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Cumulative > EKG Stuff > Flashcards

EKG Stuff Flashcards

1
Q

______ generate electrical impulses

A

myocytes

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2
Q

EKG leads measure electrical activity moving ______ the lead

A

toward the lead

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3
Q

P wave =

A

atria depolarizing

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4
Q

QRS complex =

A

ventricles depolarizing

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5
Q

Where is atrial repolarization seen on an EKG?

A

it is masked by the greater amplitude of the QRS complex

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6
Q

What does the ST segment give info about

A

ischemia

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7
Q

What condition shows ST elevations in all leeds

A

pericarditis

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8
Q

What allows for localization of findings on an EKG

A

the placement of different leads

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9
Q

define vector amplitude

A

the larger the deflection the closer you are to where that lead is providing information

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10
Q

What is this

A

Einthoven’s Triangle

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11
Q

What forms the X and Y axes of Einthoven’s triangle

A

the limb leads

Lead I: Right arm (neg) to Left arm (pos) measures laterally moving impulses

Leads 2 & 3: each arm to left leg measures inferiorly moving impulses (neg)

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12
Q

What do augmented leads do

A

reverses limb leads (I, II, III) polarity and combines them to create a hybrid lead between the contributing limb leads (adds another 3 divisions to get a total of 6 divisions 30 degrees apart)

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13
Q

What do chest leads (aka precordial leads) do

A

add a Z axis and further help localization

(surface leads are positive and AV node acts as the negative lead/anchor)

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14
Q

Describe reciprocal leads

A

What is positive from one perspective is negative from the other perspective (anterior vs posterior or left vs right)

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15
Q

what are the major components for interpreting any ECG

A
  • rate
  • rhythm
  • axis
  • hypertrophy
  • ischemia/infarct
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16
Q

Define ischemia in cardiology

A

myocardium not receiving required oxygen supply

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17
Q

define infarct

A

myocardium has been starved of oxygen to such an extent that it is experiencing cellular death

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18
Q

How is ischemia displayed on ECG in the affected territory

A

ST depression (with reciprocal changes)

w/wo T wave inversion

ECG can change/normalize as ischemia progresses

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19
Q

How is infarct displayed in the affected territory

A

ST elevation (with reciprocal changes)

w/wo T wave inversion

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20
Q

Describe the underlying pathology for ischemia/infarct

A

abnormal oxygen supply causes abnormal ion pump/gate activity causes abnormal repolarization which shows up as an abnormal ST segment

  • findings need to be present on 2 contiguous leads to qualify
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21
Q

What is shown here

A

ST depression - ischemia

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22
Q

ST elevation myocardial infarction (STEMI) occurs when the _____ ______ of myocardial wall loses perfusion

A

full thickness

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23
Q

What are Q waves and when do they develop

A

excessively wide or deep downward deflection at the beginning of a QRS complex

develop late in STEMI and are permanent (like a scar)

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24
Q

Describe stage B

A

hyperacute ST-T changes (first few mins)

elevated ST segment, upright T wave, no Q wave yet

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25
Q

Describe stage C

A

Marked ST elevation w/ hyperacute T changes

increasing ST elevation, upright T wave, no Q wave yet

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26
Q

Describe stage D

A

less ST elevation, biphasic T wave (minutes to hours)

Q waves may start to develop

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27
Q

Describe stage E

A

pathologic Q waves with T inversion (myocardial necrosis and fibrosis, recent MI within hours to weeks)

ST normalizes, T wave symmetrically inverted

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28
Q

What are the most common sites of infarcts

A

LV and septum (RV is rare)

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29
Q

What is this an example of

A

septal infarct
- ST elevation in aVR, V1-V3
- Q waves in V1-V2
- ST elevation and T inversion in III
- ST depression in I, II, aVL

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30
Q

What is this an example of

A

Anteroseptal infarct

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31
Q

What is this an example of

A

anterior infarct
- ST elevation in I, aVL, V2-V6
- Q waves V2-V4

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32
Q

What is this an example of

A

lateral infarct
- ST elevation in I, aVL, V5-V6
- Q waves in I, aVL
- ST depression in II, III, V1-V3 (reciprocal)

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33
Q

What is this an example of

A

anterolateral infarct
- ST elevation in I, aVL, V2-V6
- Q waves in V2-V6

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34
Q

what is this an example of

A

inferior infarct
- ST elevation in II, III, aVF, V4-V6
- Q waves in II, III, aVF
- ST depression in aVR, aVL, V1-V3

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35
Q

what should be on the differential for any new arrhythmia

A

ischemia

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36
Q

What are some ischemia imposters

A
  • strain pattern
  • juvenile T wave pattern
  • j point elevation
  • hyperkalemia
  • pericarditis
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37
Q

What are the rates of the SA node, AV node, and ventricular focus

A

SA: 60-100 bpm
AV: 40-60 bpm
VF: 20-40 bpm

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38
Q

How many big boxes on an ECG is 1 second

A

5 big boxes, 1 little box = 0.2 seconds

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39
Q

What are some examples of rhythms/arrhythmias

A
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40
Q

Define automaticity

A

spontaneous gradual decline in transmembrane potential until threshold is reached causing sudden depolarization

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41
Q

Define refractoriness

A

lag period after depolarization when subsequent depolarization is impossible d/t inadequate transmembrane ion gradient

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42
Q

Which myocytes have automaticity?

A

All of them, therefore they can all act as a pacemaker

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43
Q

How is the timing of impulses governed

A

by refractory periods, as long as the heart beats rhythmically the refractory periods occur predictably and keep everything working regularly

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44
Q

What is this an example of

A

normal sinus rhythm (1 P for every QRS and vice versa)

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45
Q

What is this an example of

A

sinus arrhythmia

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46
Q

What is this an example of

A

wandering pacemaker

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47
Q

What is this an example of

A

atrial fibrillation

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48
Q

What is this an example of

A

atrial flutter

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49
Q

Describe premature/escape beats

A
  • result from excess or pre-excited automaticity
  • spontaneous = premature, after sinus pause = escape
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50
Q

how is an escape/ectopic rhythm generated

A

from repeat premature/escape beats that cause refractory periods to reset, resulting in a new primary pacemaker at an ectopic focus

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51
Q

What is this rhythm

A

sinus rhythm with atrial escape rhythm

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52
Q

what is this rhythm

A

PAC

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53
Q

What is this rhythm

A

junctional escape

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54
Q

What is this rhythm

A

ventricular escape

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55
Q

Describe an idiojunctional rhythm

A

40-60 bpm (slower than normal sinus rhythm), no P wave, normal QRS

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56
Q

Describe an idioventricular rhythm

A

20-40 bpm (way slower), no P wave, wide/bizarre QRS

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57
Q

What is an accelerated idio rhythm

A

an ectopic/idio rhythm that is sped up

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58
Q

What is this an example of

A

supraventricular tachycardia
- locked in around 150bpm, no rate variation with respiration
- T wave of one cycle may overlap P wave of next obscuring the P wave
- QRS complex is narrow

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59
Q

What is this an example of

A

ventricular tachycardia (can lead to ischemia if sustained d/t strain on heart, or progress to ventricular flutter)

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60
Q

Define bigeminy and trigeminy and quadrigeminy as it relates to ectopic beats

A

Bigeminy = 1 PVC every other beat

Trigeminy = 1 PVC every 3rd beat

Quadrigeminy = 1 PVC every 4th beat

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61
Q

When do PACs/PVCs become serious

A
  • when PVC initiates during normal T wave and can cause V-fib or QT phenomenon
  • when the ectopic rate is <40 bpm
  • multifocal PVCs can progress to V-fib
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62
Q

What is this an example of

A

ventricular flutter (300 bpm, no effective perfusion, pre-Vfib/torsades)

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63
Q

What is this an example of

A

ventricular fibrillation (can progress to PAE and asystole)

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64
Q

What is this an example of

A

Wolff-Parkinson-White (WPW) showing Delta wave
- trap door pathway - bundle of kent allows impulses to progress forward or back
- does not respond to cardioversion/meds well, requires ablation

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65
Q

describe bundle branch blocks

A
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66
Q

what is a characteristic finding on ECG for a RBBB or LBBB

A

bunny ears in V1 for RBBB or V6 for LBBB

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67
Q

what is this an example of

A

sinus block (1+ dropped cycle with baseline normal sinus rhythm)

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68
Q

What is this an exmaple of

A

1st degree AV block
- delayed impulse relay thru AV node, PR prolongation

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69
Q

What are the 2 types of 2nd degree AV blocks

A

Mobitz I aka Wenkebach

Mobitz II (more dangerous)

70
Q

what is this an example of

A

Wenckebach/Mobitz I

71
Q

What is this an example of

A

Mobitz II

72
Q

What is this an example of

A

3rd degree AV block

73
Q

how long is the PR interval

A

< 0.2 seconds (5 small boxes or 1 big box) from beginning of P to end of R

74
Q

how long is the QRS interval

A

< 0.12 seconds (3 small boxes) from beginning of Q to end of S

75
Q

how long is the QT interval

A

<0.4 seconds (10 small boxes, 2 big boxes) from beginning of Q to end of T

76
Q

What happens to intervals as the rate increases

A

intervals narrow

77
Q

What is a PR prolongation characteristic of

A

AV block

78
Q

What is a QRS prolongation characteristic of

A

bundle branch block

79
Q

What direction does the axis point in infarct

A

away from the infarct because the cells create no impulse and don’t contribute positively to the axis

80
Q

what creates larger impulses in ECG, hyper or hypotrophic areas

A

hypertrophic areas, vector points more strongly toward hypertrophy

81
Q

what is the most common cause of sudden cardiac arrest in young athletes

A

hypertrophy

82
Q

What does hyperkalemia produce on ECG

A

tall tenting T waves, wide QRS

83
Q

What does hyperacute ischemia look like on ECG

A

broad T waves (not tented like hyperkalemia)

84
Q

What is this an example of

A

hypokalemia
- shallowly inverted T waves and prominent U waves
- lazy wavelength with long QTU interval

85
Q

What are the left and right examples of

A

left = hypocalcemia (prolonged QT, long ST, delayed T)
right = hypercalcemia

86
Q

What is this an example of

A

Torsades de pointes
- polymorphic VT with long QT
- deteriorates to Vfib
- results from ischemia, electrolyte abnormality, meds, poorly timed cardioversion

87
Q

what is this an example of

A

electrical alternans
- result from large pericardial effusion
- axis reverses with each beat
- QRS polarity alternates above and below isoelectric baseline

88
Q

what is this an example of

A

PE or acute cor pulmonale
- indicates right ventricular strain
- S1-Q3-T3 is classic pattern
- S wave in I, Q wave in III, flipped T in III

89
Q
A
90
Q
A
91
Q
A
92
Q

T wave =

A

ventricles repolarizing

93
Q

PR segment =

A

built-in delay at the AV node

94
Q

Which leads show lateral territory

A

I, aVL, V5, V6

95
Q

Which leads show inferior territory

A

II, III, aVF

96
Q

Which leads show septal territory

A

V1, V2

97
Q

Which leads show anterior territory

A

V3, V4

98
Q

What is a J-point elevation seen on EKG

A

early repolarization pattern in healthy hearts

99
Q

How to identify a first degree AV block

A

“if the R is far from P, then you have a first degree”
- prolonged PR interval
- benign

100
Q

How to identify a Wenckebach (2nd degree type 1/Mobitz I)

A

“PR gets longer, longer, longer, drops! Then you have a Wenckebach”
- progressively prolonging PR interval
- dropped beats in recurring pattern
- benign

101
Q

How to identify a Mobitz II (2nd degree type 2)

A

” if some R’s don’t get through, prepare to pace that Mobitz 2”
- stable PR interval
- occasional or recurring dropped beats
- high risk for sudden cardiac death

102
Q

How to identify a 3rd degree AV block

A

“If the R’s and P’s don’t agree, prepare to pace that 3rd degree”
- total dissociation of atrial/ventricular conduction
- regularly repeating P waves and QRS complexes (idioventricular morphology)
- hemodynamically unstable

103
Q

What are some causes of left axis deviation

A
  • normal variation
  • left ventricular hypertrophy
  • LBBB
  • left anterior fascicular block
  • inferior MI
104
Q

What are some causes of right axis deviation

A
  • normal variation
  • right ventricular hypertrophy
  • RBBB
  • left posterior fascicular block
  • lateral MI
105
Q

Describe the P wave seen in R atrial enlargement

A
  • p pulmonale
  • width does not change
  • amplitude increases in inferior leads (II, III, avF) (biphasic in V1)
106
Q

Describe the P wave seen in L atrial enlargement

A
  • p mitrale
  • large terminal P wave deflection in V1 with increased duration
  • M shaped p wave in II (biphasic in V1)
107
Q

What is a cause of L atrial enlargement

A

mitral stenosis

108
Q

What is a cause of R atrial enlargement

A
  • cor pulmonale
  • tricuspid stenosis
  • CHD
109
Q

What is the most common finding for R ventricular hypertrophy in limb leads & precordial leads

A

limb leads: right axis deviation

precordial leads: R wave progression disrupted
- lead V1: R wave > S wave OR R >6mm
- lead V6: S wave > R wave

110
Q

What can cause R ventricular hypertrophy

A
  • pulmonary HTN
  • COPD
  • pulmonary stenosis
  • atrial septal defect
111
Q

What is the easiest way to determine L ventricular hypertrophy on EKG

A

LVH = >35mm = S wave depth in V1 + tallest R wave in V5 or V6

112
Q

What can cause L ventricular hypertrophy

A
  • increased voltage as a normal variant in young athletic people
  • systemic HTN
  • aortic stenosis
  • ventricular septal defect
  • hypertrophic cardiomyopathy
113
Q

What are the three types of conduction blocks

A
  • sinus node block
  • AV node block
  • bundle branch block

(any obstruction or delay in normal pathways of electrical conduction)

114
Q

What causes a 1st degree AV block

A

common in normal hearts but can be caused by myocarditis or drug toxicity (no treatment)

115
Q

What causes a Mobitz 1 second degree AV block (Wenkebach)

A

occurs high up in the AV node (no treatment if asymptomatic)

116
Q

What are the symptoms, causes, and treatment for a Mobitz II second degree AV block

A

Symptoms: weakness, fatigue, light-headedness, syncope

Causes: block in bundle of His (usually organic dz)

Treatment: usually pacemaker (can progress to 3rd degree AV block)

117
Q

What are the symptoms, causes, and treatment for a 3rd degree AV block

A

Symptoms: fatigue, dyspnea, pre/syncope

Causes: MI, CMO, AV nodal blocking meds

Treatment: atropine and temporary pacing if unstable, monitoring and implanted pacemaker for stable

118
Q
A

A-fib

119
Q
A

A-fib

120
Q
A

A-fib

121
Q
A

Asystole

122
Q
A

A-flutter

123
Q
A

A-flutter

124
Q
A

RBBB

125
Q
A

LBBB

126
Q
A

1st degree AV block

127
Q
A

1st degree AV block

128
Q
A

1st degree AV block

129
Q
A

junctional rhythm

130
Q
A

junctional rhythm

131
Q
A

normal sinus rhythm

132
Q
A

normal sinus rhythm

133
Q
A

PACs

134
Q
A

PACs

135
Q
A

PVC

136
Q
A

PVC

137
Q
A

PVC

138
Q
A

R on T phenomenon

139
Q
A

Mobitz II

140
Q
A

Mobitz II

141
Q
A

Mobitz II

142
Q
A

sick sinus syndrome

143
Q
A

sick sinus syndrome

144
Q
A

sinus arrhythmia

145
Q
A

sinus arrhythmia

146
Q
A

sinus brady

147
Q
A

sinus brady

148
Q
A

sinus tach

149
Q
A

STEMI

150
Q
A

SVT

151
Q
A

SVT

152
Q
A

third degree block

153
Q
A

third degree block

154
Q
A

third degree/complete heart block

155
Q
A

torsades de pointes

156
Q
A

V-fib

157
Q
A

V-fib

158
Q
A

v-fib

159
Q
A

v-tach

160
Q
A

v-tach

161
Q
A

RBBB

162
Q
A

RBBB

prolonged QRS, RSR’ in V1, slurred S wave in V6

163
Q
A

RBBB

164
Q
A

LBBB

165
Q
A

LBBB

prolonged QRS (>3 small boxes), broad monomorphic R waves in I and V6, broad monomorphic S wave in V1

166
Q
A

LBBB

167
Q
A

LBBB

168
Q
A

left anterior fascicular block

169
Q
A

sinus arrest

170
Q
A

tachy-brady

171
Q
A

Cumulative (162 decks)

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