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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
Describe stage C
Marked ST elevation w/ hyperacute T changes increasing ST elevation, upright T wave, no Q wave yet
26
Describe stage D
less ST elevation, biphasic T wave (minutes to hours) Q waves may start to develop
27
Describe stage E
pathologic Q waves with T inversion (myocardial necrosis and fibrosis, recent MI within hours to weeks) ST normalizes, T wave symmetrically inverted
28
What are the most common sites of infarcts
LV and septum (RV is rare)
29
What is this an example of
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
30
What is this an example of
Anteroseptal infarct
31
What is this an example of
anterior infarct - ST elevation in I, aVL, V2-V6 - Q waves V2-V4
32
What is this an example of
lateral infarct - ST elevation in I, aVL, V5-V6 - Q waves in I, aVL - ST depression in II, III, V1-V3 (reciprocal)
33
What is this an example of
anterolateral infarct - ST elevation in I, aVL, V2-V6 - Q waves in V2-V6
34
what is this an example of
inferior infarct - ST elevation in II, III, aVF, V4-V6 - Q waves in II, III, aVF - ST depression in aVR, aVL, V1-V3
35
what should be on the differential for any new arrhythmia
ischemia
36
What are some ischemia imposters
- strain pattern - juvenile T wave pattern - j point elevation - hyperkalemia - pericarditis
37
What are the rates of the SA node, AV node, and ventricular focus
SA: 60-100 bpm AV: 40-60 bpm VF: 20-40 bpm
38
How many big boxes on an ECG is 1 second
5 big boxes, 1 little box = 0.2 seconds
39
What are some examples of rhythms/arrhythmias
40
Define automaticity
spontaneous gradual decline in transmembrane potential until threshold is reached causing sudden depolarization
41
Define refractoriness
lag period after depolarization when subsequent depolarization is impossible d/t inadequate transmembrane ion gradient
42
Which myocytes have automaticity?
All of them, therefore they can all act as a pacemaker
43
How is the timing of impulses governed
by refractory periods, as long as the heart beats rhythmically the refractory periods occur predictably and keep everything working regularly
44
What is this an example of
normal sinus rhythm (1 P for every QRS and vice versa)
45
What is this an example of
sinus arrhythmia
46
What is this an example of
wandering pacemaker
47
What is this an example of
atrial fibrillation
48
What is this an example of
atrial flutter
49
Describe premature/escape beats
- result from excess or pre-excited automaticity - spontaneous = premature, after sinus pause = escape
50
how is an escape/ectopic rhythm generated
from repeat premature/escape beats that cause refractory periods to reset, resulting in a new primary pacemaker at an ectopic focus
51
What is this rhythm
sinus rhythm with atrial escape rhythm
52
what is this rhythm
PAC
53
What is this rhythm
junctional escape
54
What is this rhythm
ventricular escape
55
Describe an idiojunctional rhythm
40-60 bpm (slower than normal sinus rhythm), no P wave, normal QRS
56
Describe an idioventricular rhythm
20-40 bpm (way slower), no P wave, wide/bizarre QRS
57
What is an accelerated idio rhythm
an ectopic/idio rhythm that is sped up
58
What is this an example of
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
59
What is this an example of
ventricular tachycardia (can lead to ischemia if sustained d/t strain on heart, or progress to ventricular flutter)
60
Define bigeminy and trigeminy and quadrigeminy as it relates to ectopic beats
Bigeminy = 1 PVC every other beat Trigeminy = 1 PVC every 3rd beat Quadrigeminy = 1 PVC every 4th beat
61
When do PACs/PVCs become serious
- 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
62
What is this an example of
ventricular flutter (300 bpm, no effective perfusion, pre-Vfib/torsades)
63
What is this an example of
ventricular fibrillation (can progress to PAE and asystole)
64
What is this an example of
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
65
describe bundle branch blocks
66
what is a characteristic finding on ECG for a RBBB or LBBB
bunny ears in V1 for RBBB or V6 for LBBB
67
what is this an example of
sinus block (1+ dropped cycle with baseline normal sinus rhythm)
68
What is this an exmaple of
1st degree AV block - delayed impulse relay thru AV node, PR prolongation
69
What are the 2 types of 2nd degree AV blocks
Mobitz I aka Wenkebach Mobitz II (more dangerous)
70
what is this an example of
Wenckebach/Mobitz I
71
What is this an example of
Mobitz II
72
What is this an example of
3rd degree AV block
73
how long is the PR interval
< 0.2 seconds (5 small boxes or 1 big box) from beginning of P to end of R
74
how long is the QRS interval
< 0.12 seconds (3 small boxes) from beginning of Q to end of S
75
how long is the QT interval
<0.4 seconds (10 small boxes, 2 big boxes) from beginning of Q to end of T
76
What happens to intervals as the rate increases
intervals narrow
77
What is a PR prolongation characteristic of
AV block
78
What is a QRS prolongation characteristic of
bundle branch block
79
What direction does the axis point in infarct
away from the infarct because the cells create no impulse and don't contribute positively to the axis
80
what creates larger impulses in ECG, hyper or hypotrophic areas
hypertrophic areas, vector points more strongly toward hypertrophy
81
what is the most common cause of sudden cardiac arrest in young athletes
hypertrophy
82
What does hyperkalemia produce on ECG
tall tenting T waves, wide QRS
83
What does hyperacute ischemia look like on ECG
broad T waves (not tented like hyperkalemia)
84
What is this an example of
hypokalemia - shallowly inverted T waves and prominent U waves - lazy wavelength with long QTU interval
85
What are the left and right examples of
left = hypocalcemia (prolonged QT, long ST, delayed T) right = hypercalcemia
86
What is this an example of
Torsades de pointes - polymorphic VT with long QT - deteriorates to Vfib - results from ischemia, electrolyte abnormality, meds, poorly timed cardioversion
87
what is this an example of
electrical alternans - result from large pericardial effusion - axis reverses with each beat - QRS polarity alternates above and below isoelectric baseline
88
what is this an example of
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
90
91
92
T wave =
ventricles repolarizing
93
PR segment =
built-in delay at the AV node
94
Which leads show lateral territory
I, aVL, V5, V6
95
Which leads show inferior territory
II, III, aVF
96
Which leads show septal territory
V1, V2
97
Which leads show anterior territory
V3, V4
98
What is a J-point elevation
early repolarization pattern in healthy hearts
99
How to identify a first degree AV block
"if the R is far from P, then you have a first degree" - prolonged PR interval - benign
100
How to identify a Wenckebach (2nd degree type 1/Mobitz I)
"PR gets longer, longer, longer, drops! Then you have a Wenckebach" - progressively prolonging PR interval - dropped beats in recurring pattern - benign
101
How to identify a Mobitz II (2nd degree type 2)
" 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
How to identify a 3rd degree AV block
"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
What are some causes of left axis deviation
- normal variation - left ventricular hypertrophy - LBBB - left anterior fascicular block - inferior MI
104
What are some causes of right axis deviation
- normal variation - right ventricular hypertrophy - RBBB - left posterior fascicular block - lateral MI
105
Describe the P wave seen in R atrial enlargement
- p pulmonale - width does not change - amplitude increases in inferior leads (II, III, avF) (biphasic in V1)
106
Describe the P wave seen in L atrial enlargement
- p mitrale - large terminal P wave deflection in V1 with increased duration - M shaped p wave in II (biphasic in V1)
107
What is a cause of L atrial enlargement
mitral stenosis
108
What is a cause of R atrial enlargement
- cor pulmonale - tricuspid stenosis - CHD
109
What is the most common finding for R ventricular hypertrophy in limb leads & precordial leads
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
What can cause R ventricular hypertrophy
- pulmonary HTN - COPD - pulmonary stenosis - atrial septal defect
111
What is the easiest way to determine L ventricular hypertrophy on EKG
LVH = >35mm = S wave depth in V1 + tallest R wave in V5 or V6
112
What can cause L ventricular hypertrophy
- increased voltage as a normal variant in young athletic people - systemic HTN - aortic stenosis - ventricular septal defect - hypertrophic cardiomyopathy
113
What are the three types of conduction blocks
- sinus node block - AV node block - bundle branch block (any obstruction or delay in normal pathways of electrical conduction)
114
What causes a 1st degree AV block
common in normal hearts but can be caused by myocarditis or drug toxicity (no treatment)
115
What causes a Mobitz 1 second degree AV block (Wenkebach)
occurs high up in the AV node (no treatment if asymptomatic)
116
What are the symptoms, causes, and treatment for a Mobitz II second degree AV block
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
What are the symptoms, causes, and treatment for a 3rd degree AV block
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
A-fib
119
A-fib
120
A-fib
121
Asystole
122
A-flutter
123
A-flutter
124
RBBB
125
LBBB
126
1st degree AV block
127
1st degree AV block
128
1st degree AV block
129
junctional rhythm
130
junctional rhythm
131
normal sinus rhythm
132
normal sinus rhythm
133
PACs
134
PACs
135
PVC
136
PVC
137
PVC
138
R on T phenomenon
139
Mobitz II
140
Mobitz II
141
Mobitz II
142
sick sinus syndrome
143
sick sinus syndrome
144
sinus arrhythmia
145
sinus arrhythmia
146
sinus brady
147
sinus brady
148
sinus tach
149
STEMI
150
SVT
151
SVT
152
third degree block
153
third degree block
154
third degree/complete heart block
155
torsades de pointes
156
V-fib
157
V-fib
158
v-fib
159
v-tach
160
v-tach
161
RBBB
162
RBBB prolonged QRS, RSR' in V1, slurred S wave in V6
163
RBBB
164
LBBB
165
LBBB prolonged QRS (>3 small boxes), broad monomorphic R waves in I and V6, broad monomorphic S wave in V1
166
LBBB
167
LBBB
168
left anterior fascicular block
169
sinus arrest
170
tachy-brady
171

Cardiology (15 decks)

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