Electrocardiogram

ECG is the recording of sequential sum of depolarization and repolarization of all

myocardial cells. The electrical depolarization of myocardial tissue produces a small
dipole current. It can be detected by electrode pairs on the body surface. These signals
are amplified and either printed on special graph paper or displayed on a monitor
 PQRST Terminology
• Used to describe various wave forms.
• P wave - depolarisation or contraction of atria.
• QRS complex - depolarisation or contraction of
ventricles.
• T wave - repolarisation of ventricles

• Repolarisation of atria is not recorded on a routine ECG

• Sometimes, another upright wave follows the T wave
known as U wave
 QRS Complex
• The QRS complex is subdivided into specific deflections or
waves.
• Q wave: If the initial QRS depletion in a particular lead is
negative, it is termed a Q wave, indicates septal depolarization.
• R wave: The first positive deflection is termed an R wave.
• S wave: A negative deflection after an R wave is an S wave.
• Subsequent positive or negative waves are labeled R′ (R prime)
and S′ (S prime) respectively.
• Lowercase letters (qrs) are used for waves of relatively small
amplitude. An entirely negative QRS complex is termed a QS
wave.
 Intervals
• PR Interval – onset of P wave to onset of QRS complex represents conduction time from atria to ventricles.
o It includes P wave and PR segment. It is a combination of Atrial depolisation followed by AV Nodal delay.
o Normal PR Interval is 0.12 - 0.2 seconds.
o Prolonged PR interval: more than 0.2 second occurs in cardiac conduction defects and heart blocks.
• QRS Interval - indicated time taken by impulse to spread through the two ventricles.
• QT Interval – Time taken from beginning of Q wave to end of T wave represents total electrical activity of
ventricles.
o It includes QRS complex + ST segment + T wave.
o It is a combination of ventricular depolarisation and ventricular repolarisation and is called total ventricular activity.
o Normal QT interval is 0.4 seconds.
o QT Interval changes according to heart rate of the inficidual therefore, qtc (corrected qt) is used.
o qtc = qt/√RR. This is called Bazet's formula
• RR Interval - From apex of one R wave to apex of next R wave to calculate heart rate or ventricular
contraction.
o Interval between 2 successive R waves.
o Heart rate = 1500/(number of small squares b/w 2 successive R waves).
o Prolonged RR: decreased heart rate due to effect of PNS or Vagal stimulation.
• PP Interval – Beginning of one P wave to beginning of another P wave indicates rate of atrial contractions.
 Segments
• PR Segment – End of P wave to onset of QRS complex,
there is no current flow, AV node delay is 0.10 seconds.
• ST Segment (J Point) - End of QRS Complex to onset of T
wave, there is no current flow. Also called joining point (J
Point) in ECG as it connects the end of QRS (Ventricular
Depolarisation) to start of T wave (Ventricular
Repolarisation) has not started yet.
Ideally, there will be no current flow in a healthy person but if
there is flow, its pathological, called as injury current due to
myocardial infarction which can be ST elevation or ST
depression.
 ECG Leads
• The standard 12–lead ECG record the difference in
potential between ten physical electrodes placed on the
surface of the body. The term twelve ‘leads’ of the ECG
is for twelve number of recordings made from pairs or
sets of these electrodes.
• ECG leads are divided into two groups: (1) six limb (extremity)
leads and (2) six chest (precordial) leads. The limb leads record
potentials transmitted onto the frontal plane, and the chest leads
record potentials transmitted onto the horizontal plane.

• Every lead has a negative end and a positive end which measures
potential difference that produce deflections represented in the
form of waves.
Significance of Limb Leads (Einthoven Leads):
He considered human body into triangle called Einthoven triangle.
To prevent electrical shock, grounding is needed. So right foot is
grounded.
Lead I: Potential difference b/w left arm and right arm. (LA → RA)
Lead II: Potential difference b/w left leg and right arm. (LL → RA)
Lead III: Potential difference b/w left leg and left arm. (LL → LA)
 Augmented Leads

aVR – Augmented unipolar lead of Right arm

Right arm is +ve
Left arm and Left foot are –ve
aVL – Augmented unipolar lead of Left arm
Left arm is +ve
Right arm and Left foor are –ve
aVF - Augmented unipolar lead of Left leg
Left foot is +ve
Right arm and Left arm are -ve
 ECG Leads and Surfaces
• II, III and aVF: inferior surface leads
• V1 and V2: septal leads
• V3 and V4: anterior surface leads
• V1, V2, V3, V4: antro septal leads
• V5, V6, lead I and aVL: lateral surface
ECG: Poor man's Echocardiogram

Surface Distribution Supplied By

II, III, aVF: Inferior surface Right coronary artery

V1, V2: Septal leads Left Anterior Descending (LAD) most

V3, V4: Anterior surface leads commonly affected

V5, V6, I, aVL: Lateral surfaces Left circumflex artery

 Cardiac Axis
• Related to direction of overall electrical activity.
• Mean QRS Axis: Usually around +59 degrees.
• Normal cardiac Axis: -30 to +110 degrees.
• Leads that are close to mean QRS Axis will always show +ve
deflection.
• Maximum +ve deflection is seen in Lead II.
• Leads that are away from mean QRS Axis will show –ve
deflection.
• Maximal –ve deflection is seen in aVR.
• aVR looks into the cavity of the heart.
Cardiac Axis Causes
Left axis deviation Left ventricular hypertrophy, left BBB,
inferior wall infarct.
Right axis deviation Right ventricular hypertrophy, right BBB,
anterior wall infarct.

Atrial hypertrophy – P wave in Lead II

Left atrial hypertrophy (Mitral valve disease)
• Wide notched P wave more than 2.5 squares known as P mitrale
Right atrial hypertrophy – Tall peaked P wave (more than 2.5 squares width
less than 2.5 squares) known as P pulmonale seen in pulmonary hypertension
 Steps in reading ECG
• Calculate rate
• Determine rhythm
• Determine QRS axis
• Check individual waves
• Calculate intervals
• Assess for hypertrophy
• Look for evidence of infarction/dyselectrolytemia drug
effects
Step 1: Determining the heart rate
• The ECG is normally recorded at a speed of 25 mm/second. Each
small, square, in the graph is 1 mm and represents 0.04 seconds
and big boxes with heavier lines represents 0.20 s (200 ms).
• Rule of 300/1500: For regular rhythms, count the number of ‘big
boxes’ between two QRS complexes, and divide this into 300. The
heart rate (beats per minute) can also be computed readily from
the interbeat (Rnumber of small (0.04 s) units into 1500.
• 6-second rule: For irregular rhythms, ECGs record 6 seconds of
rhythm per page, count the number of beats present on the ECG,
multiply by 10
Step 2: Determine regularity
• Look at the R-R distances.
• Regular (are they equidistant apart)? Occasionally irregular?
Regularly irregular?
• Irregularly irregular-atrial fibrillation.
Step 3: Determining the axis
• Normal QRS axis from –30° to +110°, –30° to –90° is
referred to as a left axis deviation (LAD), +110° to
+180° is referred to as a right axis deviation (RAD) and
–180° to –90° is referred as north-west axis/extreme
axis/axis in no man’s land/indeterminate axis.
• QRS complex in leads I and aVF determine if they are
predominantly positive or negative.
Step 4: Check individual waves
• Assess P waves
• Normal: Always positive in lead I and II, always negative in
lead aVR. Commonly biphasic in lead V1 and best seen in
leads II. <2.5 small squares in duration and <2.5 small
squares in amplitude.
• Abnormal P waves and its causes.
o Tall (> 2.5 mm), pointed P waves (P pulmonale): Suggests right
atrial enlargement. Seen in COPD, ASD, TS, Ebstein anomaly
(Himalayan P waves)
o Notched/bifid (‘M’ shaped) P wave (P ‘mitrale’) in limb leads:
Suggests left atrial enlargement. Seen in MS, MR, and systemic
hypertension. Coarse atrial fibrillation suggests LAE
o Absent P waves: Atrial fibrillation/flutter
o Inverted P waves in lead II: Dextrocardia
Step 5: Calculate intervals
PR interval: Normal is 0.12–0.20 seconds.
• Long PR interval may indicate heart block
• Short PR interval: Tachycardia and pre-excitation syndromes (e.g. Lown-Ganong-Levine
syndrome, Wolff-Parkinson-White syndrome).
QRS-complex
• Normal characteristics: Duration is 0.04–0.11 seconds.
• Broad/wide QRS (>0.12s): Ventricular hypertrophy, intraventricular conduction disturbance,
bundle branch blocks, aberrant ventricular conduction, ventricular preexcitation, ventricular
ectopic or escape pacemaker, ventricular pacing by cardiac pacemaker
• Height of QRS–Sokolow index (SV2 + RV5) <35 mm (<45 mm for young)
• Increased height: In RV/LV hypertrophy
• Decreased height: Low voltage QRS (<5 mV in limb leads/<10 mV in chest leads): Obese
patient, restrictive cardiomyopathy, pericardial effusion, hypothyroidism, hypothermia, and
myocarditis.
Q Waves
• The normal Q wave in lead I is due to septal depolarization. It is small in amplitude (less than
25% of the succeeding R wave, or less than 3 mm). Its duration is <0.04 sec or one small box.
It is seen in L1 and sometimes in V5, V6.
• Pathological Q wave of infarction in the respective leads is due to dead muscle. May also be
seen in cardiomyopathies i.e. hypertrophic (HOCM), infiltrative myocardial disease.
• Absent Q waves in V5-6 is most commonly due to LBBB.
ST Segment
• ST segment is isoelectric and at the same level as subsequent PR-interval. The length between the
end of the S wave (end of ventricular depolarization) and the beginning of repolarization. From J point
on the end of QRS complex, to inclination of T wave.
Causes of ST segment elevation.
• Ischemia
• Early repolarization
• Acute pericarditis: ST elevation in all leads except aVR
• Pulmonary embolism
• Hypothermia
• Hypertrophic cardiomyopathy
• High potassium
• Cerebrovascular accident (CVA)
• Acute sympathetic stress
• Brugada syndrome
• Cardiac aneurysm
• Left ventricular hypertrophy
• Idioventricular rhythm including paced rhythm
T Wave
• Normally, a repolarization directs from epicardium to endocardium = T wave is
concordant with QRS complex
• Causes of T wave inversions
• Tall T waves (height more than 2/3 of neighboring QRS): Hyperkalemia (steeple T
waves), hyperacute MI.
QT-interval
• Represents the time taken for ventricular depolarization and repolarization. The duration
of the QT interval is proportionate to the heart rate. The faster the heart beats, the
faster the ventricles repolarize so the shorter the QT interval. Therefore, what is a
‘normal’ QT varies with the heart rate. QT interval should be 0.35–0.45 seconds.
• For each heart rate you need to calculate an adjusted QT interval, called the ‘corrected
QT’ (QTc):
• QTc = QT/square root of RR interval—Bazett’s formula
• Prolonged QTc (>440 ms) (Box 7.17): A prolonged QT can be very dangerous. It can
predispose an individual to a type of ventricular tachycardia—Torsades de pointes.
• Short QTc (<350 ms): Hypercalcemia, digoxin effect.
U Waves
• U wave need not be always seen on an electrocardiogram. It is small, round, symmetrical and
follows the T wave and seen positive in lead II. U waves are due to repolarization of the
papillary muscles or Purkinje fibers. It is the same direction as T wave in that lead.
• Prominent U waves: Seen in hypokalemia, hypercalcemia, thyrotoxicosis, or exposure to
digitalis, epinephrine, and Class 1A and 3 antiarrhythmics.
• An inverted U wave may represent myocardial ischemia or left ventricular volume overload.
Causes of ST segment depression.
• Myocardial ischemia/NSTEMI
• Reciprocal change in STEMI
• Posterior MI
• Digoxin effect (Reverse tick mark/‘sagging’ morphology, resembling Salvador Dali’s
moustache)
• Hypokalemia
• Bundle branch block
• Ventricular hypertrophy
• Ventricular pacing
Step 6: Assess for hypertrophy
Left ventricular hypertrophy (LVH)
Right ventricular hypertrophy (RVH)
Step 7: Look for evidence of infarction/dyselectrolytemia
• ECG in myocardial infarction (MI): There are two types
of MI. STEMI and NSTEMI
– STEMI Criteria
♦ ST elevation in >2 chest leads >2 mm elevation
♦ ST elevation in >2 limb leads >1 mm elevation
♦ Q wave > 0.04s (1 small square).
ECG findings depending on the location of myocardial infarct
are presented in Table 7.32. Sequential ECG Changes in STEMI
are presented in Figures 7.33A to F.