ECG Notes

1 small square = 1mm = 40ms (horizontal) = 0.1mV (vertical)

1 big square = 5mm = 200ms = 0.5mV
Lead Placement
V1 4th ICS R sternal edge
V2 4th ICS L sternal edge
V3 middle of 2 and 4

LA wrist
RA wrist
LL ankle
Feature

Normal Range

Rate
Rhythm

60-100
Regular

Axis

-30 to +90

P wave shape

<2.5mm high
<120ms wide
Biphasic in lead V1
Upright

V4 5th ICS MCL

V5 middle of 4 and 6
V6 6th ICS MAL

Abnormalities
Irregularly irregular
Regularly irregular
QRS < 120 = Ventricular
hypertrophy, or hemiblock
QRS >= 120 = abnormal
conduction pathway e.g. L or R
BBB, prior MI, WPW, ASD

Prolonged >120ms (+/- bifid

>40ms) = LA enlarged
Peaked >2.5mm & <80ms = RA
enlarged
Prolonged + Peaked = Bilateral
enlargement
Asymmetry in V1= Atrial
enlargement
Inversion = junctional or ectopic
depolaristn.

Physiological
Representation

Average direction of
electrical depolarisation

Atrial contraction, RA first

LA last, middle third is
overlap.

P-R interval

120-200ms

Q waves

Deeper in III and aVR

Septal Q waves V5/6 < 2mm
deep, 40ms duration
Absent in V1-3

QRS duration

70-110ms

QRS voltage

V1 S wave + Tallest V5/6 R wave

< 35mm
R waves > 10mm
V3/4 transition

QRS progression
QRS shape
QT Interval

Proportional to heart rate,

correct to QT at 60bpm
At 60bpm: 350ms-450ms

< 120 + P-wave inversion =

junctional rhythm
< 120 + P-wave upright + delta
wave = WPW
< 120 + P-wave upright + normal
QRS = LGL (Lown Ganong Levine)
>120 = 1st degree block
Absence of septal Q waves (V5-6) =
LBBB
> 40ms
> 2mm or > 25% QRS depth
Any Q found in V1-3
Any abnormality = MI,
cardiomyopathy, cardiac rotation or
abnormal lead placement
>= 120ms = aberrant ventricular
conduction
- bundle branch block
- intraventricular conduction delay
(LVH)
> 35mm = LVH
< 10mm = dampening, MI,
infiltration
V4/5 = RVH
Delta wave (slurred upstroke) =
WPW
Prolonged by drugs
Hypokalemia/calcemia/magnesemia
MI
Hypothermia

V5/6: L to R depol in septum

In full thickness MI q waves
are cavity potentials
ventricle depolarises from
inside to outside, so all
depolarisation is away from
the lead

QTc = QT/sqrt (RR)

Correct by dividing by sqrt
of RR interval.

ST interval

Isoelectric

T wave shape

Normally inverted in VR, V1

also III normal variant
also V2 if young
also V3 if black

Shortened
Hypercalcemia
Digoxin
Focal ST elevation = MI (1st change)
Widespread ST elevation =
Pericarditis
J waves = hypothermia (start of ST
segment)
ST depression = ischemia (e.g.
exercise, angina)
ST downsloping = digoxin
Inversion
New T-wave inversion = MI (2nd
change w/ Q-waves if full thickness)
= Bundle branch block
= Ventricular hypertrophy/strain
= HOCM
Abnormally Upright
Tall, upright in V1 work= coronary
artery disease
New Tall T V1 = acute ischemia
Biphasic
Up-down = Myocardial ischemia
In V2-3 = LAD ischemia (Wellens
syndrome)
Down-up = Hypokalemia
Camel Appearance
= Due to U-waves - Hypokalemia
= Due to hidden P waves heart
block

T Wave Physiology
T wave represents
repolarisation.
Depolarisation and
repolarisation currents flow
in the same direction, but
have opposite polarity.
Hence T-waves should be
inverted! However they are
upright as innermost
muscles of the heart take
longer to depolarise. So
while the myocardium
depolarises from inside to
out, it repolarises from
outside to in! Thus it is
double inverted and
appears upright.
In myocardial infarction,
the innermost muscle is
destroyed first so direction

of repolarisation reverts to
inside-out, and T-waves
become inverted.
U wave

Become visible when HR <

65bpm
<25% height of T wave (aka 1-2
mm)
Same direction as T waves

ECG Report
Rate Rhythm
Axis
Intervals PR, QT
QRS complex description
-

Duration
Height
Transition point
Spot diagnoses

ST segments
T waves

>25% of T wave or >1-2mm

indicates severe hypokalemia (or
hypomagnesaemia, hypothermia,
raised ICP, LVH, medications)
U wave inversion is specific for =
CAD, HTN, VHD, congenital heart
disease, cardiomyopathy,
hyperthyroidism.

Delayed or prolonged
repolarisation of cells.

Dilation and Hypertrophy

LVH: LAD, Tall R + Deep S, R > 13 in aVL S > 15 in III, U wave in V2 and V3. Strain pattern lateral ST and T wave changes
RVH: RAD > 110, Dominant R wave in V1, dominant S wave in V5/6, QRS < 120ms

Important Diseases to Know

Myocardial Infarction
Time
until
appeara
nce
Minutes

Change

Physiology

Hyperacute
T waves

Tall T-waves and ST- elevation represent reversible ischemic damage. Hypoxia reduces available
ATP which causes potassium to leave the myocytes:

(earliest
sign, lasting
up to 30
minutes)

>15mm V16

>5mm limb
lds
ST
elevation

Hours

T wave
inversion
+

Accelerated opening of K+ channels => Rapid myocyte repolarisation => and hyperacute Twaves ST elevation
Develops seconds after ischemia develops and lasts only a few minutes
New Upright T-Wave in V1 (normally inverted) earliest sign of ACS (concern if V1 > V6)
o DDx: LBBB, LVH, High LV Voltage, misplaced lead

Decreased intracellular K+ => Decreased resting membrane potential => TQ depression

(everything except ST segment lowers)
Develops a few minutes after onset of ischemia
Delayed depolarisation => ST elevation
Develops 30 minutes after onset of ischemia
Usually concave down
Pathological Q waves due to electrical window by infarction
Ventricular muscle is depolarised from inside to outside, so all impulses are moving away from the
lead.

Q waves if
full
thickness
Days

T waves become inverted in leads with ST-elevation.

Wellens Syndrome inverted or biphasic T-waves in V2-3 is highly specific for critical
LAD stenosis
ST elevation resolves
Q waves persist as the electrical window is not impaired
T waves remain inverted

Pulmonary Embolism

S1Q3T3 + inferior & right-precordial T-wave inversion

Hyperkalemia
Change
Moderate Hyperkalemia
High hyperkalemia

Physiology
Peaked T-waves due to altered repolarisation
Rising K+ => Lowers resting membrane potential
Atrial paralysis and prolonged QRS
Ventricular arrhythmia

Hypokalemia (Causes myocardial hyperexcitability; Appears on ECG at K<2.7)

Increased amplitude and width of P wave, with longer PR interval

ST depression
T wave inversion
Precordial U waves

Hypomagnesemia

Long QTc

Bundle Branch Block (WiLLiaM MoRRoW)

RBBB

V1 RSR
Incomplete if <120ms
Complete if >120ms

LAFB

Initial LPF depolarisation

o Small Q waves in superior-leftward leads (I, AVL)
o Small R waves in inferior-rightward leads (avF, II, III)
Full LV depolarisation
o Left axis deviation < -45o
o Minimally prolonged QRS (<20ms)

LPFB

Right axis deviation > 120

Normal QRS duration
Similar presentation to right-ventricular hypertrophy

Incomplete Trifascicular block

bifascicular block RBBB + Left axis deviation

1st or 2nd degree heart block

Hypothermia
1. Bradycardia
2. Osborn waves (J waves) positive deflection at the J point
3. Shivering artefact
Hypercalcemia

1. Short QT
2. J waves if severe
Massive Pericardial Effusion

Low voltage
Tachycardia
Electrical Alternans

PACs

Followed by compensatory pause

Normal or can indicate hyperthyroidism, electrolyte abnormalities or medication toxicity

Pericarditis

QRST-T 0-60degrees
STE angle is an injury current STD is not localising T wave inversion is nonspecific
STE

Horizontal
Coved
Slurred (low)

Terminal T wave inversion is specific for ischemia

Long QT is sign of severe electrolyte disruption or ischemia
Q waves = infarction
Takotsubo Cardiomyopathy

Apical wall dyskinesia

Mild STEMI on ECG
Troponins 4000
Coronary angiography shows no blockage