Download - ECG: Indication and Interpretation
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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