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

Exam 1: Arrhythmias & ECG Flashcards

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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
Second Degree AV Block Type II Characteristics
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.)
26
Third Degree AV Block (Complete Heart Block) Characteristics
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)
27
Cardiac Arrest Rhythms
VT VF PEA Asystole
28
Common Etiologies of Cardiac Arrest Rhythms
H’s and T’s
29
C-A-B
Chest compression, Airway, Breathing
30
C-A-B: Compressions
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.
31
C-A-B: Airway
Cricoid pressure not recommended
32
C-A-B: Breathing
Briefly check fo no breathing or no normal breathing. | AFTER 30 compressions, the airway is opened then deliver 2 breaths.
33
AED Automatic External Defibrillator
Children 1-8 years old | Infants <1 year old
34
SA node
Start of impulse Dominant stimulator Sends impulse all throughout the atrium -> atrium contraction
35
Distance from SA to AV node allows
Emptying of the atrium
36
Bundle of His
Separates into right and left ventricles | Time to get bundle of his allows filling of ventricles
37
Purkinje Fibers
Stimulates ventricles to contract -> CO
38
Vagus Nerve
Decreases firing of SA node
39
Depolarization
Contraction
40
Repolarization
Relaxation
41
Nerve Fibers of sympathetic
Increases firing of SA node
42
Most common Lead ECG’s include
Lead 2 and 5
43
Lead 2
Easiest way to see P wave | Do NOT rely on paper only; assess patient to what you see on lead 2.
44
12 Leadd ECG shows changes suggesting
Structural and conduction disturbances Damage Electrolyte Imbalances Drug toxicity
45
Dysrhythmias result from disorders of:
Impulse formation Conduction of impulse formation OR both
46
When SA fires more slowly then secondary pacemakers,
AV node rate = 40-60 times/min | His-purkinje system = 20-40 times/min
47
When the secondary pacemakers fire more rapidly than normal SA,
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
Holster monitor
Continuous recording of ECG while pt is ambulatory/ADLS; pt records activities and symptoms
49
What drugs can contribute to sinus bradycardia?
B-blockers, CCB
50
Treating Sinus Bradycardia
Atropine (anticholinergic drug) | If ineffective, give transcutaneous pacing or dopamine or epinephrine infusion.
51
Treatment for Premature Atrial Contractions
Treat underlying cause. Caffeine or sympathomimetic drugs may be needed. B Blockers.
52
Premature Ventricular Contractions
Premature (early) occurrence of a QRS complex. | It is wide and distorted in shape compared to QRS complex.
53
Asystole
Represents the total absence of ventricular electrical activity. Patients are unresponsive, pulseless and apneic.
54
Aystole Clinical Associations
Usually a result of advance heart disease, severe cardiac conduction system disturbances or end-Stage HF.
55
Clinical Significance of Asystole
End-stage heart disease and prolonged arrest cannot be resuscitated.
56
Treatment of Asystole
Consists of CPR w/ initiation of ACLS measures. | Includes drug therapy, epinephrine, and/or vasopressin and intubation.
57
Treatment for sinus tachycardia
Underlying cause IV beta-adrenergic blockers Adenosine CCB
58
Premature Atrial Contraction
Starts from an ectopic focus in the atrium and comes sooner than the next expected sinus beat.
59
Premature Atrial Contraction can be a result from
Emotional stress or physical fatigue Caffeine, tobacco or alcohol. Hypoxia, electrolyte imbalances. Hyperthyroidism, COPD, heart disease
60
Clinical Significance of Premature Atrial Contractions
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
Supraventricular Tachycardia
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
Supraventricular Tachycardia Clinical Associations
..
63
Supraventricular Tachycardia
Clinical Significance
64
Treatment for Supraventricular Tachycardia
Fatal stimulation Drug of choice: IV adenosine If it is ineffective, pt become hemodynamically unstable, synchronized cardioversion is used.
65
Atrial Flutter Clinical Associations
..
66
Atrial Flutter Clinical Significance
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
Atrial Flutter Treatment
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
Atrial Fibrillation Clinical Associations
..
69
Atrial Fibrillation Clinical Association
Decreases CO | Thrombi form in the atria d/t blood stasis -> stroke (accounts for 17% of strokes)
70
Atrial Fibrillation Treatment
``` CCB (diltiazem) BB Dronedarone Digoxin Some pt. Pharmacologic or electrical conversion may be considered. ```
71
Premature Ventricular Contractions Clinical Association
..
72
Premature Ventricular Contraction Clinical Significance
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
For patients with premature ventricular contractions, assess
Apical pulse and peripheral pulse since PVC often does not generate a sufficient ventricular contraction -> which an lead to a pulse deficit.
74
Treatment of Premature Ventricular Contractions
Hemodynamics status is important to determine if tx w/ drugs is needed (BB, procainamide or amiodarone) O2 therapy for hypoxia and electrolyte replacement.
75
PVC: Ventricular bigeminy
Every other beat is PVC
76
PVC: Ventricular trigeminy
Every third beat is PCV
77
PVC: Couplet
Two consecutive PVC
78
PVC: Ventricular tachycardia
3 or more consecutive PVCs
79
Ventricular Tachycardia Clinical Associations
..
80
Ventricular Tachycardia Clinical Significance
``` Stable = pulse Unstable = no pulse Hypotension Pulmonary edema Decreased cerebral blood flow Cardiopulmonary arrest ```
81
Treatment of Ventricular Tachycardia
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
VT: Monomorphic/Stable Patient =
IV procainamide, sotalol or amiodarone is used.
83
VT: Polymorphic/QT prolonged =
IV magnesium, isoproterenol, phenytoin, or antitachycardia pacing.
84
Ventricular Fibrillation Clinical Associations
..
85
Ventricular Fibrillation Clinical Significance
Unresponsive | Pulseless and apneic state (If not treated rapidly, patient will not recover)
86
Treatment for Ventricular Fibrillation
CPR and Advanced Cardiac Life Support (ACLS) w/ use of defibrillator and definitive drug therapy (epinephrine, vasopressin)
87
First Degree AV Block: Clinical Associations
..
88
First Degree AV Block Clinical Significance
*Asymptomatic | Usually not serious but can be a sign of higher degrees of AV block
89
Treatment for First Degree AV Block
No treatment, monitor
90
Second Degree AV Block Type I: Clinical Associations
..
91
Second Degree AV Block Type I: Clinical Significance
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
Treatment for Symptomatic Second Degree AV Block Type I
Atropine (increases HR) or a temporary pacemaker may be needed (especially if pt has MI)
93
Treatment for Asymptomatic Second Degree AV Block Type I
Monitor w/ transcutaneous pacemaker on standby. | Bradycardia is more likely to become symptomatic when hypotension, HR or shock is present.
94
Second Degree AV Block Type II Clinical Associations
Rheumatic heart disease CAD Anterior MI Drug Toxicity
95
Second Degree AV Block Type II Clinical Significance
Poor prognosis can lead to third degree AV block. | Reduced HR -> reduces CO = hypotension -> Myocardial ischemia.
96
Treatment for Second Degree AV Block Type II
Permanent Pacemaker (If pt becomes symptomatic (hypotension, angina) insertion of a temporary pacemaker may be necessary before the insertion of the permanent one)
97
Third Degree AV Block: Clinical Associations
Severe Heart Disease (CAD, MI, myocarditis, cardiomyopathy, systemic disease, progressive system sclerosis)
98
Third Degree Block: Clinical Significance
``` Decreased CO Ischemia HR Shock Syncope Bradycardia or even periods of asystole ```
99
Treatment for Third Degree Block
Symptomatic: Transcutaneous pacemaker. Atropine, dopamine, epinephrine (temporarily increases HR and supports BP) Permanent pacemaker ASAP

NURS 313R (18 decks)

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