2. • DEFINITION: An ECG is recording(gram) of the electrical activity(electro)
generated by the cells of the heart(cardio) that reaches the body surface.
• It basically plots
---> Voltage on its vertical axis which is the summation of electrical activation
of all cardiac cells on the body surface. Indicates chamber enlargement and axis.
---> Time on its horizontal axis which indicates HR, Rhythm & intervals
during electrical activity.
3. HISTORY
• 1842 - Italian scientist Carlo Matteucci realizes that electricity is associated with the
heart beat.
• 1876 - Irish scientist Marey analyzes the electric pattern of frog’s heart.
• 1895 - William Einthoven , credited for the invention of EKG.
• 1906 - using the string electrometer EKG, William Einthoven diagnoses some heart
problems.
• 1924 - the noble prize for physiology/medicine is given to William Einthoven for his
work on EKG.
• 1938 - AHA and Cardiac society of Great Britain defined the position of chest leads.
• 1942- Goldberger increased Wilson’s Unipolar lead voltage by 50% and made
Augmented leads(aVR, aVL & aVF).
10. ECG LEADS
• The standard ECG has 12 leads:
---> 3 Standard Limb Leads which are bipolar – I, II, III
---> 3 Augmented Limb Leads which are unipolar– aVR, aVL, aVF
---> 6 Precordial Leads which are unipolar – V1 to V6
• The axis of a particular lead represents the viewpoint from which it looks at the
heart.
• The standard and augmented leads represent the heart’s orientation in frontal
plane.
• Precordial leads represent the heart’s orientation in transverse plane.
17. • The electrocardiogram records only Lead I & II and then calculate the voltage in
remaining leads in real time on the basis of Einthoven law
• I+III = II
• The algebraic outcome of the formulas for calculating the voltages in aV leads
from Lead I, II & III are:
aVR = - ½ (I + II)
aVL = I - ½ (II)
aVF = II – ½ (I)
• Thus, aVR + aVL + aVF = 0
18. EKG CALIBRATION
EKG graphs:
• 1 mm small squares
• 5 mm large squares
Paper Speed:
• 25 mm/sec standard
Voltage Calibration:
• 10 mm/mV standard
25. Rule of 300
• 300 divided by number of big boxes between RR interval.
• EKG speed is 25mm/sec ---> 5 big box ---> so, per minute
is 5 x 60 = 300 box.
• This works only when rhythm is regular.
• Better applicable when HR < 100.
26. Rule of 1500
• 1500 divided by number of small boxes between RR
interval.
• Each big box contains 5 small boxes, hence 300 x 5 = 1500.
• Better applicable during tachycardia ( HR > 100).
27. Rule of 10
• Used when rhythm is irregular
• Rhythm strip runs for 10 sec ---> count number of QRS in
10sec strip & multiply by 6
30. Axis determination
• The QRS axis represents the net overall direction of the heart’s electrical activity.
• Abnormalities of axis can hint at:
---> Ventricular enlargement
---> Conduction blocks (i.e. hemiblocks)
31. • Axis can be determined by two approach
Quadrant approach
Equiphasic approach
32. QRS genesis
• QRS complex represents ventricular depolarization.
• A deflection is only referred to as wave if it crosses the baseline.
• The first negative wave is called the Q-wave. If the first wave is not negative,
then the QRS complex doesn’t possess a Q-wave.
• All positive waves are referred to as R-waves. The first positive wave is R-wave,
the second positive wave is referred as R’-wave.
• Any negative wave appearing after a positive wave is referred as S-wave.
• Large waves are designated by their capital letters – Q, R, S.
• Small waves are designated by their lower case letters – q, r, s.
33. Contd..
• Ventricular septum receives fibers from left bundle branch and hence gets activated first.
• Hence, depolarization of septum proceeds from left to right. The vector is directed forward and
to right.
• The ventricular septum is relatively small, which is why lead V1 displays a small ‘r’ wave and
V5, V6 displays small negative ‘q’ wave.
• Electrical impulses then progresses to ventricular free walls via purkinje fibres from
endocardium to epicardium from the apical region.
• The endocardium depolarizes first with subsequent spread of action potential from one
contractile cell to another heading to the epicardium generating a myocardial vector which is
oriented downward and to left.
• Vector generated from RV doesn’t come to expression as it is drowned by the many times
larger vector generated by LV.
• Finally the basal part of the ventricle gets depolarized giving rise to a vector which is directed
backward and upward. It moves away from V5, V6 giving rise to small ‘s’ wave in V5 & V6.
34.
35. Contd..
• q – waves are present only in leftward oriented leads – I, aVL, V5, V6.
• Presence of ‘q’ in V1, V2, V3 is pathological.
• Presence of ‘q’ wave in rightward oriented leads should not qualify for the
criteria of pathological ‘q’ wave.
• Pathological q-wave - > 40msec in width and > 25% of QRS amplitude present in
two contiguous lead.
• R-wave should progress from V1---->V5. Tallest in V5 & V6 having a dominant
R-wave.
37. Quadrant approach
• Examine the QRS complex in leads I and aVF to determine if they are
predominantly positive or predominantly negative. The combination should
place the axis into one of the 4 quadrants below:
42. Lead I positive, Lead aVF negative but Lead II
positive ---> non pathologic LAD (Normal axis)
43. Equiphasic approach
• Most equiphasic QRS complex.
• Identified Lead lies 90° away from the equiphasic lead.
• The fact that QRS complex is equally positive and negative indicates that the net
vector is perpendicular to the axis of this particular lead.
• Next see if in perpendicular lead QRS is upright or negative.
• If upright, that is the QRS axis.
• If negative, move 90 degree away in the opposite direction of the perpendicular
lead.
44. Lead aVF is equiphasic --> perpendicular lead I is
positive --> axis is 0 degree
46. Causes of axis deviation
LAD
• LBBB, LVH
• LAFB
• INFERIOR WALL MI
• WPW – right accessory pathway
• OSTIUM PRIMUM ASD
• TRICUSPID ATRESIA
• HYPERKALEMIA
• OBESITY
• RV PACING / ECTOPICS
• HIGH DIAPHRAGM – PREGNANCY, ASCITES
RAD
• RBBB, RVH
• LPFB
• ANTEERIOR WALL MI
• CHRONIC LUNG DISEASES
• PULMONARY EMBOLISM
• WPE - left accessory pathway
• OSTIUM SECUNDUM ASD
• LV PACING / ECTOPICS
• NORMAL VARIANT - TALL
47. ‘T’ wave morphology
• Represents repolarization.
• Same direction as the preceding QRS complex.
• Blunt apex with asymmetric limbs – longer ascending limb.
• Can be biphasic ( initial positive and terminal negative ) in Lead V1.
• When biphasic the terminal portion of the ‘T’ wave determines if it is positive or
negative.
• Diminish with age and larger in males than females.
• Amplitude: 0.5 mV in limb lead, 1.5 mV in precordial lead.
• Should not exceed > 2/3rd of preceding ‘R’ wave.
• Same axis as QRS.
• Inversion in V1--->V3 – normal variant in females.
49. ‘PR’ interval
• It is the time required for electrical impulse to travel from SA node to AV node &
AV nodal conduction delay.
• Major portion ( later 2/3rd ) reflects the conduction delay in AV node.
• Duration: 0.12 – 0.2 sec.
• Tends to increase with age.
• Controlled by balance between sympathetic and parasympathetic divisions of
ANS.
52. ‘ST’ SEGMENT MORPHOLOGY
• Represents preliminary phase of repolarization.
• Forms ‘J’ point at its junction with QRS – forms a distinct angle with the
downslope of ‘R’ or upslope of ‘S’ wave.
• Proceeds horizontally and curves gently into ‘T’ wave.
• Located at same horizontal level as the baseline formed by ‘TP’ segment.
• Displacement upto 1mm ( upward or downward) is common in precordial leads
especially V1--->V3.
• Early repolarization variants are considered normal except in symptomatic and
high risk individuals.
56. Causes of ST segment elevation
• Acute MI
• Left bundle branch block (brugada)
• Acute pericarditis
• Benign early repolarization
syndrome
• Hyperkalemia
• LV aneurysm
• Brugada syndrome
• Pulmonary embolism
• Pneumothorax
• Aortic dissection
• Hypothermia
• CNS pathologies with raised ICT
• Prinzmetals’s angina
• Post electrical cardioversion
• Short QT syndrome ( V3 to V5)
• Cholecystitis / subdiaphragmatic
abscess
• Cocaine abuse
• Drugs- digoxin, isoprenaline,
quinidine, procainamide, TCA’s
57. Causes of ST segment depression
• Ischemia
• LVH
• Hypokalemia
• Hypomagnesemia
• ICH
• Digoxin effect
• Post electrical cardioversion
• Exercise and deep inspiration
58. ‘QT’ interval
• Represents duration of electrical activation and recovery of the ventricular
myocardium.
• Measurement: QT interval is best determined in a lead with an initial q wave by
tangential method.
59. Contd..
• QT interval is rate dependent. To ensure complete recovery from one cardiac
cycle before the next cardiac cycle begins, the duration of recovery must decrease
as the rate of activation increases.
• Therefore normality of QT interval can be determined only by correcting for the
heart rate ----> QTc
• Bazett: QTcB = QT/RR1/2
• Fridericia: QTcFri = QT/RR1/3
• Framingham: QTcFra = QT+0.154 (1−RR)
• Hodges: QTcH = QT+0.00175 ([60/RR]−60)
• Rautaharju: QTcR = QT−0.185 (RR−1) + k (k=+0.006 seconds for men and
+0 seconds for women)
60. Contd..
Normal QTc values:
• QTc is prolonged if > 440ms in men or > 460ms in women.
• QTc > 500 is associated with increased risk of torsades de pointes.
• QTc is abnormally short if < 350ms.
• A useful rule of thumb is that a normal QT is less than half the preceding RR
interval.
61. Causes for QT prolongation:
• Electrolytes – hypo K+, Mg2+, Ca2+
• Increasing age
• Females
• Bradycardia
• MI / LVF
• ROSC - post cardiac arrest
• Hypothermia
• Recent cardioversions
• Congenital long QT
• Raised ICT
• Hepatic dysfunction
64. ECG change in dextrocardia
• Right axis deviation
• Positive QRS complexes (with upright P and T waves) in aVR
• Lead I: inversion of all complexes, aka ‘global negativity’ (inverted P wave,
negative QRS, inverted T wave)
• Absent R-wave progression in the chest leads (dominant S waves throughout)
• These changes can be reversed by placing the precordial leads in a mirror-image
position on the right side of the chest and reversing the left and right arm leads.
• D/D – Accidental lead reversal, specifically reversal of the left and right arm
electrode.