Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Ngozi's Challenges > Cardiac Rhythm Drugs COPY > Flashcards

Cardiac Rhythm Drugs COPY Flashcards

Exam 1

1
Q

What is conductivity? simple

A

Ability to pass an impulse through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the properties of cardiac cells?

A

Automaticity, excitability, conductivity, contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is automaticity? simple

A

generates their own electric impulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is excitability? simple

A

Ability to receive an impulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is conductivity? applied

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is contractility? simple

A

Ability to shrink and squeeze the movement of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where do pacemaker cells usually exist?

A

SA Node, AV junction, Purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is automaticity? applied

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T/F You would choose to medicate a patient before shocking a patient during a code.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is excitability? applied

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can cause a excitability in any cardiac cell?

A

Mechanical, chemical, or electrical impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens when impulses travel too fast or too slow?

A

Dysrhythmia occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F Contractility is a electrical event, not mechanical?

A

False, contractility is a mechanical event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is contractility? applied

A

ability of cardiac cells to shorten in response to electrical stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is PEA?

A

Conductivity without contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name three drugs that enhance contractility.

A

Digoxin, dopamine, and epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does Digoxin affect heart rate and contractility?

A

Slows HR and increase strength of contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is Dopamine not the first choice for septic patients?

A

Increase HR, which may be already fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of Epinephrine on conductivity and contractility?

A

Increase conductivity and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does Levophed primarily work?

A

Vasoconstriction, then moves to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does PEA stand for?

A

Pulseless electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you treat PEA?

A

Like Asystole with Epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does PEA look like?

A

Looks like a sinus rhythm, BUT patient has NO pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is cardiac action potential?

A

Change in electrical charge inside cardiac cell when stimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the three events that occur during cardiac action potential?

A

Polarization, Depolarization, Repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is an action potential?

A

Change in electrical potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where does an action potential occur?

A

Along the membrane of a muscle cell or nerve cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is polarization?

A

Electrical state when cardia cell membrane is at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is happening during polarization?

A

No electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does an ECG display during polarization?

A

Iso-electric line baseline” “

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is depolarization?

A

Opposite of polarization – when the actual contraction occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes depolarization?

A

Reversal of electrical charges at the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the significance of depolarization in the cardiac muscle?

A

Results in a contraction of the cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What does atrial depolarization represent?

A

P wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does ventricular depolarization represent?

A

QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the refractory period?

A

Unresponsiveness from nerve or muscle after stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the resistance of the cell membrane to a stimulus called?

A

Refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the three kinds of refractory period?

A

Absolute, relative, supernormal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the absolute refractory period?

A

Brief period when cells will not respond to further stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When does the absolute refractory period occur in the cardiac rhythm?

A

From the beginning of the QRS to the peak of the T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does the absolute refractory period mean for cardiac contractions?

A

Nothing can interfere with a cardiac contraction once it has started

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the key requirement for administering a shock in cardioversion?

A

Synchronization with the QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When would cells in the relative refractory period respond?

A

the cells may respond if there is a “stronger than normal” stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

T/F absolute refractory period only goes thorough the first half of the T wave?

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the relative refractory period also known as?

A

vulnerable period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

When does the relative refractory period occur?

A

when some cells have repolarized

and end of t wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What can happen if there is a stronger-than-normal stimulus during the relative refractory period?

A

R on T phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When does the R on T phenomenon occur?

A

when a stimulus that causes QRS depolarization lands on the last half of the T wave

51
Q

Why is R on T phenomenon dangerous?

A

it may lead to ventricular fibrillation

52
Q

When is the refractory period?

A

QRS complex to the middle of t wave is the refractory period

53
Q

What is the supernormal period?

A

Period after relative refractory period

54
Q

What happens during the supernormal period?

A

Weaker-than-normal stimulus can cause cells to depolarize

55
Q

When does the supernormal period occur?

A

End of the T wave

56
Q

When do we do synchronized cardioversion for a patient?

A

Only for patients with a heartbeat and no pulse means we defibrillate

57
Q

How does electricity move through the heart?

A
  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
Q

What is the 6 second method for measuring heart beats?

A

Count the number of QRSs in a 6 second strip and multiply by 10.

59
Q

What do cardiac rhythm drugs do?

A

Alter cardiac electrophysiologic function to treat/prevent dysrhythmias

60
Q

What can cardiac rhythm drugs affect?

A

AV node (increasing or reducing conduction speed) and ectopic pacemakers and the SA node

61
Q

What can cardiac rhythm drugs reduce?

A

Myocardial excitability

62
Q

What can cardiac rhythm drugs lengthen?

A

Refractory period

63
Q

What can cardiac rhythm drugs stimulate?

A

Autonomic nervous system

64
Q

What are the four groups of anti-dysrhythmic drugs?

A

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

65
Q

What is the major concern with all these anti-dysrhythmic drugs?

A

Toxicity

66
Q

What is the major problem associated with toxicity of anti-dysrhythmic drugs?

A

Dysrhythmias

67
Q

What are Class 1 Anti-dysrhythmic: Sodium Channel Blockers (Procainamide and Lidocaine) used for?

A

Drugs designed to SLOW cardiac conduction velocity

68
Q

What are the Class 1a sodium channel blockers?

A

Procainamide, quinidine, disopyramide

69
Q

What are the indications for Class 1a sodium channel blockers (Procainamide)?

A

SVT, V-tach, Atrial Flutter, Atrial Fibrillation

70
Q

What are the Class 1b sodium channel blockers?

A

Lidocaine, mexiletine, phenytoin

71
Q

What are the indications for Class 1b sodium channel blockers (Lidocaine)?

A

Short-term for ventricular dysrhythmias

72
Q

What are the Class 1c sodium channel blockers?

A

Propafenone, flecainide

73
Q

What are the indications for Class 1c sodium channel blockers?

A

SVT

74
Q

What does cardio toxicity caused by sodium channel blockers 1a (Procainamide) present with?

A

toxicity presents as confusion, drowsiness, vomiting

75
Q

What are the complications of Sodium Channel Blockers 1A (Procainamide)?

A

Systemic Lupus Syndrome, Neutropenia/thrombocytopenia/agranulocytosis, Cardio toxicity, Hypotension

76
Q

What are the monitoring and interventions for Systemic Lupus Syndrome caused by Sodium Channel Blockers 1A (Procainamide)?

A

Monitor for butterfly rash, give NSAIDs PRN, discontinue for rising ANA titer

77
Q

How should neutropenia, thrombocytopenia, and agranulocytosis be managed when caused by Sodium Channel Blockers 1A (Procainamide)?

A

CBC weekly for 12 weeks, then periodically; Watch for infection/bleeding; Stop with bone marrow suppression

78
Q

What are the monitoring and presenting symptoms of cardio toxicity caused by Sodium Channel Blockers 1A (Procainamide)?

A

Monitor for dysrhythmias (widened QRS); Procainamide level should be 4-10mcg/ml; (toxicity presents as confusion, drowsiness, vomiting)

79
Q

When should Sodium Channel Blockers 1A (Procainamide) be held in case of hypotension?

A

Hold med if patient is hypotensive

80
Q

What is V tach?

A

Widening QRS

81
Q

What are the complications associated with 1b sodium channel blockers (lidocaine)?

A

CNS Effects, Respiratory Arrest, Bradycardia, Hypotension

82
Q

What are the complications associated with 1C sodium channel blockers (Propafenone, flecainide)?

A

Bradycardia, heart failure, dizziness, weakness, hypotension, bronchospasm

83
Q

What are the symptoms that can occur when there is a drop in HR and BP?

A

Various symptoms

84
Q

What are some examples of beta blockers?

A

Propranolol, esmolol, acebutolol

85
Q

How do beta blockers (Propranolol, esmolol, acebutolol) work?

A

Preventing sympathetic nervous system stimulation of the heart

86
Q

What are the therapeutic uses of beta blockers?

A

Afib, aflutter, paroxysmal SVT, hypertension, angina, PVCs, severe recurrent ventricular tachycardia, exercise inducted tachycardias, paroxysmal atrial tachycardia

87
Q

What do beta blockers (Propranolol, esmolol, acebutolol) decrease?

A

Lowers HR and BP

88
Q

What levels should the MAP of BP be at?

A

Greater than 65

89
Q

What are some complications of beta blockers (Propranolol)?

A

Bradycardia, weakness, heart failure, dizziness, hypotension, bronchospasm

90
Q

In case of beta blocker overdose or severe adverse effects what is done?

A

Fluid bolus given to increase volume and atropine given to increase heart rate

91
Q

Why is the MAP more important than BP in the ICU?

A

Look at BP less and MAP more

92
Q

How does chest pain relate to hypoxia?

A

Not getting good blood mvmt

93
Q

Why do you lay a patient flat when they have chest pain related to hypoxia?

A

To help heart move blood easier

94
Q

T/F Vfib has a pulse?

A

False, Vfib never has a pulse

95
Q

What are the dosages given for potassium channel blocker (Amiodarone)?

A

Amiodarone 300 mg bolus if no pulse 150 if they do have pulse

96
Q

How do potassium channel blockers (amiodarone) affect the cardiac cycle?

A

By prolonging the action potential and refractory period of the cardiac cycle

97
Q

What is the mechanism of action of a potassium channel blocker?

A

It delays repolarization

98
Q

Besides affecting the cardiac cycle, what other effect does a potassium channel blocker have?

A

It dilates blood vessels

99
Q

Which types of dysrhythmias are targeted by potassium channel blockers (amiodarone)?

A

Afib, Vfib, vtach

100
Q

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

A

Pulmonary toxicity, sinus brady, visual disturbances

101
Q

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

A

Phlebitis (inflammation of a vein)

102
Q

What are some cardiovascular complications of amiodarone?

A

Hypotension, bradycardia, AV block

103
Q

What is the mechanism of action of adenosine?

A

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

104
Q

What are the indications for using adenosine?

A

SVT or Wolff-Parkinson-white syndrome (WPW)

105
Q

What are the potential complications of adenosine?

A

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

106
Q

What should be done when administering adenosine?

A

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

107
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

108
Q

Where should adenosine be administered?

A

Give at site closest to heart

109
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.

110
Q

How is Adenosine given?

A

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

111
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

112
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

113
Q

What conditions can digoxin be used to treat?

A

Heart failure, Afib, A-flutter, SVT

114
Q

What are the potential side effects of digoxin?

A

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

115
Q

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

A

<60 bpm

116
Q

What is the therapeutic level range for digoxin?

A

0.5-0.8 ng/ml

117
Q

What should be monitored while taking digoxin?

A

Potassium levels because hypokalemia increase risk of digoxin toxicity

118
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

119
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

120
Q

What does an increase in inotropic mean?

A

Increase in squeezing

121
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).

122
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).

123
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.

Ngozi's Challenges (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions