Electrocardiogram (ECG) Flashcards
Why are there 3 parts to the QRS complex?
- Different parts of the ventricles depolarise at slightly different times.
1. Interventricular Septum depolarises from left to right (Q wave)
2. R wave: bulk of ventricle depolarises from endocardial to epicardial surface
3. Upper part of interventricular septum depolarises.
What is the PR interval?
Start of P wave to start of QRS complex
Its the time from the start of atrial depolarisation to the start of ventricular depolarisation, mainly transmission in the AV node.
What is the QT interval?
Time from the start of the QRS complex to the end of the T wave.
Essentially the time the ventricle spends depolarised.
How long is the QT interval?
It varies with HR.
The standard is 0.42 seconds at 60 BPM.
How do you calculate rate from ECG?
Regular rhythm
Irregular rhythm
Regular rhythm - 300/no of R waves
Irregular rhythm - No of R waves in 10s rhythm strip x 6
Complete the sequence:
300, ___, ___, ___, 60.
300, 150, 100, 75, 60
Intervals
How long should the PR interval last?
How long should the QRS complex last?
PR interval
0.12-0.2 seconds
3-5 small squares
QRS complex
~0.08 seconds
<3 small squares
Systemic approach to ECG
Rate Rhythm Axis Intervals Everything else
Prolonged PR interval? Think Heart Blocks List the features of: 1) First Degree [1] 2) Mobitz Type 1 [2] 3) Mobitz Type 2 [2] 4) Third Degree [3]
1) First Degree - constantly prolonged PR
2) Mobitz Type 1 - progressively prolonged PR, dropped beat
3) Mobitz Type 2 - constantly prolonged PR, dropped beat every couple of beats
4) Third Degree - no relationship between atrial and ventricular depolarization, bradycardia
BBB: WIDE QRS
Describe the 3 features of RBBB
Whats the mnemonic?
Broad QRS >0.12
RSR’ in V1 [m]
Slurred S wave in V6 [w]
Normal Axis
MARROW
BBB: WIDE QRS
Describe the features of LBBB
Broad QRS >0.12
Dominant S wave in V1 [w]
RSR’ in V6 [m]
Left axis deviation
WILLIAM
Myocardial infarction/Acute Coronary Syndrome
Localisation: state which leads the changes are most likely to be seen and what artery is most commonly involved
Anterior
Septal
Inferior
Lateral
Anterior
V1-V4, LAD
Septal
V2-V4, Septal branches of LAD
Inferior
III, AVF, II
80% RCA, 20% LCA
Lateral
V5, V6, AVL, I
Left Circumflex Artery
AXIS
Which leads to look for net deflection
What should we see in the leads if axis is normal
Right axis deviation - what should we see in the leads
Left axis deviation - what should we see in the leads
I, AVF > II
If lead 1 is positive, lead II negative> LAD
If Lead 1 is negative, AVF is positive > RAD
How to spot an RV infarction?
Suspect in patients with _______ in the presence of:
1)
2)
Suspect RV infarction in patients with inferior STEMI picture
ST elevation in V1
ST elevation in lead III > lead I
WPW syndrome
What is the problem in WPW? [2]
ECG features [3]
In WPW the accessory pathway is often referred to as theBundle of Kent [1] which bypasses the AV node causing early activation of ventricles [1]
Delta wave
PR short
QRS prolongation
Sinus tachycardia ~ 100 bpm
What ECG changes in a dyspneic patient would suggest COR pulmonale due to massive PE?
However these ECG changes are not specific to PE and may be seen in other conditions of RV dilation and pulmonary HTN eg COPD
Sinus tachycardia
RV strain pattern in V1-V4
= T wave inversion in right precordial leads (V1-V4)
3 ECG features that would make massive pericardial effusion highly suspect
- Tachycardia
- Low QRS voltages
- Electrical alternans
ECG pattern characteristic of raised ICP (classically seen in context of massive intracranial hemorrhage)
- Giant T wave inversion
2. Marked QT prolongation
Posterior infarction ECG features [4]
Which set of infarct patients should you look for evidence of posterior infarction [1]
How to confirm that it is a posterior infarction if in doubt [1]
Look at V2 for:
Horizontal ST depression
Tall broad R wave
Upright T wave
Changes in V1-3
Look for evidence of posterior involvement in any patient with aninferiororlateral STEMI.
Confirm with recording posterior lead ECG V7-9
ST elevation in MI [3]
○ >1mm in height
○ New: hyperacute T waves, ST elevation
○ Old: pathological Q waves
Causes of ST elevation other than MI [9]
Pericarditis Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm =Brugada syndrome Ventricular paced rhythm Raised intracranial pressure Takotsubo Cardiomyopathy
ST depression MI (NSTEMI) [2]
ST depression
T wave inversions
What are the features of ST depression that [3]
Three types of ST depression
- ST depression ≥ 0.5 mm at the J-point
- in ≥ 2 contiguous leads
- Upsloping
- Downsloping
- Horizontal
ST segment depression - what do these mean?
- Upsloping
- Horizontal
- Upsloping
- LAD occlusion - Horizontal
- Posterior MI in V1-V3 + upright T waves and tall R waves
Other causes of ST depression [8]
Reciprocal change in STEMI Posterior MI Digoxin effect Hypokalaemia SVT LBBB, RBBB LVH, RCH Ventricular paced rhythm
Conduction disease and arrhythmias: overview
- AV node disease
- Bundle branch disease or fascicle disease
- Escape rhythms i.e. tachyarrhythmias (when no impulse arise…)
Describe what axis you may see in single fascicle blocks
Left anterior fascicular block causes LEFT AXIS DEV
Left posterior fascicular block causes RIGHT AXIS DEV
Bifascicular blocks:
- RBBB + LAFB
- RBBB + LPFB
- RBBB + LAFB: Left axis deviation
2. RBBB + LPFB: Right axis deviation
Trifascicular block
Bifascicular block + PR interval up i.e. there is heart block
Bradycardia algorithm:
What will cause bradycardia + narrow complex QRS [5]
Sinus bradycardia 1st degree HB 2nd degree HB 3rd degree HB Junctional rhythm
What differentiates junctional rhythm from HB or sinus bradycardia? [3]
Junctional Rhythm:
- QRS narrow and regular rhythm
- BUT there are no P waves or they are buried in QRS/T
- HR 40-60 bpm
Heart block, p waves will be seen
What can cause bradycardia + wide QRS complex + regular rhythms
Sinus brady with BBB First degree HB with BBB Mobitz type 2 AV block Complete HB AF with complete HB
What can cause bradycardia + wide QRS complex + IRREGULAR rhythms
AF with slow response
BBB pattern
Tachyarrhythmias algorithm:
What can cause QRS narrow + regular rhythms [5]
Atrial flutter Ectopic atrial tachycardia Sinus tachycardia AVNRT AVRT
What tachyarrhythmia cause QRS narrow + irregular rhythms + no P waves?
How to distinguish Atrial flutter Ectopic atrial tachycardia Sinus tachycardia AVNRT AVRT
Tachyarrhythmia, QRS narrow + irregular rhythms + no P waves = Atrial fibrillation
Atrial flutter: continuous and fluttery P waves ‘sawtooth’
Ectopic atrial tachycardia and Sinus tachycardia = discrete P waves
AVNRT and AVRT = No p waves
What tachyarrhythmias have BROAD QRS + regular rhythms [7]
SVT with BBB SVT with aberrancy WPW antidromic Ventricular tachycardia AF with BBB or AF with aberrancy Torsades des pointes, other polymorphic VTs Ventricular fibrillation
Tachyarrhythmias: BROAD QRS + regular rhythm
How are they distinguished from each other? [3]
Typical BBB pattern > SVT + BBB/Aberrancy
Delta wave > WPW antidromic
Unlike BBB pattern, fusion and capture beats > VT
Tachyarrhythmias: BROAD QRS + irregular rhythm
How are they distinguished from each other? [2]
Tachyarrhythmias: BROAD QRS + irregular rhythm:
Tall QRS
Flat wavy QRS = Ventricular fibrillation
If you suspect that it is VT and the patient has a wide complex tachycardia, do you wait for investigation before treating?
No, any wide complex Tachycardia is VT until proven otherwise
What is VT characterized by? [3]
Types of VT [2]
Regular rhythm P waves absent 3 or more ventricular beats Capture or fusion beats Types: 1. Monomorphic 2. Polymorphic
Explain Torsades des Pointes - it is a type of polymorphic VT
Twisting of the points
Changing in amplitudes of ventricular impulses
Several escape beats are happening and they take turns
SVT with aberrancy [3]
Narrow complex tachycardia + other conduction defect e.g. BBB (regular + broad QRS) so it has a WIDE QRS complex
AV dissociation
Extreme axis deviation
Causes of right axis deviation [2]
acute, chronic, congenital, normal variants.
- right ventricular hypertrophy
- left posterior hemiblock
- lateral myocardial infarction
- chronic lung disease → cor pulmonale
- pulmonary embolism
- ostium secundum ASD
- Wolff-Parkinson-White syndrome - left-sided accessory pathway
- normal in infant < 1 years old
- minor RAD in tall people
Causes of LAD
- left anterior hemiblock
- left bundle branch block
- inferior myocardial infarction
- Wolff-Parkinson-White syndrome - right-sided accessory pathway
- hyperkalaemia
- congenital: ostium primum ASD, tricuspid atresia
- minor LAD in obese people
Describe how digoxin toxicity can manifest as ECG changes [4]
down-sloping ST depression (‘reverse tick’, ‘scooped out’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia
Hypokalemia in ECG [5]
- U waves
- small or absent T waves (occasionally inversion)
- prolong PR interval
- ST depression
- long QT
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT
When would bradycardia and a J wave be seen?
ECG: hypothermia
The following ECG changes may be seen in hypothermia
* bradycardia
* ‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
* first degree heart block
* long QT interval
* atrial and ventricular arrhythmias
Causes of LBBB
New LBBB is always pathological
- myocardial infarction
- diagnosing a myocardial infarction for patients with existing LBBB is difficult
- rhe Sgarbossa criteria can help with this - please see the link for more details
- hypertension
- aortic stenosis
- cardiomyopathy
- rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
Causes of ST elevation [7]
Causes of ST elevation
* myocardial infarction
* pericarditis/myocarditis
* normal variant - ‘high take-off’
* left ventricular aneurysm
* Prinzmetal’s angina (coronary artery spasm)
* Takotsubo cardiomyopathy
* rare: subarachnoid haemorrhage
Name normal variants in athletes that can be misinterpreted as pathological on an ECG
The following ECG changes are considered normal variants in an athlete:
* sinus bradycardia
* junctional rhythm
* first degree heart block
* Mobitz type 1 (Wenckebach phenomenon)
Causes of a prolonged PR interval
- idiopathic
- ischaemic heart disease
- digoxin toxicity
- hypokalaemia
- rheumatic fever
- aortic root pathology e.g. abscess secondary to endocarditis
- Lyme disease
- sarcoidosis
- myotonic dystrophy
Prolonged ECG monitoring
methods
- Holter- 24h to 7d
- External recorders: patient places monitor on chest at onset of symptoms
- Wearable loop recorder: continuous monitoring, patient activates recorder when symptoms occur, records minutes before, during after event
- Implantable loop recorders: records when there is pre-specified alarm criteria, implanted for 3y.
Cardiac action potentials
Describe the movement of Na, K or Ca at each stage of the cardiac AP
* Rapid depolarisation
* Early depolarisation
* Plateau
* Final repolarisation
* Restoration of ionic concentrations
Rapid depolarisation
* Rapid sodium influx
Early depolarisation
* Efflux of potassium
Plateau
* Slow influx of calcium
Final repolarisation
* Efflux of potassium
Restoration of ionic concentrations
* Na/K/ATPase - slow entry of Na into cell decreasing potential difference until threshold potential reached.
Heart block
Bundle branch block
- RBBB
- LBBB
- LAFB
- LPFB
- Bifascicular block
- Trifascicular block
RBBB vs LBBB
One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6 in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
New LBBB is always pathological. Causes of new LBBB [6]
myocardial infarction
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
What is the Sgarbossa criteria?
In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG can be difficult.
1. Concordant ST elevation ≥ 1 mm in ≥ 1 lead
2. Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
3. Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave
ECG criteria for LAFB, LPFB
◆ Left anterior hemiblock: left axis deviation, rS pattern inferior leads.
◆ Left posterior hemiblock: right axis deviation, tall R wave in inferior leads.
What is a bifascicular block?
What is a trifascicular block?
- Bifascicular block:
RBBB + left anterior or left posterior hemiblock.
LBBB (due to involvement of both fascicles). - Trifascicular block:
first degree heart block and RBBB
AND
either left anterior or left posterior hemiblock.
Features suggesting VT rather than SVT with aberrant conduction
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
Brugada syndrome ECG features
ECG changes
* convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
* partial right bundle branch block
* the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
