ecg_easy
Table of Contents
The basics of reading an ECG
see also in this wiki:
see also:
- EMRAPTV videos:
The ECG:
Lead placement:
- Limb leads:
- all in a coronal plane & thus can be used to measure the mean frontal axis
- Chest leads:
- V1: right sternal edge, 4ICS
- V2: left sternal edge, 4ICS
- V3: half-way between V2 & V4
- V4: pt's apex beat
- V5: AAL
- V6: MAL
- additional leads:
- V7: PAL
- NB. all leads subsequent to V4 are horizontal to V4
Paper speed:
- usually 25mm/sec which results in:
- each “big” square = 0.2secs
- each “small” square = 0.04secs
- can speed paper up to 50mm/sec esp. when interpreting tachycardias looking for P waves, etc.
- NB. modern ECG machines, record ECG in 5 discrete, sequential time periods so pt's ECG status may have altered during the performance of the ECG and this will be reflected as differences between the ECG sectors:
- I, II & III are recorded together
- avR, avL & avF are recorded together
- V1-3 are recorder together
- V4-6 are recorded together
- finally, the rhythm strip is recorded which is usually lead II
Systematic ECG interpretation:
What is the rate?
- count number of large squares in one RR interval and divide into 300:
- 1.5 squares = 200 bpm
- 2 squares = 150 bpm (could this be atrial flutter with 2:1 block)
- 3 squares = 100 bpm (faster than this is tachycardia)
What is the rhythm & how has the depolarisation been initiated?
- regular:
- tachycardias:
- narrow complex:
- sinus tachycardia
- AV nodal reentrant tachycardia
- atrial tachycardia
- atrial flutter with fixed AV conduction
- wide complex (see wide complex tachycardia):
- VT
- Torsade de Pointes
- SVT with BBB or aberrancy
- atrial flutter with WPW conduction
- pre-excited (circus movement) tachycardia (WPW anterograde conduction)
- bradycardias:
- sinus bradycardia
- AV block
- irregularly irregular:
- AF:
- narrow complex
- broad complex if WPW anterograde conduction or intraventricular conduction defect
- atrial flutter with variable block
- VF
- regularly irregular:
- multifocal atrial tachycardia
- tachycardia
what is the mean frontal QRS axis?
- the mean frontal axis is the sum of all the ventricular forces during ventricular depolarisation
- determined by analysing the 6 limb leads which are in a coronal plane
- axis directions of the limb leads (NB. 0 degrees is taken here as being the East position of a compass):
- aVL = -30deg
- I = 0 deg
- II = 60deg
- aVF = 90deg
- III = 120deg
- aVR = -150deg (ie. 210deg)
- normal axis is -30deg to + 120deg
- left axis deviation (LAD):
- more negative than -30deg
- aetiology includes:
- LAHB
- right axis deviation (RAD):
- more positive than +120deg
- aetiology includes:
- rules of thumb:
- if there is an isoelectric complex in the limb leads then the axis is 90deg to that lead, check which way by looking at direction in other leads
- if predominantly +ve in both I & II then it is normal
- if predominantly -ve in all I, II & III then it is in “no man's land” ie NW quadrant & +ve in aVR:
- ventricular focus highly likely if leads are correctly placed
- mathematical determination:
- create a right angle triangle from 2 resultant vectors:
- horizontal vector side determined by net sum of lead I complex:
- length = net sum in mm (ie. subtract height of negatively directed components from height of positively directed components)
- direction of vector: to right if net sum is +ve
- vertical side determined by net sum aVF is attached to arrow end of horizontal vector:
- length = net sum in mm
- directed downwards if net sum +ve
- the axis is the angle between the horizontal vector & the hypotenuse:
- ie. Inverse Tan (net sum aVF / net sum I) (nb. ensure + or - included here)
P wave shape:
- P waves are best seen in leads II & V1
- if inverted in lead I and upright in aVR then arm leads are reversed or dextrocardia is present, but in dextrocardia there is loss of R waves in V4-6
- P mitrale:
- wide P waves >= 0.12secs
- notching of wide P wave in lead II with distance b/n peaks > 0.04sec
- biphasic P wave in V1 - if P-terminal force (depth of inversion x width) > 0.04
- P pulmonale:
- tall, peaked P waves:
- height in lead III > lead I
- >= 3mm in an inferior lead
P-R interval:
- normally 0.12-0.21sec
- shortened PR interval:
- WPW
- normal variant
- low atrial or upper AV junctional rhythms
- accelerated AV conduction
- phaeochromocytoma
- glycogen storage disease
- Fabry's disease
- prolonged PR interval:
- no dropped beats ⇒ 1st degree heart block
- dropped beats:
- dropped beat after successive increasingly long PR interval ⇒ Wenckebach (Mobitz type I)
- at least 2 regular, consecutive impulses conducted with same PR ⇒ Mobitz type II
- no conduction ⇒ complete HB
QRS width:
- normally < 0.12sec
QRS height:
- LVH
QRS morphology:
Tall R waves in V1:
- thin chest wall or normal variant
- RBBB - NB. slurred S wave in leads I, V5 & V6
- RVH
- WPW
- true posterior infarction - assoc. inf. AMI & no slurred S in V5/6, T wave upright in V1-2
- HOCM
- Duchenne's muscular dystrophy
- low placement of leads V1-2
RSR' or RSr' pattern in V1 or V2 (ie. M-shape):
- QRS > 0.10sec and slurred S in leads I, V5/6:
- QRS 0.09-0.10sec and slurred S in leads I, V5 or 6:
- incomplete RBBB:
- < 1% of normal individuals
- secundum ASD (90% of these pts have incomplete RBBB)
- QRS < 0.08sec and no slurred S in leads I, V5 or 6:
- RSr' variant:
- aetiology:
- 5% of normal individuals
- recording artifacts
- chest deformities - straight back syndrome, pectus excavatum
- CHD eg. ASD & rarely VSD or coarctation aorta
- acquired heart disease - eg. MS
- RVH
- RV diastolic or volume overload
- cor pulmonale
- pulm. embolism
- WPW
- AVNRT - should have pseudo-S wave in leads II, III & avF
- Duchenne's muscular dystrophy
- late activation of outflow tract of RV eg. crista supraventricularis
LBBB:
- ECG:
- QRS duration > 0.11sec
- M shape in leads I, V5 or V6
- QS complex usually present in leads facing RV ie. V1
- but <50% have small r wave in V1
- ST elevation common in V1-4 with ST-T waves opposite in direction to terminal QRS direction
- aetiology:
- normal hearts but extremely rare in children
- IHD - these pts have high incidence of LV dysfunction & CCF
- cardiomyopathy
- degenerative diseases
- if present, cannot make diagnosis of LVH & Dx of AMI is difficult - see ECG Diagnosis of AMI
- see LBBB
Pathologic Q waves:
- > 25% of succeeding R waves
- > 0.04secs wide
Q-T interval:
- the QT interval on the ECG is measured from the start of QRS complex to end of the T wave
- QTc refers to a QT interval “corrected” for the effect of differing heart rate to give a QT value as if the heart rate is 60bpm
- if rate 60-100bpm, then QT should be less than half the RR interval
- Bazett's formula: QTc = QT / square root (RR interval)
prolonged QTc:
- prolonged QTc represents delayed repolarisation & predisposes to early after-depolarisations, re-entrant tachycardias, especially potentially fatal torsade de pointes VT which is most likely if bradycardia is present too.
- see prolonged QTc
shortened QTc:
- not of significance
- aetiology:
- hypercalcaemia
- hyperkalaemia
- digoxin intoxication
ST segment:
- ST elevation:
- see also:
- aetiology:
- AMI, variant angina
- Left Bundle Branch Block (LBBB) or left ventricular hypertrophy (LVH) (right precordial leads)
- mechanical (pericardiocentesis needle striking ventricle)
- electrical artefacts (artificial pacemaker, monitor)
- ventricular aneurysm
T wave:
- normal T wave is asymmetric with steeper descending limb than ascending limb
- inverted T waves:
- normal in V1-3 in prepubertal children
- V1-3 in older patients may represent Wellens syndrome
- aVL T inversion may represent a mid segment LAD stenosis
- Tinv in ant and inf leads with SOB is most likely due to PE
- Tinv in many leads with prolonged QTc suggests SAH
- myocardial ischaemia
- myocardial strain
- eg PE
- very deep inverted T waves with prolonged QTc suggests raised intracranial pressure (ICP) such as subarachnoid haemorrhage (SAH)
- peaked T waves:
- aetiology:
- acute myocardial ischaemia (the hyperacute T wave) - symmetric wave form esp. if > 5-7mm height
- Left Bundle Branch Block (LBBB) or left ventricular hypertrophy (LVH) (right precordial leads)
- acute haemopericardium
- flattened T waves:
- aetiology:
- normal newborn infants
- myocarditis
- myocardial ischaemia
- biphasic T waves:
- consider life threatening Wellen's syndrome
- long sinus like inverted T waves with prominent U wave suggests life threatening severe hypokalaemia
- De Winter's waves
- combination of ST depression with rocket-shaped T waves in the precordial leads V1-6
- becoming increasingly recognised as an anterior STEMI equivalent (~2% of LAD occlusions)
U wave:
- may be prominent in hypokalaemia but may be present in normal pts
ecg_easy.txt · Last modified: 2025/08/02 11:44 by wh