ECG Interpretation Flashcards
Pericarditis - common findings
Widespread ST elevation.
PR depression.
Define the following intervals/segments.
a) PR interval (normal value?)
b) QRS duration (normal value?)
c) ST segment
d) QT interval
a) Start of P wave to start of QRS (normal: 120 - 200 ms)
b) Start of QRS to end of QRS (normal: <120 ms)
c) End of QRS to start of T wave
d) Start of QRS to end of T wave
Reading an ECG (step 1: assess rate)
a) 1 small square (1 mm) = ? milliseconds
b) 1 large square (5 mm) = ? milliseconds
c) A rhythm strip = ? seconds
d) To calculate HR - 2 techniques
a) 40 ms (0.04 seconds)
b) 200 ms (0.2 seconds)
c) 10 seconds (hence number of QRS complexes multiplied by 6 gives HR)
d) - Total QRS number x 6
- 300 / number of large squares between successive RR intervals (only if regular rhythm)
Step 2: assess rhythm
a) Sinus rhythm
b) AF - pattern
c) Other patterns
a) Normal P wave precedes each QRS complex. Normal rhythm with narrow complexes.
Indicates normal conduction from SA node to AVN, down Bundle of His and Purkinje fibres
b) Irregularly irregular
c) Regularly irregular
Step 3: axis
a) Normal - ?
b) LAD - ? - causes?
c) RAD - ? - causes?
a) Leads I and aVF - both positive
- Normal axis: -30 degrees to +90 degrees
b) Leaving: Lead I positive, Lead aVF negative
- Causes: LVH, inferior MI, LBBB, left anterior hemiblock
c) Reaching: Lead I negative, aVF positive
- Causes: RVH, lateral MI, RBBB, left posterior hemiblock, acute lung disease (PE), chronic lung disease
Step 4: P waves
a) Absent
b) If present, are they always followed by…?
c) If absent, is there another pattern of atrial activity? - give 2 examples
d) P mitrale - explain? - causes?
e) P pulmonale - explain? - causes?
a) AF
b) QRS complex (is there a pattern of association?, are they completely dissociated?)
c) Flutter waves (sawtooth), fibrillation (wandering baseline)
d) ‘M’ shaped notched P wave - caused by increased left atrial pressure (e.g. mitral stenosis/regurgitation)
e) Tall pointed P wave - caused by increased right atrial pressure (e.g. cor pulmonale, pulmonary stenosis, ASD)
Step 5: PR interval
a) Normal range
b) Describe 1st degree HB (give site of pathology)
c) Describe 2nd degree HB (Mobitz type 1/ Wenckebach)
d) Describe 2nd degree HB (Mobitz type 2)
e) Describe 3rd degree HB
f) Shortened PR - causes?
a) 0.12 - 0.2 seconds
b) Fixed prolonged PR (> 0.2 seconds). Occurs within atria (between SA node and AV node)
c) PR interval increases gradually and then a QRS is dropped (occurs within AVN)
d) Fixed PR with occasional dropped beats; may follow a ratio, e.g. 3:1 (occurs after AVN: partial conduction block)
e) Complete dissociation between atrial (P waves) and ventricular (QRS complexes) activity (occurs after AVN: total conduction block)
f) - Normal physiological phenomenon (some people have smaller atria or less distance between SAN/AVN)
- WPW - accessory pathway (Bundle of Kent) look for delta waves
Step 6: QRS complexes
a) Width - normal? prolonged?
b) Causes of wide QRS
c) Height - causes of tall QRS complexes?
d) Height - causes of short QRS complexes?
e) Q waves - when are they pathological?
f) Poor R wave progression
a) Normal: 80-100 ms (prolonged: >120 ms)
b) - Conduction block: LBBB, RBBB, bifascicular block
- Ventricular rhythm
c) LVH, normal variant in tall thin people
d) Fat, fluid (pericardial effusion, pleural effusion), air (emphysema, pneumothorax), restrictive cardiomyopathy
e) - >25% height of QRS, or
- greater than 2mm, or
- > 40ms (wide), or
- in leads V1 - V3
Note: a single Q wave may not be pathological - look at entire territory for evidence of previous MI
f) Transition from negative to positive should occur around V3/V4. If later than this, could be a sign of previous anterior MI
Step 6: ST segment
a) What is the J (junction) point?
b) How can pathological ST elevation be distinguished from benign early repolarisation (high take-off)?
c) What value of ST elevation is pathological?
d) In what situation can the ST segment not be evaluated?
a) The JUNCTION between the QRS and the ST segment
b) - BER: tends to be common in younger healthy patients, leads to widespread concave ST elevation (high J point) with large prominent T waves that are concordant with the QRS complexes, changes do not evolve over time
- STEMI: generally convex, often older patients (more likely to have MI), generally in one region, T waves usually same size, may have T wave changes (eg inversion), reciprocal changes in other regions, evolving changes over time
c) >1 mm in >1 contiguous limb leads, or >2 mm in >1 contiguous chest lead (in V2 and V3)
d) If there is a LBBB
Step 7: T waves
a) Represent what?
b) Tall T waves - give 2 causes
c) Inversion - normal in what leads?
d) Pathological inversion - causes?
e) Biphasic T waves - causes?
f) Flattened T waves - causes?
a) Ventricular repolarisation
b) Hyperkalaemia, hyperacute STEMI
c) V1, III and aVR
- However, if there is TWI in >1 contiguous leads (eg. in leads II and III), this is likely pathological
- Also, look for concordance between QRS and T waves (to account for any axis changes)
d) - Ischaemia, infarction, PE, general illness
- Intracranial haemorrhage: deep TWI
- HCM: TWI in leads V1 - V3 is common
- Brugada: coved ST elevation and TWI in >1 of leads V1-V3
e) Ischaemia, hypokalaemia
f) Ischaemia, hypokalaemia
Step 8: QT interval
a) What does it measure?
b) Effect of heart rate and reason for QTc
c) Normal QTc duration in men and in women
d) Causes of long QT (think HYPO) - risk of what arrhythmia?
e) Causes of short QT? (defined as < ? ms)
a) The start of the Q wave to the end of the T wave. It represents the time taken for ventricular depolarisation and repolarisation
b) Slower = longer QT; faster = shorter QT
c) Men: <440 ms, Women <460 ms
d) - Hypo…K+, Mg2+, Ca2+, thermia
- Myocardial ischemia
- ROSC Post-cardiac arrest
- Raised intracranial pressure
- Congenital long QT syndrome (e.g. Romano-Ward)
- Medications/Drugs (e.g. TCAs, citalopram, antiarrhythmics, macrolides, antipsychotics)
e) Short QT syndrome (congenital)
Likely pathophysiological difference between a STEMI and an NSTEMI
STEMI - full thickness infarct
NSTEMI - smaller vessel infarct
When should you look at troponins?
When you suspect ACS
Never on a whim, as they may be raised for other reasons (e.g. AF, CCF, sepsis, PE, kidney disease) and then you’re in a pickle
Progressively prolonged PR, then a dropped QRS.
- diagnosis?
- give the other types of heart block
2nd degree HB (Mobitz type 1 - Wenckeback)
Others:
- 1st degree = fixed prolonged PR; sinus rhythm
- Mobitz type 2 = fixed PR with dropped QRS (may have a ratio of dropped QRS)
- Complete (3rd degree) = complete AV dissociation
ACS on ECG.
a) Sequence of ECG changes in typical STEMI
b) Other than ST/T/Q abnormalities, what new feature on ECG may indicate an MI?
a) 1. Large peaked T waves (or hyperacute T waves)
2. ST elevation
3. Negative T waves
4. Finally pathological Q waves develop
b) New LBBB - considered equivalent to ST elevation in context of cardiac-sounding chest pain (for PCI)
- use Sgarbossa criteria
