Indication and Interpretation of ECG

GuideDr. J. Singh Madam Rakesh Verma

The electrocardiogram (EKG) is a graphical representation of the electrical events of the cardiac cycle.

1895 - William Einthoven, credited for the invention of EKG

1924 - William Einthoven got the Noble prize for the same

ECG

THE CONDUCTING SYSTEM

SA node is the pacemaker where the electrical impulse is generated.

Located along the posterior wall of the right atrium right beneath the opening of the SVC.

It is crescent shaped and about 3 mm wide and 1 cm long.

The impulse travels from the SA node through the internodal pathways to the atrioventricular node (AV node).

SA Node

The AV node is responsible for conduction of the impulse from the atria to the ventricles.

The impulse is delayed slightly at this point to allow complete emptying of the atria before the ventricles contract.

The impulse continues through the AV bundle and down the left and right bundle branches of the Purkinje fibers.

AV Node

The Purkinje fibers conduct the impulse to all parts of the ventricles

Purkinje Fibers

Turn on machine Calibrate to 10mm/ mV Rate at 25mm/ s Record and print Label the tracing - Name, DOB, Hospital

number, date and time

Recording an ECG

10 electrodes in total are placed on the patient

The 10 leads are lubricated with jelly then placed over the respective sites

Electrode Placement

Limb Leads

Chest Leads

Chest Leads

Chest leads are labelled “V”(vector) and are numbered from 1 to 6.

The placement of these electrodes needs to be exact to give the optimum information.

Chest Leads

V1 fourth intercostal space, right sternal edge

V2 fourth intercostal space, left sternal edge V4 at the apex (fifth ICS mid clavicular line) V3 midway between V2 and V4 V5 same level as V4 but on the anterior

axillary line V6 same level as V4 and V5 but on the mid

mid-axillary line

Where to place?

Electrical impulse (wave of depolarisation) picked up by placing electrodes on patient

The voltage change is sensed by measuring the current change across 2 electrodes – a positive electrode and a negative electrode

If the electrical impulse travels towards the positive electrode this results in a positive deflection

If the impulse travels away from the positive electrode this results in a negative deflection

How ECG work?

P wave: Activation (depolarization) of the right and left atria

QRS complex: right and left ventricular depolarization

T wave: ventricular repolarization

Conduction system and ECG

PR interval: time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)

QRS duration: duration of ventricular muscle depolarization

QT interval: duration of ventricular depolarization and repolarization

RR interval: duration of ventricular cardiac cycle (an indicator of ventricular rate)

PP interval: duration of atrial cycle (an indicator of atrial rate)

Conduction system and ECG

Symtoms Palpitation, cyanosis, chest pain, syncope, seizure, poisoning

Signs tachycardia, bradycardia, hypothermia, murmur, Shock Evaluation of rheumatic heart disease, congenital heart diseases Evaluation of suspected electrolyte imbalance Evaluation of cases like drowning, electrocution During cardiopulmonary resuscitation (CPR). Evaluation of patients with implanted defibrillators and pacemakers To detect myocardial injury, ischemia, and the presence of prior

infarction as well. Effects and side effects of pharmacotherapy Evaluation of metabolic disorders processes among others.

Contraindications No absolute contraindications

patient refusal, exist. patients allergies to adhesive used to affix the leads

Indications

EINTHOVEN’S TRIANGLE

Electrodes

Limb leads Poles E.g.

Bipolar Positive and negative poles

I, II, III

Unipolar Positive and zero poles

aVL, aVR, aVF, chest leads

How to remember axis

Hexaxial system

NORMAL ECG

Calibration Rate Rhythm Axis

ECG - Interpretation

The ECG Paper Horizontally

◦ One small box - 0.04 s◦ One large box - 0.20 s

Vertically◦ One large box - 0.5 mV

◦ 25mm = 1s

Height 10mm = 1mV

Half standardisation 5mm=1mV One fourth standardisation 2.5mm= 1mV (only amplitude is changed not speed)

Paper speed = 25mm/ s 25 mm (25 small squares / 5 large squares)

equals one second

Calibration

If the heart rate is regular Count the number of large squares

between R waves i. e. the RR interval in large squares

Rate = 300/RR(no. of large boxes) = 1500/RR(no. of small boxes)

Rate

If the rhythm is irregular it may be better to estimate the rate using the rhythm strip at the bottom of the ECG (usually lead II)

The rhythm strip is usually 25cm long (250mm i. e. 10 seconds)

Count the number of R waves on that strip and multiple by 6 you will get the rate

Rate

Heart rate

Regular slow 300/RR (large square)

Regular fast 1500/RR (small square)

Irregular R wave in rhythm strip X 6

New born 110-150/min 2year 85-125/min 4year 75-125/min 6year 65-100/min > 6 year 60-100/min

Heart rates

Tachycardia Sinus tachcardia Supraventrical Ventricular Atrial flutter and

fibrillation

Bradycardia Sinus bradycardia Heart block

Normal rhythm must have a P wave before each QRS complex

The easiest way to tell is to take a sheet of paper and line up one edge with the tips of the R waves on the rhythm strip.

Mark off on the paper the positions of 3 or 4 R wave tips Move the paper along the rhythm strip so that your first

mark lines up with another R wave tip See if the subsequent R wave tips line up with the

subsequent marks on your paper If they do line up, the rhythm is regular. If not, the

rhythm is irregular

Rhythm

Absent P wave – indicate non sinus rhythm SA block AV rhythm (may be present) Atrial fibrillation Idioventricular rhythm

Multiple P waves◦ Atrial flutter◦ Atrial fibrillation◦ 2nd ar 3rd degree block

Changing P wave shape◦ Wandering atrial pacemaker

Abnormal rhythm

The axis is the overall direction of the cardiac impulse or wave of depolarisation of the heart

An abnormal axis (axis deviation) can give a clue to possible pathology

Axis

Axis

Quadrant Approach Lead I

Lead aVF

Mean axis

Lead I Lead aVF

Mean axis

Quadrant Approach

Equiphasic method

Graphical method

Lead (mm) = R-S amplitude

Lead I = 4-0 = 4mmLead aVF = 13-2 = 11mm

Lead I

Lead aVF

Mean axis

Lead I

Lead aVF

Lead I = 5+ (-10)= -5mmLead aVF = 17-4 = 13mm

Right Axis Deviation - Right ventricular hypertrophy, Anterolateral MI, Left Posterior Hemi-block, COPD, pulmonary arterial hypertension or large pulmonary embolism

Left Axis Deviation- Ventricular tachycardia, Left ventricular hypertrophy, Left Anterior hemi-block

Wolff-Parkinson-White syndrome can cause both Left and Right axis deviation

Axis deviation - Causes

P-wave

Normal values1. up in all leads

except aVR.2. Duration.

< 2.5 mm.3. Amplitude. < 2.5 mm.

Abnormalities1. Inverted P-wave Junctional rhythm.2. Wide P-wave (P- mitrale) LAE3. Peaked P-wave (P-

pulmonale) RAE4. Saw-tooth appearance Atrial flutter5. Absent normal P wave Atrial fibrillation

Saw-tooth appearance

Absent normal P wave

Inverted P-wave

PR interval

Definition: the time interval between beginning of P-wave to beginning of QRS complex.

Normal PR interval<3yrs – 0.08sec3-16 yrs – 0.10sec>16 – 0.12sec

Abnormalities 1. Short PR interval WPW syndrome2. Long PR interval First degree heart

block

Bundle of Kent

Slide 44

1st degree heart block, after each P must be QRS

If the PR interval is constant with a missed QRS complex: 2nd degree heart block, Mobitz type II, each QRS followed after P wave

If there is no relationship between the P waves and the QRS complexes: 3rd degree heart block

PR Interval

Block Relation Electrical origin

1st degree Each P has QRS SA node

2nd degree Each QRS has P SA node

3rddegree No Relation Fasciular,Ventricular, or other

Q WAVES Q waves <0.04 second.

That’s is less than one small square duration.

Present commonly in I,II,III,aVF, and always present in V5 and V6 (lateral leads)

Absent in V1

Height < 1/4 of R wave height.

Chest Leads

Q wave in septal hypertrophy

The width of the QRS complex should be less than 0.12 seconds (3 small squares)

Height of R wave is (V1-V6) >8 mm in at least one of chest leads.

Morphology: progression from Short R and deep S (rS) in V1 to tall R and short S in V6 (qRs).

QRS Complexes

New born +125 1 month +90 3 years +60 Adult +50

QRS Axis Preterm

0.04s Full term 0.0.5s 1 -3yrs

0.06s >3 years 0.07s Adult

0.08s

QRS duration

LAD◦ LVH◦ LBBB◦ Left anterior hemiblock

RAD◦ RVH◦ RBBB

Superiorly oriented axis◦ Left anterior

hemiblock, particularly with endocardial cushion defect

◦ RBBB

Bundle branch block Preexication (WPW) Intraventricular

block Idioventricular

rhythm Ventricular

implanted pacemaker

Abnormal QRS axis

Abnormal QRS duration (wide)

Abnormally large deflections (positive or negative)◦ Ventricular

hypertrophy◦ Ventricular

conduction defects like - BBB, preexication,artificial ventricular pacemaker

Low voltage complex – limb lead less than 5mm◦ Myocarditis◦ Pericardial effusion◦ Hypothyroidism◦ Pericarditis

QRS amplitude

Right ventricular hypertrophy

Right axis deviation of +110° or more.

Dominant R wave in V1

Dominant S wave in V5 or V6

Right atrial enlargement (P pulmonale).

Right ventricular strain pattern = ST depression / T wave inversion in the right precordial (V1-4) and inferior (II, III, aVF) leads.

Right ventricular hypertrophyDominant R wave in V1-V4Dominant S wave in V5-V6 Right vent. strain pattern with ST depression and T-wave inversion in V1-V4

Left ventricular hypertrophy

Left axis deviation

Increased R wave amplitude in the left-sided ECG leads (I, aVL and V4-6) and

Increased S wave depth in the right-sided leads (III, aVR, V1-3).

The thickened LV wall leads to prolonged depolarisation and delayed repolarisation (ST and T-wave abnormalities) in the lateral leads.

Left atrial enlargement (P mitrale).

Left ventricular strain pattern = ST depression / T wave inversion in the lateral (I, aVL,V5-V6) leads.

Left ventricular hypertrophyIcreased R wave amplitude in the left-sided ECG leads (I, aVL and V5-6) and Increased S wave depth in the right-sided leads (III, aVR, V1-3).Left vent. strain pattern with ST depression and T-wave inversion in I,aVL,V5-46

Right Bundle Branch Block (RBBB)

In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle.

The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged.

The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads (V5-6)

Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads (V1-3)

QRS duration ≥ 120ms rSR’ pattern or notched R wave in V1-3 along with T

wave inversion Wide S wave in I and V6

Right Bundle Branch Block

Left Bundle Branch Block (LBBB) Normally the septum is activated from left to right, producing small Q waves

in the lateral leads.

In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the RV to the LV via the septum.

Eliminates the normal septal Q waves in the lateral leads. . The overall direction of depolarisation (from right to left) produces tall R

waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3)

As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the lateral leads.

QRS duration ≥ 120ms Broad R wave in I, aVL, and V5-6 Prominent QS wave in V1-3

Absence of q waves (including physiologic q waves) in I and V6

Left Bundle Branch Block

The ST segment should sit on the isoelectric line (at least in the begining)

It is abnormal if there is planar (i.e. flat) elevation or depression of the ST segment

ST Segment

1. ST elevation:More than one smallsquare Infarcts Angina. Acute pericarditis. Early repolarization

Abnormalities

ST depression:More than one smallsquare Ischemia. Ventricular strain. BBB. Hypokalemia. Digoxin effect.

Abnormalities of ST- segment

ST depression

T wave is best measured in left precordial leads

In V5 <1yr 11mm>1yr 14mm

T Wave

Abnormalities:

1. Peaked T-wave:Posterior wall MI.Hyperkalemia.

.2. T- inversion:

Ischemia. Myocardial

infarction. Myocarditis Ventricular strain BBB. Hypokalemia. Digoxin effect.

Hyperkalemia

The normal range for QT is 0.38-0.42 (≤ 11mm )

QT Interval

Definition: Time interval between beginning of

QRS complex to the end of T wave. QT interval varies with heart rate - As the heart rate gets faster, the QT interval gets shorter It is possible to correct the QT interval with respect to rate by using the following formula:

Bazzet’s formula QTc = QT/ √RR (QTc = corrected QT)

Long QTc – causes◦Drugs – procanamide, quinidine◦Hypocalcemia, ◦hypomagnesemia,◦hypokalemia◦Hypothermia ◦AMI◦Congenital Jerwell and Lange-Neilsen syndrome Romano- Ward syndrome

Short QT interval: hypercalcemia, digitalis

Abnormalities:

Osborn wave in hypothermia

U waves occur after the T wave and are often difficult to see

They are thought to be due to repolarisation of the atrial septum

Prominent U waves can be a sign of hypokalaemia

U Wave

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