ECG Flashcards
what type of tissue should you attach electrodes over
bone
what position should patient be in
lying at 30-40 degrees
where does V1 go
4thIC right sternal angle
where does V2 go
4thIC space left sternal angle
where does V4 go
5thIC space mid clavicular line
where does V3 go
midway between v2 and v4
where does V5 go
5thIC space anterior axillary line
where does V6 go
5thIC space mid axillary line
where do the limb leads go
ride your good bike red arm - right left arm - yellow left foot- green right foot - black (earth)
what does AC interference look like
(electrical equipment, noise)
comb
how do you prevent muscle tremor interference
improve contact with abrasive pad- get off dead skin
what does baseline wander mean (slow undulation)
patient movement
how do you calculate rate
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
how long is a small square
0.04 seconds
how long is a large square
0.2 seconds
what is a good method to go through an ECG
- is there electrical activity present
- are there P waves present
- QRS rate
- QRS rhythm (regular/ irregular?)
- QRS narrow/ broad
- relationship between P waves and QRS complexes
- Axis
- P wave progression
what is the cardiac axis
the direction of sum electrical activation
towards lead= +ve
away from lead= -ve
perpendicular= isoelectric
where do you look to determine cardiac axis
QRS complexes in lead I and aVF
lead I left hand, aVF right hand
what shows normal cardiac axis
lead I +ve
lead aVF +ve
(-30 to 90 degrees)
what shows right axis deviation
lead I -ve
lead aVF +ve
(90-180 degrees)
what shows left heart deviation
Lead I +ve
Lead aVF -ve
(-30 to -180 degrees)
what shows an indeterminate heart axis
both Lead I and avf -ve
what can cause RAD
can be normal- inspiration RV hypertrophy RBBB posterior hemiblock dextrocardia ventricular ectopic WPW
what can cause LAD
normal- expiration left anterior hemiblock LBBB congenital lesions WPW emphysema hyperkalaemia
how long should a PR interval be
120-200ms (3-5 small squares)
what is a PR interval
AV node delay (ventricles re-filling)
from start of atrial depolarisation to start of ventricular depolarisation
where do you measure PR interval from
onset of P wave to QRS onset
how long should a QRS be
<120ms (3 small squares)
what is the QT interval
ventricular repolarisation
where do measure QT from
start of QRS to end of T wave
how do you calculate corrected QT interval
square root of RR interval (seconds) / QTi (ms)
what is the P wave
atrial depolarisation
when is the P wave positive and rounded
leads II, III and aVF
when is the P wave inverted normally
aVR
what should happen to the amplitude of the QRS complex from v1-6
should increase (R gets taller)
what should T wave be in relation to QRS complex
usually in same direction (+ve or -ve)
should not be >1/2 preceeding QRS height
how should you place chest leads on women
under mammary tissue
how should you do ECG on patient with dextrocardia
place leads normal way first then do another with them reversed
what are the augmented leads
aVF, aVR and aVL (form wilsons central terminal)
what are the precordial leads
V1-6
what are the standard limb leads
I-III
what should you do if ECG shows something odd e.g. abnormal axis
repeat ECG to make sure its correct
what is the vertical plane in the ECg
limb leads
what is the horizontal plane in an ECG
R wave progression
what does R wave progression show
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
what should the R wave be in V1-2
mostly negative: if positive then RVH or RV problem
where does a supraventricular rhythm originate
above the AV node
what does a supraventricular rhythm usually have
narrow QRS
ANYTHING NARROW HAS COME FROM THE AV NODE
name 8 SV rhythms
sinus A fib A flutter sinus arrhythmia SVT AVN re-entry tachycardia AVNRT (WPW) wandering atrial pacemaker
what does sinus arrhythmia look like
normal shape and ECG other than rhythm (regularity irregular)
this due to breathing (vagal tone)
what does A fib look like
disorganised activity in atria
irregularly irregular QRS
absent P waves/ not clearly reproducible
chaotic baseline
can occur with range of ventricular rates
what causes A fib
lots of causes (CHD, hypertension, valvular heart disease, hyperthyroidism) make atrium continually send chaotic impulses to AV nodes which are intermittently transmitted to ventricles
what are some presenting features of a fib
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)
what is the most common rhythm problem
AF
what does A flutter look like
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)
where does junctional rhythm originate
@AV node (not sinoatrial node)- pulse travels to atria and ventricles at the same time via the purkinje system
what does junctional rhythm look like
retrograde P waves in ST segment
regular
normal QRS morphology
rate can be normal or tachy-/bradycardic
what is an SVT
tachycardia that originates above/ involves the AV node (excluding sinus, Afib, A flutter)
can be an accessory pathway or re-entry pathway involving AVN
what does SVT look like
regular, narrow, often no clear P waves
what do SV ectopic look like
sinus rhythm
differing P morphology on beats 3,6 and 9 which also come early
varying PR and RR intervals
can ventricular rhythms be normal
no always pathological
what is always present in ventricular rhythm
QRS>120ms
what do premature ventricular complexes look like
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
what is a premature ventricular complex
when beat initiated in purkinje fibres
what does VTV look like
regular broad can be monomorphic or polymorphic (torsades de points) always abnormal, may have haemodynamic compromise
what can VT deteriorate into
VF or MI
what does VF look like
irregular random baseline
no discernible waveforms
LOC always
what is a capture beats
when sinus beat reaches AV node before wide QRS VT beat and produces a QRS of normal duration
what is a fusion beat
when sinus beat and VT beat fuse to produce a hybrid complex
what do capture and fusion beats show in VT
the independent rhythms of atria and ventricles
why is it hard to tell ventricular rhythms from SV rhythms in patients with BBB
as both have broad QRS’
how do you estimates whether its ventricular or SV with BBB
v: pre-existing coronary disease, capture/ fusion beats present
SV with aberrancy: pre-existing BBB
what is aberrancy
abnormal conduction e.g. BBB
where is heart block affecting
AV nodal dysfunction
NOT bundle branches
what can cause heart block
drugs
ischaemia
age
what does 1st degree heart block look like
PRi >200ms (1 big square)
stable
what is the common theme of 2nd degree heart block
P wave blocked from initiating QRS
what are the types of 2nd degree heart block
mobitz 1 and 2
what does mobitz 1 look like
increasing delays
eventual missed beat
may be normal
what does mobitz 2 look like
constant PRi with subsequent missed beat
always abnormal, may deteriorate
what does 3rd degree heart block look like
no relationship between P wave and QRS
broad QRS= ventricular escape rhythms
always abnormal
what does a ventricular escape rhythm look like
300-400 bpm
broad
not linked to atrial activity
when does a ventricular escape rhythm occur
in heart block
what are the fascicles
anterior and posterior fascicles branch off the left bundle branch
right bundle branch
what is bi fascicular block and what does it look like
when 2 of LAFB, LPFB, RBBB occur 2 of: PRi >200ms LAD (LAHB) RBBB
what is tri-fascicular block
when RBB, LAF and LPF all block all of: PRi >200ms LAD (LAHB) RBBB or alternating LBBB and RBBB
what are the cardiac arrest rhythms and their treatments
VT and VF (shockable rhythms)
complete AV block (give IV atropine and isoprenaline until venous pacing wire)
pulseless electrical activity (CPR)
what can VT deteriorate into
VF then asystole
where do you look for BBB
V1 and V6
what can you see in RBBB
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
what can you see in LBBB
V1-V6 WilliaM
W QRS in V1
M QRS in V6 (wide notched QRS in I, aVL, V5-6)
prolonged QRS
which of LBBB and RBBB is always pathological
LBBB can be MI or other left heart disease
what should you do to interpret signs of ischaemia on ECG
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
what leads show inferior heart
what CA is this
II
III
aVF
RCA
what leads show lateral heart
what CA is this
I
aVL
V5
V6
circumflex
what leads show anterior heart
what CA is this
V3
V4
LADA
what are the ECG markers of ischaemia
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)
name something other that ischaemia that can cause ST depression
pericarditis
what on an ECG means you should thrombolyse
ST elevation:
- > 1mm in 2 contiguous limb leads
- > 2mm in 2 contiguous chest leads
- posterior MI (V1-3)
- LBBB
what shows a posterior infarction
ST elevation in leads v1-3
what are the ECG signs of infarction
ST elevation
LBBB
Q wave formation
T wave peaking/ inversion
what is a Q wave
the loss of R waves, happens at 2-24 hours
shows myocardial necrosis
when are Q waves pathological
if in V1-3
>0.03 seconds in I, II, aVF, A4-6
must be present in2 contiguous leads and be >1mm in depth
what else can cause ST elevation
benign early repolarisation LBBB LVH ventricular aneurysm coronary vasospasm pericarditis brugada syndrome subarachnoid haemorrhage
what should you think when there is new LBBB in an acute MI
infarction
what is the general rule for thrombolysis
unless they look like they are having an MI do not thrombolyse
what constitutes a STEMI with LBBB
ST depression >1mmin V1-2
ST elevation >1mm where +ve QRS
ST elevation >5mm where -ve QRs
what is pericarditis
pericardial inflammation post MI/ viral infection
what are the symptoms of pericarditis
pleuritic chest pain
fever
pericardial friction rub
what is seen on ECG in pericarditis
upward concave ST elevation that doesn’t evolve
and is widespread (>1 vascular region)
what is the Tx for pericarditis
analgesia and NSAIDs
when is ventricular hypertrophy pathological
when in response to stress/ disease e.g. hypertension, MI, HF, neurohormones
what does VH look like on ECG
v high QRS complexes
what leads show the right ventricle
V1-2
what leads show the left ventricle
V5-6
what leads show the IV septum
V1-2
when is it partial/ full BBB
full= QRS> 0.12 seconds partial= BBB present but QRS not >0.12 seconds
what happens in RBBB
RV depolarises late
what can cause RBBB
can be normal cor pulmonale/RVH PE MI CHD mechanical damage congenital heart disease (e.g. septal defect) myocarditis cardiomyopathy lev disease
what hemi bundles are injured in LBBB
both anterior and poster fascicles
what happens in LBBB
delayed LV activation
what can cause LBBB
HD IHD MI cardiomyopathy hypertension
what is hemi block
block in either hemifascicles of LBB
which is the most common hemiblock
LAHB
what does LAHB look like
LAD without other causes for it
initial R waves in inferior leads
what does LPHB look like
(is rare)
RAD without other causes
normal/ slightly prolonged QRS
S1 Q3 pattern
what is mobitz type 1 associated with
high vagal tone e.g. athletes (not worrying)
does mobitz 2 need intervention
yes as may deteriorate
does 3rd degree heart block need intervention
yes may deteriorate
what can tachycardia be associated with
sudden death
why is tachycardia bad
less efficient (pre load and afterload reduced)
increased myocardial demand
risk of stroke
risk of cardiomyopathy long term
what is tachycardia
> 100bpm
what is sinus rhythm
regular rhythm
when is a tachycardia sinus
if regular and every P wave followed by a QRS and every QRS preceded by a P wave
will sinus tachycardia always stay at same rate
no often fluctuates
what is not included in narrow complex tachycardias
AF
A flutter
sinus tachycardia
how do you treat narrow complex tachycardias
AV node block:
vagal manoeuvres (stimulating vagal nerve by valsalva, cough, gag reflex, hold knees against chest, carotid sinus massage)
adenosine (gives transient block)
what condition should you not give adenosine in
severe asthma
can also block some other drugs metabolism so look for interactions
what is AVNRT
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
where is the best place to look for atrial activation in AVNRT
V1
what is AVRT
re-entry tachycardia that can use either AV node on way to ventricles or separate accessory pathway
what do QRS’ in AVRT look like
broad QRS complex
slurred upstrokes on QRS complex (delta wave) with small PR interval=?
WPW (a AVRT)
what do atrial tachycardias and heart block have in common
both have more P waves then QRS’
how do you tell the difference between atrial tachycardias and heart block
in atrial tachycardias atria will influence ventricles
in heart block QRS will be regular but not related at all to what atria doing
if the qrs is narrow can there be bundle branch block
no
what is partial branch block
when there is a bit of delay but QRS not >120ms
how many boxes should it be from start of p wave to start of qrs
within one big box
what do you see in RBBB
RSR in v1 or v2
how to tell RBBB from LBBB
right v1/2 qrs positive and notched
left v5/6 qrs notched or no M’s (RSR) in v1/2
where could a broad complex tachycardia have originated
in ventricles or transmitted there with aberrancy
define VT, sustained VT and idioventricular rhythm and accelerated idioventricular rhythm
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
what are the two forms of VT
monomorphic and polymorphic
what does pre-existing BBB and atrial tachycardia make
a broad complex tachycardia
how do you diagnose SVT with aberrancy
vagal manoeuvres/ adenosine to try and terminate tachycardia and then assess QRS’s
how do you treat SVTs
adenosine
if re-enters sinus rhythm then confirms tachycardia originates within the atria
is SVT a diagnosis
no is a finding on ECG, lots of different things can cause it e.g. re-entry tachycardias
ectopic vs escape beats
ectopic beats come early
escape beats come late
what is the method for going through an ECG
check name patient rhythm: sinus, AF, sinus arrhythmia rate, where P waves are (heart block) cardiac axis R wave progression QRS
how many ECG do you need to do in ACS patients
always do more than one
what is ST elevation
when ST segment is above isoelectric line
why are serial ecgs in ischaemia good
show changes in T waves
how many patients with infarction will have typical changes on ECG
50%
what does a posterior MI look like
ST depression usually in V1-4 stops at V4
if it was anterior would go to v4-5
what rhythms are common in MI patients
idioventricular
what are reciprocal changes in MI
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
are there P waves in SVT
no (how to tell it from a sinus tachycardia)
what do capture and fusion beats tell you
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)
what are dynamic ST changes
ST changes that come with pain and go when symptoms absent
what are fixed ST changes
there all the time
how do you tell pericarditis from a STEMI
pericarditis doesn’t follow a vascular territory, has saddle shaped ST elevation, also causes PR segment depression
none of this happens in STEMI
what must you have to diagnose WPW
delta waves
what are important exams findings to look for in chest pain
JVP
murmur
pericardial rub
crepitations
what is important to add in ecg notes
if patient is in pain
what bloods for chest pain
troponin
U+Es
FBC
ABGs if hypoxic
d dimers if indicated
what does emphysema look like on chest x ray
(pulmonary emphysema is the abnormal permanent enlargement of airspaces distal to the terminal bronchioles)
big hyperexpanded lungs with lots of air
what are the 3 big DDx for chest pain
acute coronary syndrome (STEMI, NSTEMI, unstable angina, coronary spasm)
acute aortic syndrome (dissection, rupture, penetrating ulcer)
pulmonary embolism
what is the treatment for a myocardial infarction
morphine + antiemetic
oxygen if hypoxic
nitrate
aspirin 300mg chewed
heparin/LMWH/clopidogrel/tricagrelor b blocker CCV angiography +/- plasty IV GTN
what is the different pathologicallu between stable and unstable angina
unstable angina is a ruptured atheroma, stable angina is a stable plaque
when do you give angiogram for angina
if symptoms when on medical treatment (aspirin, statin, b blocker, GTN)
what is the difference clinically between STEMI and NSTEMI
STEMI artery completely blocked- needs immediate cath lab or thrombolysis
NSTEMI artery still has flow both critically narrowed- unpredictable symptoms
why should people with chest pain (suspected MI) be admitted by ambulance)
as has defib on board
what are you suspecting on ecg in a young patient with dizziness, syncope/ palpitations
abnormal PR interval
abnormal qt interval
LVH
etc
what are you looking for in an older patient with IHD/ dizziness
heart block
AF
MI
what are you looking for in a patient with HF/ valvular disease
AF
LBBB
what do Q waves show
a older (maybe few hours) stemi
quick way to differentiate BBB
QRS broad
QRS mainly down in V1= LBBB
QRS mainly up in V1= RBBB
what is:
tall QRS
peaked T waves
inverted T waves also
LVH with strain
what can cause widespread T wave inversion
PE
broken heart syndrome
what can cause anterior ST depression
posterior MI
what should you do if patient sick with arrhythmia
immediate TX
iv anti-arrthymic
get help
what rate are the P waves in atrial flutter
300BPM
what are the P waves like in 3rd degree HB
marching through
what do ectopic beats look like
come early, followed by compensatory pause
is broad or narrow QRS heart block worse
broad QRS- admit asap, risk of stopping ventricular activity
what is RBBB with left axis deviation
bi-fasicular block
what rhythm is a heart in if there is fusion beats
VT
what should you look for in other territories when there is ST elevation
reciprocal changes
what is widespread st elevation that doesn’t follow a vascular territory and no reciprocal changes
pericarditis
which lead is the reference lead that tells you leads are on right
AvR (reference) - should go up
do escape beats come early or late
early
what do junctional beats not have
P waves before them
what is seen on ECG in PE
sinus tachycardia
RBBB
RV strain, RAD
SIQIIITIII (S wave, Q wave, inverted T wave)
