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NURS 313R > Exam 1: Arrhythmias & ECG > Flashcards

Exam 1: Arrhythmias & ECG Flashcards

1
Q

Anatomy of the Cardiac Conduction System include

A
  1. SA node
  2. Bachmann’s Bundle
  3. AV node
  4. Bundle of His
  5. Left and Right Bundle Branch
  6. Purkinje Fibers
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2
Q

Polarization includes

A

Positive or negative

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3
Q

Types of Polarization include

A
  1. Atrial Depolarization
  2. Ventricular Depolarization
  3. Ventricular Repolarization
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4
Q

ECG Cardiac Cycle

A
  1. P Wave
  2. PR Interval
  3. QRS Interval
  4. ST Segment
  5. T Wave
  6. QT Interval
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5
Q

EKG Paper

A

Time measure in seconds

Amplitude measured in mV

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6
Q

Small box

A

0.04 secs and 0.1 mV amplitude

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7
Q

Large box

A

5x5 small boxes = 0.2 secs and 0.5 mV amplitude

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8
Q

Methods of Measuring Rate

A
  1. Number of QRS complexes in one minute
  2. Six second strip
  3. Number of small boxes between two R waves
  4. Triplicate method
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9
Q

What are the three types of sinus rhythms?

A

Normal Sinus Rhythm
Sinus Tachycardia
Sinus Bradycardia

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10
Q

Normal Sinus Rhythm Characteristics

A 
Rate: Normal Duration
P Wave: 0.06-0.12 sec
P-R interval: 0.12-0.20 sec
QRS: <0.12 sec
Rhythm: 60-100 bpm
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11
Q

Sinus Tachycardia Characteristics

A 
Rate: Normal Duration
P Wave: Normal
P-R Interval: Normal
QRS: Normal
Rhythm: 101-200 bpm
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12
Q

Sinus Bradycardia Characteristics

A 
Rate: Normal Duration 
P Wave: Normal
P-R Interval: Normal
QRS: Normal
Rhythm: <60 bpm
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13
Q

The four types of Atrial Rhythms include

A
  1. Premature Atrial Contraction
  2. Atrial Flutter
  3. Atrial Fibrillation
  4. Supraventricular Tachycardia
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14
Q

Premature Atrial Contraction Characteristics

A

P Wave: Distorted (d/t ectopic signal travels across the atria by an abnormal pathway) OR hidden by the T-wave
P-R Interval: May be shorter/or longer but still falls w/in normal limits
QRS: Normal <0.12 or Abnormal >0.12
Rhythm: irregular

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15
Q

Atrial Flutter Characteristics

A

Atrial rate 200-350 bpm & Ventricular rate about 150 bpm
P Wave: Recurring, regular, saw tooth shape waves
P-R Interval: Variable and not measurable.
QRS: Usually normal
Rhythm: Tachydsyrhytmia

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16
Q

Atrial Fibrilation Characteristics

A 
Atrial: 350-600 bpm Ventricular: 60-100 bpm
P Wave: Chaotic, fibrillatory waves
P-R Interval: Not measurable
QRS: Usually normal shape and duration
Rhythm: Irregular
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17
Q

Supraventricular Tachycardia Characteristics

A 
Rate: 150-220 bpm
P Wave: Often hidden in the preceding T wave
P-R: Shorten or normal
QRS: Usually normal
Rhythm: Regular/slightly irregular
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18
Q

The three types of Ventricular Rhythms include

A
  1. Premature Ventricular Contraction
  2. Ventricular Tachycardia
  3. Ventricular Fibrillation
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19
Q

Premature Ventricular Contraction Characteristics

A 
Rate: Ectopic focus in the ventricles
P Wave: Rarely visible, usually lost in the QRS complex
QRS: wide/distorted shape; >0.12
T-Wave: Large and opposite in direction
Rhythm: Irregular
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20
Q

Ventricular Tachycardia Characteristics

A

P Wave: Occurs independently of QRS complex; usually buried in the QRS complex
P-R Interval: Not measurable
QRS: Wide/distorted in appearance; >0.12 sec
T Wave: Opposite direction of QRS complex
Rhythm: Regular or irregular

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21
Q

Ventricular Fibrillation Characteristics

A

Rate: Not measurable
P Wave: Not measurable
QRS: Not measurable
Rhythm: Irregular and chaotic

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22
Q

AV Block Types

A

First Degree
Second Degree Type I
Second Degree Type II
Third Degree

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23
Q

First Degree AV Block Characteristics

A 
Rate: HR normal
P Wave: Normal
P-R interval: PROLONGED >0.20 sec
QRS: Shape/duration usually normal
Rhythm: Regular
(Wife(P Wave) waits for husband(QRS) to come home. He comes home later than normal but he always comes home at the same time each night.)
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24
Q

Second Degree AV Block Type I Characteristics

A 
Rate: Normal, maybe bradycardia
P Wave: Normal shape
P-R Interval: GRADUAL LENGTHENING
QRS: Normal
Rhythm: PROGRESSIVE LENGTHENING
(Wife(P Wave) waits for husband(QRS) to get home. Each night he comes home later and later, until he doesn’t come home at all.)
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25
Q

Second Degree AV Block Type II Characteristics

A

P Wave: Normal shape
P-R Interval: Normal or prolonged in duration; remains constant on conducted beats.
QRS: Usually >0.12 d/t bundle branch block.
Rhythm: Atrial = regular, Ventricular = may be irregular.
(Wife(P Wave) waits for her husband(QRS) to come home. Sometimes he comes home, sometimes he doesn’t. But when he does come home, he shows up at the same time each night.)

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26
Q

Third Degree AV Block (Complete Heart Block) Characteristics

A

P Wave: Normal shape
P-R interval: Variable, no relationship between the P wave and the QRS complex
Rhythm: atrial and ventricular rhythms are regular but unrelated to each other.
(Wife(P Wave) is no longer waiting for her husband(QRS). They are on completely different schedules. There is no longer a relationship)

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27
Q

Cardiac Arrest Rhythms

A

VT
VF
PEA
Asystole

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28
Q

Common Etiologies of Cardiac Arrest Rhythms

A

H’s and T’s

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29
Q

C-A-B

A

Chest compression, Airway, Breathing

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30
Q

C-A-B: Compressions

A

Should be initiated within 10 second of recognition of arrest
Given at a rate of at least 100/min and each set of 30 compression should take 18 seconds or less.
Depth at least 2 inches for adult, 1/3 of chest for children, 1/3 of chest for infant.

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31
Q

C-A-B: Airway

A

Cricoid pressure not recommended

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32
Q

C-A-B: Breathing

A

Briefly check fo no breathing or no normal breathing.

AFTER 30 compressions, the airway is opened then deliver 2 breaths.

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33
Q

AED Automatic External Defibrillator

A

Children 1-8 years old

Infants <1 year old

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34
Q

SA node

A

Start of impulse
Dominant stimulator
Sends impulse all throughout the atrium -> atrium contraction

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35
Q

Distance from SA to AV node allows

A

Emptying of the atrium

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36
Q

Bundle of His

A

Separates into right and left ventricles

Time to get bundle of his allows filling of ventricles

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37
Q

Purkinje Fibers

A

Stimulates ventricles to contract -> CO

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38
Q

Vagus Nerve

A

Decreases firing of SA node

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39
Q

Depolarization

A

Contraction

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40
Q

Repolarization

A

Relaxation

41
Q

Nerve Fibers of sympathetic

A

Increases firing of SA node

42
Q

Most common Lead ECG’s include

A

Lead 2 and 5

43
Q

Lead 2

A

Easiest way to see P wave

Do NOT rely on paper only; assess patient to what you see on lead 2.

44
Q

12 Leadd ECG shows changes suggesting

A

Structural and conduction disturbances
Damage
Electrolyte Imbalances
Drug toxicity

45
Q

Dysrhythmias result from disorders of:

A

Impulse formation
Conduction of impulse formation
OR both

46
Q

When SA fires more slowly then secondary pacemakers,

A

AV node rate = 40-60 times/min

His-purkinje system = 20-40 times/min

47
Q

When the secondary pacemakers fire more rapidly than normal SA,

A

Triggered beats (early or late) can come from an area outside the normal conduction pathway (ectopic focus/accessory pathway) in atria, AV node or ventricle.

48
Q

Holster monitor

A

Continuous recording of ECG while pt is ambulatory/ADLS; pt records activities and symptoms

49
Q

What drugs can contribute to sinus bradycardia?

A

B-blockers, CCB

50
Q

Treating Sinus Bradycardia

A

Atropine (anticholinergic drug)

If ineffective, give transcutaneous pacing or dopamine or epinephrine infusion.

51
Q

Treatment for Premature Atrial Contractions

A

Treat underlying cause.
Caffeine or sympathomimetic drugs may be needed.
B Blockers.

52
Q

Premature Ventricular Contractions

A

Premature (early) occurrence of a QRS complex.

It is wide and distorted in shape compared to QRS complex.

53
Q

Asystole

A

Represents the total absence of ventricular electrical activity.
Patients are unresponsive, pulseless and apneic.

54
Q

Aystole Clinical Associations

A

Usually a result of advance heart disease, severe cardiac conduction system disturbances or end-Stage HF.

55
Q

Clinical Significance of Asystole

A

End-stage heart disease and prolonged arrest cannot be resuscitated.

56
Q

Treatment of Asystole

A

Consists of CPR w/ initiation of ACLS measures.

Includes drug therapy, epinephrine, and/or vasopressin and intubation.

57
Q

Treatment for sinus tachycardia

A

Underlying cause
IV beta-adrenergic blockers
Adenosine
CCB

58
Q

Premature Atrial Contraction

A

Starts from an ectopic focus in the atrium and comes sooner than the next expected sinus beat.

59
Q

Premature Atrial Contraction can be a result from

A

Emotional stress or physical fatigue
Caffeine, tobacco or alcohol.
Hypoxia, electrolyte imbalances.
Hyperthyroidism, COPD, heart disease

60
Q

Clinical Significance of Premature Atrial Contractions

A

In people with healthy hearts, isolated PACs are not significant.
Patients may report palpitations or a sense that heart skipped a beat.
In people with heart disease, may indicate enhanced automaticity of the atria or a reentry mechanism. (May warn of or start more serious dysrhythmias.)

61
Q

Supraventricular Tachycardia

A

Starts in ectopic focus anywhere above the bifurcation of the bundle of His.
Occurs because of reentrant phenomenon (reexcitation of the atria when there is a one-way block).
Abrupt onset and ending. Termination is sometimes followed by a brief perio of asystole.

62
Q

Supraventricular Tachycardia Clinical Associations

63
Q

Supraventricular Tachycardia

A

Clinical Significance

64
Q

Treatment for Supraventricular Tachycardia

A

Fatal stimulation
Drug of choice: IV adenosine
If it is ineffective, pt become hemodynamically unstable, synchronized cardioversion is used.

65
Q

Atrial Flutter Clinical Associations

66
Q

Atrial Flutter Clinical Significance

A

Can cause HF w/ pt w/ underlying heart disease

Increases risk for stroke (d/t risk of thrombus formation/stasis of blood in the atrium)

67
Q

Atrial Flutter Treatment

A

Warfarin (to prevent stroke = decrease ventricular response by increase AV block)
CCB, BB, antidysrhythmia drugs
Electrical cardioversion (for unstable pt)
Radio frequency catheter ablations - treatment of choice

68
Q

Atrial Fibrillation Clinical Associations

69
Q

Atrial Fibrillation Clinical Association

A

Decreases CO

Thrombi form in the atria d/t blood stasis -> stroke (accounts for 17% of strokes)

70
Q

Atrial Fibrillation Treatment

A 
CCB (diltiazem)
BB
Dronedarone
Digoxin
Some pt. Pharmacologic or electrical conversion may be considered.
71
Q

Premature Ventricular Contractions Clinical Association

72
Q

Premature Ventricular Contraction Clinical Significance

A

usually normally not harmful in patients w/ normal heart
In pts w/ heart disease: decrease CO -> angina and possible HF.
In CAD or acute MI indicates Ventricular irritability.

73
Q

For patients with premature ventricular contractions, assess

A

Apical pulse and peripheral pulse since PVC often does not generate a sufficient ventricular contraction -> which an lead to a pulse deficit.

74
Q

Treatment of Premature Ventricular Contractions

A

Hemodynamics status is important to determine if tx w/ drugs is needed (BB, procainamide or amiodarone)
O2 therapy for hypoxia and electrolyte replacement.

75
Q

PVC: Ventricular bigeminy

A

Every other beat is PVC

76
Q

PVC: Ventricular trigeminy

A

Every third beat is PCV

77
Q

PVC: Couplet

A

Two consecutive PVC

78
Q

PVC: Ventricular tachycardia

A

3 or more consecutive PVCs

79
Q

Ventricular Tachycardia Clinical Associations

80
Q

Ventricular Tachycardia Clinical Significance

A 
Stable = pulse
Unstable = no pulse 
Hypotension
Pulmonary edema
Decreased cerebral blood flow
Cardiopulmonary arrest
81
Q

Treatment of Ventricular Tachycardia

A

W/o pulse is life threatening. To like VF; CPR, rapid defibrillation (first line of treatment)
Follow with administration of vasopressors (epi), antidysrhythmics (amiodarone) if defib is unsuccessful.

82
Q

VT: Monomorphic/Stable Patient =

A

IV procainamide, sotalol or amiodarone is used.

83
Q

VT: Polymorphic/QT prolonged =

A

IV magnesium, isoproterenol, phenytoin, or antitachycardia pacing.

84
Q

Ventricular Fibrillation Clinical Associations

85
Q

Ventricular Fibrillation Clinical Significance

A

Unresponsive

Pulseless and apneic state (If not treated rapidly, patient will not recover)

86
Q

Treatment for Ventricular Fibrillation

A

CPR and Advanced Cardiac Life Support (ACLS) w/ use of defibrillator and definitive drug therapy (epinephrine, vasopressin)

87
Q

First Degree AV Block: Clinical Associations

88
Q

First Degree AV Block Clinical Significance

A

*Asymptomatic

Usually not serious but can be a sign of higher degrees of AV block

89
Q

Treatment for First Degree AV Block

A

No treatment, monitor

90
Q

Second Degree AV Block Type I: Clinical Associations

91
Q

Second Degree AV Block Type I: Clinical Significance

A

Results from MI or inferior MI.
Generally transient and well tolerated.
May be a sign for a more serious AV conduction disturbance (complete heart block)

92
Q

Treatment for Symptomatic Second Degree AV Block Type I

A

Atropine (increases HR) or a temporary pacemaker may be needed (especially if pt has MI)

93
Q

Treatment for Asymptomatic Second Degree AV Block Type I

A

Monitor w/ transcutaneous pacemaker on standby.

Bradycardia is more likely to become symptomatic when hypotension, HR or shock is present.

94
Q

Second Degree AV Block Type II Clinical Associations

A

Rheumatic heart disease
CAD
Anterior MI
Drug Toxicity

95
Q

Second Degree AV Block Type II Clinical Significance

A

Poor prognosis can lead to third degree AV block.

Reduced HR -> reduces CO = hypotension -> Myocardial ischemia.

96
Q

Treatment for Second Degree AV Block Type II

A

Permanent Pacemaker
(If pt becomes symptomatic (hypotension, angina) insertion of a temporary pacemaker may be necessary before the insertion of the permanent one)

97
Q

Third Degree AV Block: Clinical Associations

A

Severe Heart Disease (CAD, MI, myocarditis, cardiomyopathy, systemic disease, progressive system sclerosis)

98
Q

Third Degree Block: Clinical Significance

A 
Decreased CO
Ischemia
HR
Shock
Syncope
Bradycardia or even periods of asystole
99
Q

Treatment for Third Degree Block

A

Symptomatic: Transcutaneous pacemaker. Atropine, dopamine, epinephrine (temporarily increases HR and supports BP)
Permanent pacemaker ASAP

NURS 313R (18 decks)

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