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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

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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

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3
Q

What are the properties of cardiac cells?

A

Automaticity, excitability, conductivity, contractility

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4
Q

What is automaticity? simple

A

generates their own electric impulse

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5
Q

What is excitability? simple

A

Ability to receive an impulse

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6
Q

What is conductivity? applied

A

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

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7
Q

What is contractility? simple

A

Ability to shrink and squeeze the movement of the heart

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8
Q

Where do pacemaker cells usually exist?

A

SA Node, AV junction, Purkinje fibers

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9
Q

What is automaticity? applied

A

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

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10
Q

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

A

TRUE

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11
Q

What is excitability? applied

A

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

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12
Q

What can cause a excitability in any cardiac cell?

A

Mechanical, chemical, or electrical impulses

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13
Q

What happens when impulses travel too fast or too slow?

A

Dysrhythmia occurs

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14
Q

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

A

False, contractility is a mechanical event

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15
Q

What is contractility? applied

A

ability of cardiac cells to shorten in response to electrical stimulation

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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

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17
Q

What is PEA?

A

Conductivity without contraction

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18
Q

Name three drugs that enhance contractility.

A

Digoxin, dopamine, and epinephrine

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19
Q

How does Digoxin affect heart rate and contractility?

A

Slows HR and increase strength of contractility

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20
Q

Why is Dopamine not the first choice for septic patients?

A

Increase HR, which may be already fast

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21
Q

What is the effect of Epinephrine on conductivity and contractility?

A

Increase conductivity and contractility

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22
Q

How does Levophed primarily work?

A

Vasoconstriction, then moves to the heart

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23
Q

What does PEA stand for?

A

Pulseless electrical activity

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24
Q

How do you treat PEA?

A

Like Asystole with Epinephrine

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25
Q

What does PEA look like?

A

Looks like a sinus rhythm, BUT patient has NO pulse

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26
Q

What is cardiac action potential?

A

Change in electrical charge inside cardiac cell when stimulated

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27
Q

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

A

Polarization, Depolarization, Repolarization

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28
Q

What is an action potential?

A

Change in electrical potential

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29
Q

Where does an action potential occur?

A

Along the membrane of a muscle cell or nerve cell

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30
Q

What is polarization?

A

Electrical state when cardia cell membrane is at rest

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31
Q

What is happening during polarization?

A

No electrical activity

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32
Q

What does an ECG display during polarization?

A

Iso-electric line baseline” “

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33
Q

What is depolarization?

A

Opposite of polarization – when the actual contraction occurs

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34
Q

What causes depolarization?

A

Reversal of electrical charges at the cell membrane

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35
Q

What is the significance of depolarization in the cardiac muscle?

A

Results in a contraction of the cardiac muscle

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36
Q

What does atrial depolarization represent?

A

P wave

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37
Q

What does ventricular depolarization represent?

A

QRS

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38
Q

What is the refractory period?

A

Unresponsiveness from nerve or muscle after stimulation

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39
Q

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

A

Refractory period

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40
Q

What are the three kinds of refractory period?

A

Absolute, relative, supernormal

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41
Q

What is the absolute refractory period?

A

Brief period when cells will not respond to further stimulation

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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

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43
Q

What does the absolute refractory period mean for cardiac contractions?

A

Nothing can interfere with a cardiac contraction once it has started

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44
Q

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

A

Synchronization with the QRS complex

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45
Q

When would cells in the relative refractory period respond?

A

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

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46
Q

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

A

TRUE

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47
Q

What is the relative refractory period also known as?

A

vulnerable period

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48
Q

When does the relative refractory period occur?

A

when some cells have repolarized

and end of t wave

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49
Q

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

A

R on T phenomenon

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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?

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?

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?

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)

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