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Cardiac Rhythm Drugs Flashcards

Exam 1

1
Q

What are some non medicine interventions for SVT?

A

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.

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2
Q

When should digoxin dose be held?

A

If adverse effects: digoxin toxicity include bradycardia, headache, dizziness, confusion, nausea, and visual disturbances (blurred vision or yellow vision).

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3
Q

What is a possible s/s of digoxin toxicity?

A

signs and symptoms of digoxin toxicity include bradycardia, headache, dizziness, confusion, nausea, and visual disturbances (blurred vision or yellow vision).

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4
Q

What does an increase in inotropic mean?

A

Increase in squeezing

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5
Q

What does digoxin to the cardiovascular system?

A

Slow HR down and HR good squeeze strong and have a good contraction with a lot of blood flow
Increase inotropic – mean squeezing

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6
Q

What should be included in the patient’s diet while taking digoxin?

A

High potassium foods
bananas, oranges, apricots, dates, raisins, broccoli, green beans, potatoes, tomatoes, meats, fish, wheat bread, legumes, green leafy vegetables

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7
Q

What should be monitored while taking digoxin?

A

Potassium levels because hypokalemia increase risk of digoxin toxicity

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8
Q

What is the therapeutic level range for digoxin?

A

0.5-0.8 ng/ml

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9
Q

What is the recommended heart rate threshold for holding a dose of digoxin?

A

<60 bpm

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10
Q

What are the potential side effects of digoxin?

A

Bradycardia, hypotension, cardiotoxicity, GI disturbances, fatigue, visual disturbances

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11
Q

What conditions can digoxin be used to treat?

A

Heart failure, Afib, A-flutter, SVT

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12
Q

What are the effects of digoxin on the heart?

A

Decreases electrical conduction through AV node, decreases automaticity in SA node, INCREASES myocardial contraction

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13
Q

Why would you ask a patient to bear down?

A

To relieve pressure in the chest and help return the heart to a normal rhythm

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14
Q

How is Adenosine given?

A

Closest to the heart, with an 18 G, and a 3 stopcock

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15
Q

What is the significance of given Adenosine in the AC?

A

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.

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16
Q

Where should adenosine be administered?

A

Give at site closest to heart

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17
Q

What is the recommended dosing regimen for adenosine?

A

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

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18
Q

What should be done when administering adenosine?

A

Monitor the ECG. Effects usually last 1 min or less, have IV bolus prepared

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19
Q

What are the potential complications of adenosine?

A

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

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20
Q

What are the indications for using adenosine?

A

SVT or Wolff-Parkinson-white syndrome (WPW)

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21
Q

What is the mechanism of action of adenosine?

A

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

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22
Q

What are some cardiovascular complications of amiodarone?

A

Hypotension, bradycardia, AV block

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23
Q

What is a potential complication of administering potassium channel blocker (amiodarone)?

A

Phlebitis (inflammation of a vein)

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24
Q

What are some complications of potassium channel blockers (amiodarone)?

A

Pulmonary toxicity, sinus brady, visual disturbances

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25
Which types of dysrhythmias are targeted by potassium channel blockers (amiodarone)?
Afib, Vfib, vtach
26
Besides affecting the cardiac cycle, what other effect does a potassium channel blocker have?
It dilates blood vessels
27
What is the mechanism of action of a potassium channel blocker?
It delays repolarization
28
How do potassium channel blockers (amiodarone) affect the cardiac cycle?
By prolonging the action potential and refractory period of the cardiac cycle
29
What are the dosages given for potassium channel blocker (Amiodarone)?
Amiodarone 300 mg bolus if no pulse 150 if they do have pulse
30
T/F Vfib has a pulse?
False, Vfib never has a pulse
31
Why do you lay a patient flat when they have chest pain related to hypoxia?
To help heart move blood easier
32
How does chest pain relate to hypoxia?
Not getting good blood mvmt
33
Why is the MAP more important than BP in the ICU?
Look at BP less and MAP more
34
In case of beta blocker (lol) overdose or severe adverse effects what is done?
Fluid bolus given to increase volume and atropine given to increase heart rate
35
What are some complications of beta blockers (Propranolol)?
Bradycardia, weakness, heart failure, dizziness, hypotension, bronchospasm
36
What levels should the MAP of BP be at?
Greater than 65
37
What do beta blockers (Propranolol, esmolol, acebutolol) decrease?
Lowers HR and BP
38
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
39
How do beta blockers (Propranolol, esmolol, acebutolol) work?
Preventing sympathetic nervous system stimulation of the heart
40
What are some examples of beta blockers?
Propranolol, esmolol, acebutolol
41
What are the symptoms that can occur when there is a drop in HR and BP?
Various symptoms
42
What are the complications associated with 1C sodium channel blockers (Propafenone, flecainide)?
Bradycardia, heart failure, dizziness, weakness, hypotension, bronchospasm
43
What are the complications associated with 1b sodium channel blockers (lidocaine)?
CNS Effects, Respiratory Arrest, Bradycardia, Hypotension
44
What is V tach?
Widening QRS
45
When should Sodium Channel Blockers 1A (Procainamide) be held in case of hypotension?
Hold med if patient is hypotensive
46
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)
47
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
48
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
49
What are the complications of Sodium Channel Blockers 1A (Procainamide)?
Systemic Lupus Syndrome, Neutropenia/thrombocytopenia/agranulocytosis, Cardio toxicity, Hypotension
50
What does cardio toxicity caused by sodium channel blockers 1a (Procainamide) present with?
toxicity presents as confusion, drowsiness, vomiting
51
What are the indications for Class 1c sodium channel blockers?
SVT
52
What are the Class 1c sodium channel blockers?
Propafenone, flecainide
53
What are the indications for Class 1b sodium channel blockers (Lidocaine)?
Short-term for ventricular dysrhythmias
54
What are the Class 1b sodium channel blockers?
Lidocaine, mexiletine, phenytoin
55
What are the indications for Class 1a sodium channel blockers (Procainamide)?
SVT, V-tach, Atrial Flutter, Atrial Fibrillation
56
What are the Class 1a sodium channel blockers?
*Procainamide*, quinidine, disopyramide
57
What are Class 1 Anti-dysrhythmic: Sodium Channel Blockers (Procainamide and Lidocaine) used for?
Drugs designed to SLOW cardiac conduction velocity
58
What is the major problem associated with toxicity of anti-dysrhythmic drugs?
Dysrhythmias
59
What is the major concern with all these anti-dysrhythmic drugs?
Toxicity
60
What are the four groups of anti-dysrhythmic drugs?
Sodium Channel Blockers, Beta-Adrenergic Blockers, Potassium Channel Blockers, Calcium Channel Blockers
61
What can cardiac rhythm drugs stimulate?
Autonomic nervous system
62
What can cardiac rhythm drugs lengthen?
Refractory period
63
What can cardiac rhythm drugs reduce?
Myocardial excitability
64
What can cardiac rhythm drugs affect?
AV node (increasing or reducing conduction speed) and ectopic pacemakers and the SA node
65
What do cardiac rhythm drugs do?
Alter cardiac electrophysiologic function to treat/prevent dysrhythmias
66
What is the 6 second method for measuring heart beats?
Count the number of QRSs in a 6 second strip and multiply by 10.
67
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
68
When do we do synchronized cardioversion for a patient?
Only for patients with a heartbeat and no pulse means we defibrillate
69
When does the supernormal period occur?
End of the T wave
70
What happens during the supernormal period?
Weaker-than-normal stimulus can cause cells to depolarize
71
What is the supernormal period?
Period after relative refractory period
72
When is the refractory period?
QRS complex to the middle of t wave is the refractory period
73
Why is R on T phenomenon dangerous?
it may lead to ventricular fibrillation
74
When does the R on T phenomenon occur?
when a stimulus that causes QRS depolarization lands on the last half of the T wave
75
What can happen if there is a stronger-than-normal stimulus during the relative refractory period?
R on T phenomenon
76
When does the relative refractory period occur?
when some cells have repolarized and end of t wave
77
What is the relative refractory period also known as?
vulnerable period
78
T/F absolute refractory period only goes thorough the first half of the T wave?
TRUE
79
When would cells in the relative refractory period respond?
the cells may respond if there is a “stronger than normal” stimulus
80
What is the key requirement for administering a shock in cardioversion?
Synchronization with the QRS complex
81
What does the absolute refractory period mean for cardiac contractions?
Nothing can interfere with a cardiac contraction once it has started
82
When does the absolute refractory period occur in the cardiac rhythm?
From the beginning of the QRS to the peak of the T wave
83
What is the absolute refractory period?
Brief period when cells will not respond to further stimulation
84
What are the three kinds of refractory period?
Absolute, relative, supernormal
85
What is the resistance of the cell membrane to a stimulus called?
Refractory period
86
What is the refractory period?
Unresponsiveness from nerve or muscle after stimulation
87
What does ventricular depolarization represent?
QRS
88
What does atrial depolarization represent?
P wave
89
What is the significance of depolarization in the cardiac muscle?
Results in a contraction of the cardiac muscle
90
What causes depolarization?
Reversal of electrical charges at the cell membrane
91
What is depolarization?
Opposite of polarization – when the actual contraction occurs
92
What does an ECG display during polarization?
Iso-electric line baseline" "
93
What is happening during polarization?
No electrical activity
94
What is polarization?
Electrical state when cardia cell membrane is at rest
95
Where does an action potential occur?
Along the membrane of a muscle cell or nerve cell
96
What is an action potential?
Change in electrical potential
97
What are the three events that occur during cardiac action potential?
Polarization, Depolarization, Repolarization
98
What is cardiac action potential?
Change in electrical charge inside cardiac cell when stimulated
99
What does PEA look like?
Looks like a sinus rhythm, BUT patient has NO pulse
100
How do you treat PEA?
Like Asystole with Epinephrine
101
What does PEA stand for?
Pulseless electrical activity
102
How does Levophed primarily work?
Vasoconstriction, then moves to the heart
103
What is the effect of Epinephrine on conductivity and contractility?
Increase conductivity and contractility
104
Why is Dopamine not the first choice for septic patients?
Increase HR, which may be already fast
105
How does Digoxin affect heart rate and contractility?
Slows HR and increase strength of contractility
106
Name three drugs that enhance contractility.
Digoxin, dopamine, and epinephrine
107
What is PEA?
Conductivity without contraction
108
Which event causes the heart to squeeze blood out to the body?
depolarization start the contraction, causing the heart to squeeze blood out to body
109
What is contractility? applied
ability of cardiac cells to shorten in response to electrical stimulation
110
T/F Contractility is a electrical event, not mechanical?
False, contractility is a mechanical event
111
What happens when impulses travel too fast or too slow?
Dysrhythmia occurs
112
What can cause a excitability in any cardiac cell?
Mechanical, chemical, or electrical impulses
113
What is excitability? applied
Ability to respond to electrical impulses generated by the pacemaker cells or other external stimuli
114
T/F You would choose to medicate a patient before shocking a patient during a code.
TRUE
115
What is automaticity? applied
Pacing function/ability of cardiac pacemaker cells to spontaneously initiate an electrical impulse
116
Where do pacemaker cells usually exist?
SA Node, AV junction, Purkinje fibers
117
What is contractility? simple
Ability to shrink and squeeze the movement of the heart
118
What is conductivity? applied
ability of cardiac cells to transmit the electrical impulse to adjacent heart cells
119
What is excitability? simple
Ability to receive an impulse
120
What is automaticity? simple
generates their own electric impulse
121
What are the properties of cardiac cells?
Automaticity, excitability, conductivity, contractility
122
What characteristic do cardiac cells have?
They have their own unique characteristics that allow them to regulate the heart rate and rhythm
123
What is conductivity? simple
Ability to pass an impulse through

Ngozi's Challenges (6 decks)

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