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4th Year > ECG > Flashcards

ECG Flashcards

1
Q

what type of tissue should you attach electrodes over

A

bone

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2
Q

what position should patient be in

A

lying at 30-40 degrees

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3
Q

where does V1 go

A

4thIC right sternal angle

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4
Q

where does V2 go

A

4thIC space left sternal angle

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5
Q

where does V4 go

A

5thIC space mid clavicular line

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6
Q

where does V3 go

A

midway between v2 and v4

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7
Q

where does V5 go

A

5thIC space anterior axillary line

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8
Q

where does V6 go

A

5thIC space mid axillary line

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9
Q

where do the limb leads go

A 
ride your good bike 
red arm - right 
left arm - yellow
left foot- green 
right foot - black (earth)
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10
Q

what does AC interference look like

A

(electrical equipment, noise)

comb

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11
Q

how do you prevent muscle tremor interference

A

improve contact with abrasive pad- get off dead skin

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12
Q

what does baseline wander mean (slow undulation)

A

patient movement

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13
Q

how do you calculate rate

A

use the rhythm strip
if regular: 300/number of large squares 2 Rs

if irregular: number of QRS’ in 6 seconds (30 large squares) x 10

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14
Q

how long is a small square

A

0.04 seconds

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15
Q

how long is a large square

A

0.2 seconds

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16
Q

what is a good method to go through an ECG

A
  1. is there electrical activity present
  2. are there P waves present
  3. QRS rate
  4. QRS rhythm (regular/ irregular?)
  5. QRS narrow/ broad
  6. relationship between P waves and QRS complexes
  7. Axis
  8. P wave progression
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17
Q

what is the cardiac axis

A

the direction of sum electrical activation
towards lead= +ve
away from lead= -ve
perpendicular= isoelectric

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18
Q

where do you look to determine cardiac axis

A

QRS complexes in lead I and aVF

lead I left hand, aVF right hand

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19
Q

what shows normal cardiac axis

A

lead I +ve
lead aVF +ve
(-30 to 90 degrees)

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20
Q

what shows right axis deviation

A

lead I -ve
lead aVF +ve
(90-180 degrees)

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21
Q

what shows left heart deviation

A

Lead I +ve
Lead aVF -ve
(-30 to -180 degrees)

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22
Q

what shows an indeterminate heart axis

A

both Lead I and avf -ve

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23
Q

what can cause RAD

A 
can be normal- inspiration 
RV hypertrophy 
RBBB
posterior hemiblock 
dextrocardia 
ventricular ectopic 
WPW
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24
Q

what can cause LAD

A 
normal- expiration 
left anterior hemiblock 
LBBB
congenital lesions
WPW
emphysema 
hyperkalaemia
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25
Q

how long should a PR interval be

A

120-200ms (3-5 small squares)

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26
Q

what is a PR interval

A

AV node delay (ventricles re-filling)

from start of atrial depolarisation to start of ventricular depolarisation

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27
Q

where do you measure PR interval from

A

onset of P wave to QRS onset

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28
Q

how long should a QRS be

A

<120ms (3 small squares)

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29
Q

what is the QT interval

A

ventricular repolarisation

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30
Q

where do measure QT from

A

start of QRS to end of T wave

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31
Q

how do you calculate corrected QT interval

A

square root of RR interval (seconds) / QTi (ms)

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32
Q

what is the P wave

A

atrial depolarisation

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33
Q

when is the P wave positive and rounded

A

leads II, III and aVF

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34
Q

when is the P wave inverted normally

A

aVR

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35
Q

what should happen to the amplitude of the QRS complex from v1-6

A

should increase (R gets taller)

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36
Q

what should T wave be in relation to QRS complex

A

usually in same direction (+ve or -ve)

should not be >1/2 preceeding QRS height

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37
Q

how should you place chest leads on women

A

under mammary tissue

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38
Q

how should you do ECG on patient with dextrocardia

A

place leads normal way first then do another with them reversed

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39
Q

what are the augmented leads

A

aVF, aVR and aVL (form wilsons central terminal)

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40
Q

what are the precordial leads

A

V1-6

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41
Q

what are the standard limb leads

A

I-III

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42
Q

what should you do if ECG shows something odd e.g. abnormal axis

A

repeat ECG to make sure its correct

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43
Q

what is the vertical plane in the ECg

A

limb leads

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44
Q

what is the horizontal plane in an ECG

A

R wave progression

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45
Q

what does R wave progression show

A

R waves should get progressively bigger from V1-6 usually peaking in V5. only consider how much of R is above baseline
if poor progression (PRWP)= lack of ventricular muscle mass function due to e.g. anterior MI

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46
Q

what should the R wave be in V1-2

A

mostly negative: if positive then RVH or RV problem

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47
Q

where does a supraventricular rhythm originate

A

above the AV node

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48
Q

what does a supraventricular rhythm usually have

A

narrow QRS

ANYTHING NARROW HAS COME FROM THE AV NODE

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49
Q

name 8 SV rhythms

A 
sinus 
A fib 
A flutter 
sinus arrhythmia 
SVT 
AVN re-entry tachycardia 
AVNRT (WPW)
wandering atrial pacemaker
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50
Q

what does sinus arrhythmia look like

A

normal shape and ECG other than rhythm (regularity irregular)
this due to breathing (vagal tone)

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51
Q

what does A fib look like

A

disorganised activity in atria
irregularly irregular QRS
absent P waves/ not clearly reproducible
chaotic baseline
can occur with range of ventricular rates

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52
Q

what causes A fib

A

lots of causes (CHD, hypertension, valvular heart disease, hyperthyroidism) make atrium continually send chaotic impulses to AV nodes which are intermittently transmitted to ventricles

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53
Q

what are some presenting features of a fib

A

often asymptomatic but associated with palpitations, fainting, dyspnoea, chest discomfort, stroke/ TIA (stagnant blood in atria increases risk of thrombus and emboli)

increased risk with age (8% of 80y/0s)

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54
Q

what is the most common rhythm problem

A

AF

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55
Q

what does A flutter look like

A

regular narrow QRS tachycardia
saw tooth baseline (best seen in V1 or II)- very abrupt, tends to sit on t wave
caused by re-entry circuit in atria (atria flutter at 300bmp)
AV node filters this and creates ventricular rate of a division of 300 (150, 100, 75)
can have irregular rate but RR Interval will be a multiple of PP interval (atrial rate of 300 bpm= PPi of 200ms. RR will be 400 in 2:1 block, 600 in 3:1 block and 800 in 4:1 block. this is variable AV block).
F waves will replace P waves
adenosine (AV nodal blocking drugs can reveal underlying flutter waves)

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56
Q

where does junctional rhythm originate

A

@AV node (not sinoatrial node)- pulse travels to atria and ventricles at the same time via the purkinje system

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57
Q

what does junctional rhythm look like

A

retrograde P waves in ST segment
regular
normal QRS morphology
rate can be normal or tachy-/bradycardic

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58
Q

what is an SVT

A

tachycardia that originates above/ involves the AV node (excluding sinus, Afib, A flutter)
can be an accessory pathway or re-entry pathway involving AVN

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59
Q

what does SVT look like

A

regular, narrow, often no clear P waves

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60
Q

what do SV ectopic look like

A

sinus rhythm
differing P morphology on beats 3,6 and 9 which also come early
varying PR and RR intervals

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61
Q

can ventricular rhythms be normal

A

no always pathological

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62
Q

what is always present in ventricular rhythm

A

QRS>120ms

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63
Q

what do premature ventricular complexes look like

A

PVC= wide and bizarre shaped QRS with ST segment and T waves changes

bigeminy: 1 sinus beat couples with a PVC
trigeminy: 1 sinus beat followed by 2 PVC

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64
Q

what is a premature ventricular complex

A

when beat initiated in purkinje fibres

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65
Q

what does VTV look like

A 
regular 
broad 
can be monomorphic
or polymorphic (torsades de points) 
always abnormal, may have haemodynamic compromise
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66
Q

what can VT deteriorate into

A

VF or MI

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67
Q

what does VF look like

A

irregular random baseline
no discernible waveforms
LOC always

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68
Q

what is a capture beats

A

when sinus beat reaches AV node before wide QRS VT beat and produces a QRS of normal duration

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69
Q

what is a fusion beat

A

when sinus beat and VT beat fuse to produce a hybrid complex

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70
Q

what do capture and fusion beats show in VT

A

the independent rhythms of atria and ventricles

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71
Q

why is it hard to tell ventricular rhythms from SV rhythms in patients with BBB

A

as both have broad QRS’

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72
Q

how do you estimates whether its ventricular or SV with BBB

A

v: pre-existing coronary disease, capture/ fusion beats present
SV with aberrancy: pre-existing BBB

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73
Q

what is aberrancy

A

abnormal conduction e.g. BBB

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74
Q

where is heart block affecting

A

AV nodal dysfunction

NOT bundle branches

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75
Q

what can cause heart block

A

drugs
ischaemia
age

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76
Q

what does 1st degree heart block look like

A

PRi >200ms (1 big square)

stable

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77
Q

what is the common theme of 2nd degree heart block

A

P wave blocked from initiating QRS

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78
Q

what are the types of 2nd degree heart block

A

mobitz 1 and 2

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79
Q

what does mobitz 1 look like

A

increasing delays
eventual missed beat
may be normal

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80
Q

what does mobitz 2 look like

A

constant PRi with subsequent missed beat

always abnormal, may deteriorate

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81
Q

what does 3rd degree heart block look like

A

no relationship between P wave and QRS
broad QRS= ventricular escape rhythms
always abnormal

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82
Q

what does a ventricular escape rhythm look like

A

300-400 bpm
broad
not linked to atrial activity

83
Q

when does a ventricular escape rhythm occur

A

in heart block

84
Q

what are the fascicles

A

anterior and posterior fascicles branch off the left bundle branch
right bundle branch

85
Q

what is bi fascicular block and what does it look like

A 
when 2 of LAFB, LPFB, RBBB occur 
2 of: 
PRi >200ms 
LAD (LAHB) 
RBBB
86
Q

what is tri-fascicular block

A 
when RBB, LAF and LPF all block 
all of: 
PRi >200ms
LAD (LAHB) 
RBBB
or 
alternating LBBB and RBBB
87
Q

what are the cardiac arrest rhythms and their treatments

A

VT and VF (shockable rhythms)
complete AV block (give IV atropine and isoprenaline until venous pacing wire)
pulseless electrical activity (CPR)

88
Q

what can VT deteriorate into

A

VF then asystole

89
Q

where do you look for BBB

A

V1 and V6

90
Q

what can you see in RBBB

A 
V1-V6 MarroW 
M QRS in V1
W QRS in V6
(RSR IN V1, delayed S in V4-6) 
wide QRS
can still se abnormal Q waves in MI
91
Q

what can you see in LBBB

A

V1-V6 WilliaM
W QRS in V1
M QRS in V6 (wide notched QRS in I, aVL, V5-6)
prolonged QRS

92
Q

which of LBBB and RBBB is always pathological

A

LBBB can be MI or other left heart disease

93
Q

what should you do to interpret signs of ischaemia on ECG

A

need patient Hx
use old ECGs if possible
do serial ECGs if borderline or having symptoms of MI
ECG is a priority if patient in pain

94
Q

what leads show inferior heart

what CA is this

A

II
III
aVF

RCA

95
Q

what leads show lateral heart

what CA is this

A

I
aVL
V5
V6

circumflex

96
Q

what leads show anterior heart

what CA is this

A

V3
V4

LADA

97
Q

what are the ECG markers of ischaemia

A

T waves changes:

  • tall tented
  • biphasic
  • inverted
  • flattened

ST depression:

  • subtle, flattened ST segment that rises into T waves
  • wide spread + deep = bad disease (2-3 boxes below isoelectric line)
98
Q

name something other that ischaemia that can cause ST depression

A

pericarditis

99
Q

what on an ECG means you should thrombolyse

A

ST elevation:

  • > 1mm in 2 contiguous limb leads
  • > 2mm in 2 contiguous chest leads
  • posterior MI (V1-3)
  • LBBB
100
Q

what shows a posterior infarction

A

ST elevation in leads v1-3

101
Q

what are the ECG signs of infarction

A

ST elevation
LBBB
Q wave formation
T wave peaking/ inversion

102
Q

what is a Q wave

A

the loss of R waves, happens at 2-24 hours

shows myocardial necrosis

103
Q

when are Q waves pathological

A

if in V1-3
>0.03 seconds in I, II, aVF, A4-6
must be present in2 contiguous leads and be >1mm in depth

104
Q

what else can cause ST elevation

A 
benign early repolarisation 
LBBB
LVH
ventricular aneurysm 
coronary vasospasm 
pericarditis 
brugada syndrome 
subarachnoid haemorrhage
105
Q

what should you think when there is new LBBB in an acute MI

A

infarction

106
Q

what is the general rule for thrombolysis

A

unless they look like they are having an MI do not thrombolyse

107
Q

what constitutes a STEMI with LBBB

A

ST depression >1mmin V1-2
ST elevation >1mm where +ve QRS
ST elevation >5mm where -ve QRs

108
Q

what is pericarditis

A

pericardial inflammation post MI/ viral infection

109
Q

what are the symptoms of pericarditis

A

pleuritic chest pain
fever
pericardial friction rub

110
Q

what is seen on ECG in pericarditis

A

upward concave ST elevation that doesn’t evolve

and is widespread (>1 vascular region)

111
Q

what is the Tx for pericarditis

A

analgesia and NSAIDs

112
Q

when is ventricular hypertrophy pathological

A

when in response to stress/ disease e.g. hypertension, MI, HF, neurohormones

113
Q

what does VH look like on ECG

A

v high QRS complexes

114
Q

what leads show the right ventricle

A

V1-2

115
Q

what leads show the left ventricle

A

V5-6

116
Q

what leads show the IV septum

A

V1-2

117
Q

when is it partial/ full BBB

A 
full= QRS> 0.12 seconds 
partial= BBB present but QRS not >0.12 seconds
118
Q

what happens in RBBB

A

RV depolarises late

119
Q

what can cause RBBB

A 
can be normal 
cor pulmonale/RVH
PE
MI 
CHD
mechanical damage 
congenital heart disease (e.g. septal defect) 
myocarditis 
cardiomyopathy 
lev disease
120
Q

what hemi bundles are injured in LBBB

A

both anterior and poster fascicles

121
Q

what happens in LBBB

A

delayed LV activation

122
Q

what can cause LBBB

A 
HD
IHD
MI
cardiomyopathy 
hypertension
123
Q

what is hemi block

A

block in either hemifascicles of LBB

124
Q

which is the most common hemiblock

A

LAHB

125
Q

what does LAHB look like

A

LAD without other causes for it

initial R waves in inferior leads

126
Q

what does LPHB look like

A

(is rare)
RAD without other causes
normal/ slightly prolonged QRS
S1 Q3 pattern

127
Q

what is mobitz type 1 associated with

A

high vagal tone e.g. athletes (not worrying)

128
Q

does mobitz 2 need intervention

A

yes as may deteriorate

129
Q

does 3rd degree heart block need intervention

A

yes may deteriorate

130
Q

what can tachycardia be associated with

A

sudden death

131
Q

why is tachycardia bad

A

less efficient (pre load and afterload reduced)
increased myocardial demand
risk of stroke
risk of cardiomyopathy long term

132
Q

what is tachycardia

A

> 100bpm

133
Q

what is sinus rhythm

A

regular rhythm

134
Q

when is a tachycardia sinus

A

if regular and every P wave followed by a QRS and every QRS preceded by a P wave

135
Q

will sinus tachycardia always stay at same rate

A

no often fluctuates

136
Q

what is not included in narrow complex tachycardias

A

AF
A flutter
sinus tachycardia

137
Q

how do you treat narrow complex tachycardias

A

AV node block:
vagal manoeuvres (stimulating vagal nerve by valsalva, cough, gag reflex, hold knees against chest, carotid sinus massage)
adenosine (gives transient block)

138
Q

what condition should you not give adenosine in

A

severe asthma

can also block some other drugs metabolism so look for interactions

139
Q

what is AVNRT

A

a tachycardia which occurs within the nodal tissue itself
relies on node having two distinct pathways (slow and fast)
goes down one pathway up the other and gets stuck

140
Q

where is the best place to look for atrial activation in AVNRT

A

V1

141
Q

what is AVRT

A

re-entry tachycardia that can use either AV node on way to ventricles or separate accessory pathway

142
Q

what do QRS’ in AVRT look like

A

broad QRS complex

143
Q

slurred upstrokes on QRS complex (delta wave) with small PR interval=?

A

WPW (a AVRT)

144
Q

what do atrial tachycardias and heart block have in common

A

both have more P waves then QRS’

145
Q

how do you tell the difference between atrial tachycardias and heart block

A

in atrial tachycardias atria will influence ventricles

in heart block QRS will be regular but not related at all to what atria doing

146
Q

if the qrs is narrow can there be bundle branch block

A

no

147
Q

what is partial branch block

A

when there is a bit of delay but QRS not >120ms

148
Q

how many boxes should it be from start of p wave to start of qrs

A

within one big box

149
Q

what do you see in RBBB

A

RSR in v1 or v2

150
Q

how to tell RBBB from LBBB

A

right v1/2 qrs positive and notched

left v5/6 qrs notched or no M’s (RSR) in v1/2

151
Q

where could a broad complex tachycardia have originated

A

in ventricles or transmitted there with aberrancy

152
Q

define VT, sustained VT and idioventricular rhythm and accelerated idioventricular rhythm

A

3 or more beats of ventricular origin at HR>120BPM
sustained VT needs >30s of tachycardia
if <100 idioventricular rhythm
if 100-120bpm accelerated idioventricular rhythm

153
Q

what are the two forms of VT

A

monomorphic and polymorphic

154
Q

what does pre-existing BBB and atrial tachycardia make

A

a broad complex tachycardia

155
Q

how do you diagnose SVT with aberrancy

A

vagal manoeuvres/ adenosine to try and terminate tachycardia and then assess QRS’s

156
Q

how do you treat SVTs

A

adenosine

if re-enters sinus rhythm then confirms tachycardia originates within the atria

157
Q

is SVT a diagnosis

A

no is a finding on ECG, lots of different things can cause it e.g. re-entry tachycardias

158
Q

ectopic vs escape beats

A

ectopic beats come early

escape beats come late

159
Q

what is the method for going through an ECG

A 
check name patient 
rhythm: sinus, AF, sinus arrhythmia 
rate, where P waves are (heart block) 
cardiac axis 
R wave progression 
QRS
160
Q

how many ECG do you need to do in ACS patients

A

always do more than one

161
Q

what is ST elevation

A

when ST segment is above isoelectric line

162
Q

why are serial ecgs in ischaemia good

A

show changes in T waves

163
Q

how many patients with infarction will have typical changes on ECG

A

50%

164
Q

what does a posterior MI look like

A

ST depression usually in V1-4 stops at V4

if it was anterior would go to v4-5

165
Q

what rhythms are common in MI patients

A

idioventricular

166
Q

what are reciprocal changes in MI

A

when a deflection e.g. in ST segment in mirrored in 180
ST elevation can produce reciprocal ST depression and vice versa, just like tall T waves can produce reciprocal T wave inversion and versa—and posterior Q waves can produce tall anterior R waves. So the important question is not whether there is ST elevation, but are the ST/T changes secondary repolarization abnormalities or primary changes (or both), which is the main deflection and which is the reciprocal change, and what is the cause.

Reciprocal change can be the first sign of acute coronary occlusion, leading to serial ECGs. It can also remain the dominant sign, pointing to subtle ST elevation and hyperacute T-waves. As two recent studies found, minor ST elevation and reciprocal ST depression or T-wave inversion were the most helpful signs in identifying occlusion MI that do not meet STEMI criteria, or STEMI

167
Q

are there P waves in SVT

A

no (how to tell it from a sinus tachycardia)

168
Q

what do capture and fusion beats tell you

A

suggests its a broad complex tachycardia coming from the ventricles

capture beats are normal QRS’s occurring the the middle of a broad complex tachycardia (must be a ventricular tachycardia)

fusion beats occur when a SVT and ventricular impulse coincide to produce a hybrid complex (two foci of pacemaker cell firing simultaneously, seen in VT and accelerated idioventricular rhythm)

169
Q

what are dynamic ST changes

A

ST changes that come with pain and go when symptoms absent

170
Q

what are fixed ST changes

A

there all the time

171
Q

how do you tell pericarditis from a STEMI

A

pericarditis doesn’t follow a vascular territory, has saddle shaped ST elevation, also causes PR segment depression
none of this happens in STEMI

172
Q

what must you have to diagnose WPW

A

delta waves

173
Q

what are important exams findings to look for in chest pain

A

JVP
murmur
pericardial rub
crepitations

174
Q

what is important to add in ecg notes

A

if patient is in pain

175
Q

what bloods for chest pain

A

troponin
U+Es
FBC
ABGs if hypoxic

d dimers if indicated

176
Q

what does emphysema look like on chest x ray

A

(pulmonary emphysema is the abnormal permanent enlargement of airspaces distal to the terminal bronchioles)
big hyperexpanded lungs with lots of air

177
Q

what are the 3 big DDx for chest pain

A

acute coronary syndrome (STEMI, NSTEMI, unstable angina, coronary spasm)
acute aortic syndrome (dissection, rupture, penetrating ulcer)
pulmonary embolism

178
Q

what is the treatment for a myocardial infarction

A

morphine + antiemetic
oxygen if hypoxic
nitrate
aspirin 300mg chewed

heparin/LMWH/clopidogrel/tricagrelor
b blocker
CCV
angiography +/- plasty 
IV GTN
179
Q

what is the different pathologicallu between stable and unstable angina

A

unstable angina is a ruptured atheroma, stable angina is a stable plaque

180
Q

when do you give angiogram for angina

A

if symptoms when on medical treatment (aspirin, statin, b blocker, GTN)

181
Q

what is the difference clinically between STEMI and NSTEMI

A

STEMI artery completely blocked- needs immediate cath lab or thrombolysis
NSTEMI artery still has flow both critically narrowed- unpredictable symptoms

182
Q

why should people with chest pain (suspected MI) be admitted by ambulance)

A

as has defib on board

183
Q

what are you suspecting on ecg in a young patient with dizziness, syncope/ palpitations

A

abnormal PR interval
abnormal qt interval
LVH
etc

184
Q

what are you looking for in an older patient with IHD/ dizziness

A

heart block
AF
MI

185
Q

what are you looking for in a patient with HF/ valvular disease

A

AF

LBBB

186
Q

what do Q waves show

A

a older (maybe few hours) stemi

187
Q

quick way to differentiate BBB

A

QRS broad
QRS mainly down in V1= LBBB
QRS mainly up in V1= RBBB

188
Q

what is:
tall QRS
peaked T waves
inverted T waves also

A

LVH with strain

189
Q

what can cause widespread T wave inversion

A

PE

broken heart syndrome

190
Q

what can cause anterior ST depression

A

posterior MI

191
Q

what should you do if patient sick with arrhythmia

A

immediate TX
iv anti-arrthymic
get help

192
Q

what rate are the P waves in atrial flutter

A

300BPM

193
Q

what are the P waves like in 3rd degree HB

A

marching through

194
Q

what do ectopic beats look like

A

come early, followed by compensatory pause

195
Q

is broad or narrow QRS heart block worse

A

broad QRS- admit asap, risk of stopping ventricular activity

196
Q

what is RBBB with left axis deviation

A

bi-fasicular block

197
Q

what rhythm is a heart in if there is fusion beats

A

VT

198
Q

what should you look for in other territories when there is ST elevation

A

reciprocal changes

199
Q

what is widespread st elevation that doesn’t follow a vascular territory and no reciprocal changes

A

pericarditis

200
Q

which lead is the reference lead that tells you leads are on right

A

AvR (reference) - should go up

201
Q

do escape beats come early or late

A

early

202
Q

what do junctional beats not have

A

P waves before them

203
Q

what is seen on ECG in PE

A

sinus tachycardia
RBBB
RV strain, RAD
SIQIIITIII (S wave, Q wave, inverted T wave)

4th Year (7 decks)

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