock in cardioversion?
Synchronization with the QRS complex
45
When would cells in the relative refractory period respond?
the cells may respond if there is a “stronger than normal” stimulus
46
T/F absolute refractory period only goes thorough the first half of the T wave?
TRUE
47
What is the relative refractory period also known as?
vulnerable period
48
When does the relative refractory period occur?
when some cells have repolarized
and end of t wave
49
What can happen if there is a stronger-than-normal stimulus during the relative refractory period?
R on T phenomenon
50
When does the R on T phenomenon occur?
when a stimulus that causes QRS depolarization lands on the last half of the T wave
51
Why is R on T phenomenon dangerous?
it may lead to ventricular fibrillation
52
When is the refractory period?
QRS complex to the middle of t wave is the refractory period
53
What is the supernormal period?
Period after relative refractory period
54
What happens during the supernormal period?
Weaker-than-normal stimulus can cause cells to depolarize
55
When does the supernormal period occur?
End of the T wave
56
When do we do synchronized cardioversion for a patient?
Only for patients with a heartbeat and no pulse means we defibrillate
57
How does electricity move through the heart?
1. Electricity starts in the Sinoatrial (SA) node.
2. Intranodal Pathways
3. Intra-atrial Pathways
4. Atrioventricular (AV/Junctional) node
5. Bundle of HIS
6. Bundle Branches (left and right)
7. Purkinje Fibers
58
What is the 6 second method for measuring heart beats?
Count the number of QRSs in a 6 second strip and multiply by 10.
59
What do cardiac rhythm drugs do?
Alter cardiac electrophysiologic function to treat/prevent dysrhythmias
60
What can cardiac rhythm drugs affect?
AV node (increasing or reducing conduction speed) and ectopic pacemakers and the SA node
61
What can cardiac rhythm drugs reduce?
Myocardial excitability
62
What can cardiac rhythm drugs lengthen?
Refractory period
63
What can cardiac rhythm drugs stimulate?
Autonomic nervous system
64
What are the four groups of anti-dysrhythmic drugs?
Sodium Channel Blockers, Beta-Adrenergic Blockers, Potassium Channel Blockers, Calcium Channel Blockers
65
What is the major concern with all these anti-dysrhythmic drugs?
Toxicity
66
What is the major problem associated with toxicity of anti-dysrhythmic drugs?
Dysrhythmias
67
What are Class 1 Anti-dysrhythmic: Sodium Channel Blockers (Procainamide and Lidocaine) used for?
Drugs designed to SLOW cardiac conduction velocity
68
What are the Class 1a sodium channel blockers?
*Procainamide*, quinidine, disopyramide
69
What are the indications for Class 1a sodium channel blockers (Procainamide)?
SVT, V-tach, Atrial Flutter, Atrial Fibrillation
70
What are the Class 1b sodium channel blockers?
Lidocaine, mexiletine, phenytoin
71
What are the indications for Class 1b sodium channel blockers (Lidocaine)?
Short-term for ventricular dysrhythmias
72
What are the Class 1c sodium channel blockers?
Propafenone, flecainide
73
What are the indications for Class 1c sodium channel blockers?
SVT
74
What does cardio toxicity caused by sodium channel blockers 1a (Procainamide) present with?
toxicity presents as confusion, drowsiness, vomiting
75
What are the complications of Sodium Channel Blockers 1A (Procainamide)?
Systemic Lupus Syndrome, Neutropenia/thrombocytopenia/agranulocytosis, Cardio toxicity, Hypotension
76
What are the monitoring and interventions for Systemic Lupus Syndrome caused by Sodium Channel Blockers 1A (Procainamide)?
Monitor for butterfly rash, give NSAIDs PRN, discontinue for rising ANA titer
77
How should neutropenia, thrombocytopenia, and agranulocytosis be managed when caused by Sodium Channel Blockers 1A (Procainamide)?
CBC weekly for 12 weeks, then periodically; Watch for infection/bleeding; Stop with bone marrow suppression
78
What are the monitoring and presenting symptoms of cardio toxicity caused by Sodium Channel Blockers 1A (Procainamide)?
Monitor for dysrhythmias (widened QRS); Procainamide level should be 4-10mcg/ml; (toxicity presents as confusion, drowsiness, vomiting)
79
When should Sodium Channel Blockers 1A (Procainamide) be held in case of hypotension?
Hold med if patient is hypotensive
80
What is V tach?
Widening QRS
81
What are the complications associated with 1b sodium channel blockers (lidocaine)?
CNS Effects, Respiratory Arrest, Bradycardia, Hypotension
82
What are the complications associated with 1C sodium channel blockers (Propafenone, flecainide)?
Bradycardia, heart failure, dizziness, weakness, hypotension, bronchospasm
83
What are the symptoms that can occur when there is a drop in HR and BP?
Various symptoms
84
What are some examples of beta blockers?
Propranolol, esmolol, acebutolol
85
How do beta blockers (Propranolol, esmolol, acebutolol) work?
Preventing sympathetic nervous system stimulation of the heart
86
What are the therapeutic uses of beta blockers?
Afib, aflutter, paroxysmal SVT, hypertension, angina, PVCs, severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia
87
What do beta blockers (Propranolol, esmolol, acebutolol) decrease?
Lowers HR and BP
88
What levels should the MAP of BP be at?
Greater than 65
89
What are some complications of beta blockers (Propranolol)?
Bradycardia, weakness, heart failure, dizziness, hypotension, bronchospasm
90
In case of beta blocker overdose or severe adverse effects what is done?
Fluid bolus given to increase volume and atropine given to increase heart rate
91
Why is the MAP more important than BP in the ICU?
Look at BP less and MAP more
92
How does chest pain relate to hypoxia?
Not getting good blood mvmt
93
Why do you lay a patient flat when they have chest pain related to hypoxia?
To help heart move blood easier
94
T/F Vfib has a pulse?
False, Vfib never has a pulse
95
What are the dosages given for potassium channel blocker (Amiodarone)?
Amiodarone 300 mg bolus if no pulse 150 if they do have pulse
96
How do potassium channel blockers (amiodarone) affect the cardiac cycle?
By prolonging the action potential and refractory period of the cardiac cycle
97
What is the mechanism of action of a potassium channel blocker?
It delays repolarization
98
Besides affecting the cardiac cycle, what other effect does a potassium channel blocker have?
It dilates blood vessels
99
Which types of dysrhythmias are targeted by potassium channel blockers (amiodarone)?
Afib, Vfib, vtach
100
What are some complications of potassium channel blockers (amiodarone)?
Pulmonary toxicity, sinus brady, visual disturbances
101
What is a potential complication of administering potassium channel blocker (amiodarone)?
Phlebitis (inflammation of a vein)
102
What are some cardiovascular complications of amiodarone?
Hypotension, bradycardia, AV block
103
What is the mechanism of action of adenosine?
Decreases electrical conduction through the AV node and decreases automaticity in the SA node
104
What are the indications for using adenosine?
SVT or Wolff-Parkinson-white syndrome (WPW)
105
What are the potential complications of adenosine?
Sinus brady, hypotension, dyspnea with bronchoconstriction, flushed face from vasodilation
106
What should be done when administering adenosine?
Monitor the ECG. Effects usually last 1 min or less, have IV bolus prepared
107
What is the recommended dosing regimen for adenosine?
Dose 1: 6mg rapid IVP followed by 20 ml rapid saline bolus, Dose 2: 12 mg rapid IVP followed by 20 ml rapid saline bolus, Dose 3: 12 mg rapid IVP followed by 20 ml rapid saline bolus
108
Where should adenosine be administered?
Give at site closest to heart
109
What is the significance of given Adenosine in the AC?
It is given in the AC and above because it has an immediate on set of action, short half life, and very brief duration of action.
110
How is Adenosine given?
Closest to the heart, with an 18 G, and a 3 stopcock
111
Why would you ask a patient to bear down?
To relieve pressure in the chest and help return the heart to a normal rhythm
112
What are the effects of digoxin on the heart?
Decreases electrical conduction through AV node, decreases automaticity in SA node, INCREASES myocardial contraction
113
What conditions can digoxin be used to treat?
Heart failure, Afib, A-flutter, SVT
114
What are the potential side effects of digoxin?
Bradycardia, hypotension, cardiotoxicity, GI disturbances, fatigue, visual disturbances
115
What is the recommended heart rate threshold for holding a dose of digoxin?
<60 bpm
116
What is the therapeutic level range for digoxin?
0.5-0.8 ng/ml
117
What should be monitored while taking digoxin?
Potassium levels because hypokalemia increase risk of digoxin toxicity
118
What should be included in the patient's diet while taking digoxin?
High potassium foods
bananas, oranges, apricots, dates, raisins, broccoli, green beans, potatoes, tomatoes, meats, fish, wheat bread, legumes, green leafy vegetables
119
What does digoxin to the cardiovascular system?
Slow HR down and HR good squeeze strong and have a good contraction with a lot of blood flow
Increase inotropic – mean squeezing
120
What does an increase in inotropic mean?
Increase in squeezing
121
What is a possible s/s of digoxin toxicity?
signs and symptoms of digoxin toxicity include bradycardia, headache, dizziness, confusion, nausea, and visual disturbances (blurred vision or yellow vision).
122
When should digoxin dose be held?
If adverse effects: digoxin toxicity include bradycardia, headache, dizziness, confusion, nausea, and visual disturbances (blurred vision or yellow vision).
123
What are some non medicine interventions for SVT?
Vagal manoeuvres bearing down. breathe out with your stomach muscles but you don't let air out of your nose or mouth. To stimulate the vagal nerve.
