ecg fundamentals

ECG fundamentals

Dr. Emad EfatShebin El kom Chest hospital

July 2016

What is an ECG?

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

Each event has a distinctive waveform

the study of waveform can lead to greater insight into a patient’s cardiac pathophysiology.

With ECGs we can identify

Arrhythmias

Myocardial ischemia and infarction

Pericarditis

Chamber hypertrophy

Electrolyte disturbances (i.e. hyperkalemia, hypokalemia)

Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)

Depolarization

• Contraction of any muscle is associated with

electrical changes called depolarization

• These changes can be detected by electrodes

attached to the surface of the body

Pacemakers of the Heart

• SA Node - Dominant pacemaker with an

intrinsic rate of 60 - 100 beats/minute.

• AV Node - Back-up pacemaker with an

intrinsic rate of 40 - 60 beats/minute.

• Ventricular cells - Back-up pacemaker with

an intrinsic rate of 20 - 45 bpm.

Height

• 10mm = 1mV

• Look for a reference pulse which should be the rectangular looking wave somewhere near the left of the paper. It should be 10mm (10 small squares) tall

Electrical impulse that travels towards the electrode produces an upright (“positive”) deflection

Calibration

Impulse Conduction & the ECG

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

The “PQRST”

P wave - Atrial depolarization

T wave - Ventricular repolarization

QRS - Ventricular depolarization

The PR Interval

Atrial depolarization

+

delay in AV junction

(AV node/Bundle of His)

(delay allows time for

the atria to contract

before the ventricles

contract)

NORMAL ECG

The ECG Paper

• Horizontally

– One small box - 0.04 s

– One large box - 0.20 s

• Vertically

– One large box

0.5 mV ( 5 mm )

The 12-leads include:

–3 Limb leads

(I, II, III)

–3 Augmented leads

(aVR, aVL, aVF)

–6 Precordial leads

(V1- V6)

ECG Leads ( The 12-Leads ):

ECG Leads

Bipolar Leads: Two different points on the

body (I, II, III)

Unipolar Leads: One point on the body

and a virtual reference point with zero

electrical potential, located in the center of

the heart (aVR, aVL, aVF)

Standard Limb Leads

Augmented Limb Leads

All Limb Leads

Precordial Leads

Arrangement of Leads on the ECG

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

Determine regularity

Look at the R-R distances (using a caliper or markings on a pen or paper).

Regular (are they equidistant apart)? And

presence of same number of P waves and QRS complexes

Occasionally irregular? Regularly irregular? Irregularly irregular?

Interpretation? Regular

R R

Determining the Heart Rate

Rule of 300/1500

6 Second Rule

Rule of 300

Count the number of “big boxes” between two

QRS complexes, and divide this into 300. (smaller

boxes with 1500)

for regular rhythms.

300/R-R interval ( big boxes) or 1500/R-R

interval (smaller boxes )

What is the heart rate?

(300 / 6) = 50 bpm

6 Second Rule

Number of QRS in 6 seconds ( 30 large squares ) x 10

For irregular rhythms.

This method can be used also with regular rhythm.

the heart rate 9 x 10 = 90 bpm

3 sec 3 sec

The QRS Axis

The QRS axis represents

overall direction of the heart’s

electrical activity.

Normal QRS axis from -30° to

+90°.

-30° to -90° is referred to as a

left axis deviation (LAD)

+90° to +180° is referred to

as a right axis deviation

(RAD)

Normal QRS axis from -30° to +90°.

QRS up in I and up in aVF = Normal

QRS up in I and

up in aVF = Normal

Example

Negative in I, positive in aVF RAD

Causes of left axis deviation include:

• Normal variation (physiologic, often with age)

• Mechanical shifts, such as expiration, high diaphragm

(pregnancy, ascites, abdominal tumor)

• ventricular hypertrophy

• Left bundle branch block

• left anterior fascicular block

• Congenital heart disease (e.g. atrial septal defect)

• Emphysema

• Hyperkalemia

• Ventricular ectopic rhythms

• Preexcitation syndromes

• Inferior myocardial infarction

• Pacemaker rhythm

Causes of right axis deviation include:

• Normal variation (vertical heart with an axis of 90º)

• Mechanical shifts, such as inspiration and emphysema

• Right ventricular hypertrophy

• Right bundle branch block

• Right ventricular load, for example Pulmonary Embolism

or Cor Pulmonale (as in COPD)

• Left posterior fascicular block

• Dextrocardia

• Ventricular ectopic rhythms

• Preexcitation syndromes

• Lateral wall myocardial infarction

P wave

• Always positive in lead I and II

• Always negative in lead aVR

• < 3 small squares in duration

• < 2.5 small squares in amplitude

• Commonly biphasic in lead V1

• Best seen in leads II

Right Atrial Enlargement

• Tall (> 2.5 mm), pointed P waves (P Pulmonale)

• Causes : pulmonary diseases (pulmonary embolism and

pulmonary hypertension) - Congenital e.g. PS,ASD

• Wide more than 0.12 sec in duration (3 small

squares) & Notched in ( II,I) or biphasic in ( V1)

P wave (P ‘mitrale’ )• Causes: Valvular e.g.: MR,AR,AS – HTN - Dilated cardiomyopathy

Left Atrial Enlargement

• Inversion :

A-V junctional rhythms

-ve in lead II

+ve in lead aVR

• Absent : in some of A-V junctional rhythms.

• Replaced : by fibrillatory or flutter waves ( AF

and Atrial flutter respectively)

Other abnormalities of P wave

• the PR interval is the period, measured from the

beginning of the P wave (the onset of atrial

depolarization ) until the beginning of the QRS complex

(the onset of ventricular depolarization)

• it is normally between 0.12 – 0.20 sec in duration ( 3-5

small squares).

The PR interval

Short PR Interval

1. Low atrial or junctional

rhythms.

2. WPW (Wolff-Parkinson-

White) Syndrome:

Accessory pathway (Bundle

of Kent) allows early

activation of the ventricle

(delta wave, wide QRS

and short PR interval)

Long PR Interval

• First degree Heart Block

QRS Complexes• Comment on: ( axis, voltage, interval and abnormal Q )

• A) Voltage:

• Normally : The amplitudes of all the QRS complexes in

any of the six limb leads is > 5 mm

• low voltage when: The amplitudes of all the QRS

complexes in the limb leads is < 5 mm

QRS Complexes• Specific causes of low voltage include:

Pericardial effusion

Pleural effusion

Obesity

Emphysema

Pneumothorax

Constrictive pericarditidis

Previous massive MI

End-stage dilated cardiomyopathy

Infiltrative myocardial diseases — i.e. restrictive cardiomyopathy due

to amyloidosis, sarcoidosis, haemochromatosis

Scleroderma

Myxoedema

QRS Complexes

• High Voltage ( Ventricular hypertrophy):

A. Left Ventricular Hypertrophy (LVH) (Exaggeration of

normal)

• S wave depth in V1 + tallest R wave height in V5-V6 > 35

mm or > 7 large squares ( Voltage criteria )

• (±) the left ventricular ‘strain’ pattern : ST segment

depression and T wave inversion in the left-sided leads

• Concomitantly : left atrial enlargement may be present

• N.B. LVH can be diagnosed if S in V1 > 5 large squares

or R in V5 or V6 > 5 large squares ( Voltage criteria )

QRS Complexes• Causes of LVH:

Hypertension (most common cause), Aortic stenosis, Aortic

regurgitation, Mitral regurgitation, Coarctation of the aorta,

Hypertrophic cardiomyopathy

QRS Complexes

QRS Complexes

• Right Ventricular Hypertrophy (RVH) (opposite

normal)

Right axis deviation of +110° or more.

Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).

Dominant S wave in V5 or V6 (> 7mm deep or R/S

ratio < 1).

Right atrial enlargement (P pulmonale) may be present.

Right ventricular strain pattern = ST depression / T

wave inversion in the right precordial (V1-4)

QRS Complexes

Causes of Right Ventricular Hypertrophy (RVH) : Pulmonary hypertension, Mitral stenosis, Pulmonary embolism,

Chronic lung disease (cor pulmonale), Congenital heart disease (e.g.

Tetralogy of Fallot, pulmonary stenosis), Arrhythmogenic right

ventricular cardiomyopathy

QRS in LVH & RVH

QRS Complexes

B) Interval (duration):

The width of the QRS complex should be less than 3 small squares

(0.12 seconds )

Wide QRS Complex:

• Bundle branch block

• Hyperkalaemia

• Pre-excitation (i.e. Wolff-Parkinson-White syndrome)

• Hypothermia

• Poisoning with sodium-channel blocking agents (e.g. tricyclic

antidepressants)

• Ventricular pacing

QRS ComplexesRight Bundle Branch Block ( R.B.B.B )

Criteria:

• Broad QRS ≥ 0.12 sec ( 3 small squares )

• rsR’ with prominent final R in V1-3 (‘M-shaped’ QRS complex)

• Wide final S wave in the lateral leads (I, aVL, V5-6)

• ST depression and T wave inversion in the right precordial leads

(V1-3)

QRS Complexes

Right Bundle Branch Block ( R.B.B.B )

Causes of RBBB:

( Right ventricular hypertrophy / cor pulmonale, Pulmonary

embolus, Ischaemic heart disease, Rheumatic heart disease,

Myocarditis or cardiomyopathy, Degenerative disease of the

conduction system, Congenital heart disease (e.g. atrial

septal defect)

R.B.B.B is also called RSR pattern

Can occur in healthy people with normal QRS width

( partial RBBB )

QRS ComplexesLeft Bundle Branch Block( L.B.B.B )

Criteria:

• Broad QRS ≥ 0.12 sec ( 3 small squares )

• Dominant S wave in V1

• Prominent (often notched ) R wave (M shaped ) in lateral leads

(I, aVL, V5-V6)

• the ST segments and T waves always go in the opposite

direction to the main vector of the QRS complex

QRS Complexes

Left Bundle Branch Block( L.B.B.B )

Causes :

( Aortic stenosis, Ischaemic heart disease, Hypertension, Dilated

cardiomyopathy, Anterior MI, Primary degenerative disease

(fibrosis) of the conducting system (Lenegre disease),

Hyperkalaemia, Digoxin toxicity )

New onset LBBB with chest pain consider Myocardial

infarction

Not possible to interpret the ST segment.

Q wave• The Q wave represents the normal left-to-right

depolarisation of the interventricular septum

• Non-pathological Q waves: Small ‘septal’ Q waves are

typically seen in the left-sided leads (I, aVL, V5 and V6)

• A Q wave can be pathological if it is:

Deeper than 2 small squares (0.2mV) and/or Wider than 1 small

square (0.04s) and/or In a lead other than III or one of the leads

that look at the heart from the left (I, II, aVL, V5 and V6) where

small Qs (i.e. not meeting the criteria above) can be normal

• Pathological Q waves usually indicate current or prior

myocardial infarction.

Q wave

Poor R Wave Progression• R wave height ≤ 3 mm ( 3 small squares ) in V3.

• The R wave height normally becomes progressively

taller from leads V1 through V6.

Poor R Wave Progression• Causes:

Anterior MI

Left ventricular hypertrophy

Dilated cardiomyopathy

Inaccurate lead placement (e.g. transposition of V1

and V3)

WPW syndrome

LBBB, Left anterior fascicular block

Chronic lung disease, Left sided pneumothorax

May be a normal variant

ST Segment• The ST segment is the flat, isoelectric section of the ECG

between the end of the S wave (the J point) and the

beginning of the T wave.

• It represents the interval between ventricular

depolarization and repolarization.

• Elevation or depression of ST segment by 1 mm or

more

Variable Shapes Of ST Segment Elevations in AMI

ST Segment• Abnormalities:

• ST Segment Elevation :

• Acute myocardial infarction

• Coronary vasospasm (Printzmetal’s angina)

• Pericarditis

• Ventricular aneurysm

• Benign early repolarization

• Left bundle branch block

• Left ventricular hypertrophy

• Brugada syndrome

• Ventricular paced rhythm

• Raised intracranial pressure

ST Segment• Acute ST elevation myocardial infarction (STEMI):

There is usually reciprocal ST depression in the electrically

opposite leads.

Anterolateral STEMI

elevation

reciprocal ST depression

ST Segment

Inferior MI

elevation reciprocal ST depression

ST Segment• Pericarditis:

• Widespread concave ST elevation and PR depression

throughout most of the limb leads (I, II, III, aVL, aVF) and

precordial leads (V2-6).

• Reciprocal ST depression and PR elevation in lead aVR (± V1).

• Sinus tachycardia due to pain and/or pericardial effusion.

ST Segment

Pericarditis

elevation reciprocal ST depression

ST SegmentCoronary Vasospasm (Prinzmetal’s angina):

• ST elevation that is very similar to acute STEMI occurring during

episodes of chest pain.

• the ECG changes are transient, reversible with vasodilators and

not usually associated with myocardial necrosis. It may be impossible

to differentiate these two conditions based on the ECG alone.

ST Segment• Left Ventricular Aneursym:

• ST elevation seen > 2 weeks following an acute MI.

• Most commonly seen in the precordial leads.

• May exhibit concave or convex morphology.

ST Segment• ST Depression:

• Acute Coronary Syndrome (ACS): Unstable angina (UA) & Non-

ST-elevation MI (NSTEMI) ( subendocardial ischaemia )

• Reciprocal change in STEMI

• +ve stress E.C.G test

• Strain pattern with LVH or RVH ( asymmetrical )

• 2ry ST-T changes with BBB & WPW pattern

• Drugs e.g. Digoxin effect

• Hypokalaemia

• Posterior MI

• Variant of normal

ST Segment• Subendocardial ischaemia:

• ST depression is usually widespread — typically present in leads

I, II, V4-6 and a variable number of additional leads.

• ST depression localised to a particular territory (esp. inferior or

high lateral leads only) is more likely to represent reciprocal

change due to STEMI. The corresponding ST elevation may be

subtle and difficult to see, but should be sought.

ST Segment• Digoxin Effect:

• Down-sloping ST depression with a characteristic “sagging”

appearance (see below).

• Flattened, inverted, or biphasic T waves.

• Shortened QT interval.

T wave• It represents part of ventricular repolarisation.

• Generally follow the direction of the main deflection of QRS

• Upright in all leads except aVR and V1

• Amplitude < 5 mm in limb leads, < 10 mm in precordial leads

• T wave abnormalities:• Prominent T wave inversion

• Tall +ve T wave

• Biphasic T waves

T wave• Prominent T wave inversion ( or flat T wave ):

• Strain pattern with LVH or RVH

• 2ry ST-T changes with BBB & WPW pattern

• Hypertrophic cardiomyopathy

• subendocardial ischaemia

• Evolving phase of MI

• Pulmonary embolism

• Drugs e.g. Digoxin effect

• Normal finding in children

• Hypokalaemia

• Raised intracranial pressure

T wave• Tall +ve T wave:

• The early stages of ST-elevation MI (STEMI)

• Hyperkalaemia

• Normal variant

T wave• Biphasic T waves:

• There are two main causes of biphasic T waves:

Myocardial ischaemia

Hypokalaemia

• The two waves go in opposite directions:

Ischaemic T waves go up then down

Hypokalaemic T waves go down then up

QT interval Total duration of Depolarization and Repolarization

Measured from the start of the QRS complex to the end of the T

wave.

QT interval decreases when heart rate increases

QT interval should be 0.36–0.44 (9–11 small squares)

Should not be more than half of the interval between adjacent R

waves (RR interval).

QT interval1. A prolonged QT:

( Hypokalaemia, Hypomagnesaemia, Hypocalcaemia, Hypothermia,

Myocardial ischemia, Post-cardiac arrest, Raised intracranial pressure,

Congenital long QT syndrome, DRUGS )

2. A short QT:

1. familial/genetic:

(short Q-T syndrome)

1. Digoxin toxicity

2. Hypercalcemia

3. Hyperthermia

U wave

• The U wave is a small deflection immediately following the T wave, usually in the same direction as the T wave.

• It is best seen in leads V2 and V3.They are thought to be due to repolarisation of the atrial septum

• Prominent U waves can be a sign of hypokalaemia, hyperthyroidism

E.C.G sequence of MI

1. Acute phase:

ST segment elevation in 2 or more consecutive leads with reciprocal changes (Sometimes tall positive T wave )

At least 1mm ST elevation in limb leads and 2mm in precordial leads to be significant.

Pathological Q appear in leads that show ST elevation (8-48 h )

2. Evolving phase:

ST segment returns to the baseline with development of deep T wave inversion hours to days later in the same leads that show ST elevation

3. Chronic phase:

Regression of ST-T changes pathological Q wave without ST-T changes that usually persists for months to years (old MI )

Again localization of leads in STEMI

1. Septal (V1-2)

2. Strict anterior (V3-4)

3. Anteroseptal ( V1 V4 )

4. Lateral (I , aVL, V5-6)

5. Anterolateral ( V3 V6 ,I,aVL )

6. Extensive anterior (V1 V6, I,aVL )

7. Inferior (II, III, aVF)

Inferior Wall MI

This is an inferior MI. Note the ST elevation in

leads II, III and aVF.

Inferior Wall MI

Now how about the inferior portion of the heart?

Limb Leads Augmented Leads Precordial Leads

Leads II, III and aVF

Anterolateral MI

This person’s MI involves both the anterior wall

(V2-V4) and the lateral wall (V5-V6, I, and aVL)

Lateral MI

So what leads do you think the lateral portion of the heart is best viewed?


Leads I, aVL, and V5- V6

Anterior MI

Remember the anterior portion of the heart is

best viewed using leads V1- V4.


E.C.G Signs of Pulmonary embolism

1. Sinus tachycardia: 8-73%.

2. RBBB (complete/incomplete): 6-67%.

3. Rightward axis shift : 3-66%.

4. P Pulmonale : 6-33%.

5. Inverted T-waves in right chest leads: 50%.

6. S1Q3T3 pattern: 11-50% (S1-60%, Q3-53% ,T3-20%).

7. Clockwise rotation:10-56%.

8. AF or A flutter: 0-35%.

9. No ECG changes: 20-24%.

E.C.G Signs of Pulmonary embolism

Heart rate of 100/min & S1Q3T3 & inverted or flattened T waves in leads V1 through V3.

Hyperkalemia (according to K serum level )

Arrhythmias

1. Regular Tachyarrhythmias ( HR >100 beats/minute ):

Sinus tachycardia ( S.T )

Paroxysmal supraventricular tachycardia (PSVT)

Ventricular tachycardia ( VT) Wide QRS

Atrial flutter ( usually regular tachycardia but may be with normal or slow regular HR, or irregular HR with variable heart block )

2. Regular Bradyarrhythmias (HR < 60 beats/minute ):

Sinus bradycardia ( SB )

Nodal rhythm

Partial heart block

Complete heart block

Arrhythmias

3. Irregular rhythm ( with tachycardia, bradycardia or within normal HR ):

Atrial fibrillation ( A.F ) may be irregular tachycardia, irregular bradycardia or with controlled ( within normal ) rate.

Premature beats ( may occur with sinus tachycardia, sinus bradycardia or with normal rate.

Partial irregular ( variable ) heart block ( bradycardia ).

PSVT & Atrial flutter with variable heart block ( usually tachycardia ).

Ventricular Fibrillation

N.B. all arrhythmias are arrow QRS complex except with ventricular origin (Ventricular premature beats , Ventricular tachycardia and sometimes with complete heart block ) Wide QRS complex.

Arrhythmias

Regular Tachyarrhythmias :

1. Sinus tachycardia ( S.T ) ( like normal but rapid ):

Regular sinus rhythm.

Each normal P is followed by a normal QRS complex.

Rapid HR ( 100-180 beats/m )

Arrhythmias2. Paroxysmal supraventricular tachycardia (PSVT) :

( Very rapid > 140/ min ), usually no P wave )

Rapid HR ( 100-250 beats/m ), regular QRS complexes of normal morphology

P wave are either a) Abnormal (deformed or has different shape) atrial tachycardia or b) Inverted ( retrograde ) or usually absent ( buried in QRS ) junctional tachycardia

Arrhythmias3. VT ( ventricular tachycardia ) : ( wide rapid regular )

QRS complexes are wide ( usually > 0.14 sec ), bizarre shaped with rapid HR ( 120-250 beats/m )

P wave are of normal ( 60-100/m) rate and usually obscured by QRS complexes but sometimes may be superimposed on QRS complexes with A-V dissociation.

Arrhythmias4. Atrial flutter : ( Saw-tooth appearance, usually regular

tachycardia, exclusion. DD from AF )

P wave is replaced by flutter waves (“saw-tooth” pattern) best seen in leads II, III, aVF . may be more easily spotted by turning the ECG upside down!

Atrial rate = 250-350/m with a ventricular rate that is often fraction of the atrial rate ( 1/2, 1/4 , etc )

Atrial rate = 1500/ F-F interval ( small squares ) or simply ( no of F waves before QRS +1) X HR ( ventricular rate )

Arrhythmias

Regular Bradyarrhythmias :

1. Sinus bradycardia ( like normal but slow ):

Regular sinus rhythm.

Each normal P is followed by a normal QRS complex.

Slow HR (< 60 beats/m)

Arrhythmias

2. Nodal ( junctional ) rhythm :

( Slow, no or retrograde P wave ).

QRS complexes are regular, narrow, slow ( usually 40-60 beats/m ) of normal morphology.

P wave is either : a) absent b) Inverted (retrograde)

Arrhythmias

3. Heart block :

a) First degree HB: constant prolongation of P-R interval > 0.20 sec (> 5 small squares )

b) Second degree HB 2 subtypes:

Mobitz type I HB ( Wenckebach ):

Progressive prolongation of the PR interval from beat to beat until a dropped or non conducted beat then the sequence is repeated.

ArrhythmiasMobitz type II HB :

Intermittent non-conducted P waves without progressive prolongation of the PR interval (compare this to Mobitz I).

The PR interval in the conducted beats remains constant.

The block may be fixed ( 2:1, 3:1 ) or variable.

Arrhythmias

c) Third degree HB ( complete HB ): ( No relation between QRS and P waves)

QRS may be normal width or abnormally wide of slow regular rate ( 30- 60 beats/m)

P waves are of normal regular rate and may be superimposed on QRS complex and T wave. Atrial rate is almost always faster than ventricular rate. P-R interval is constantly changing. There is complete A-V dissociation.

Arrhythmias 1St & 2nd degree HB are considered incomplete or partial HB.

Arrhythmias3. Irregular rhythm :

1) A.F.: ( irregular)

• Irregularly irregular rhythm. No P waves.

• Variable ventricular rate. QRS complexes usually rapid ( 100-200 beats/m) but may be slow from drug toxicity e.g. digitalis or disease of A-V junction or controlled by drugs e.g. digitalis.

• Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).

• Fibrillatory waves may mimic P waves leading to misdiagnosis.

Arrhythmias2. Premature beats = Extrasystole:

• Comes prematurely followed by compensatory pause.

• Premature peats may occur with sinus tachycardia, sinus bradycardia or with normal heart rate.

Atrial premature beats ( APB )

( Like normal but comes early followed by slight compensatory pause )

A premature abnormal ( deformed or has different shape ) P wave with different PR interval followed by normal QRS complex followed by slight compensatory pause.

ArrhythmiasVentricular premature beats ( VPB )

( wide, bizarre, comes early and followed by full compensatory pause)

Abnormal ( Wide > 0.12 sec, bizarre ) premature QRS complex not preceded by P wave followed by full compensatory pause. The T wave is of opposite direction to QRS . ( uniform VPBs : the same shape in a single lead, multiform VPBs : different shapes in the same lead ).


N.B.

When a VPB occurs regularly after each normal beat Ventricular bigemini ( common with digitalis toxicity )


When the rhythm is two normal beats followed by a VPB ventricular trigemini


When two VPBs in a row ventricular couplet

Arrhythmias1. When a APB occurs regularly after each normal beat Atrial

bigemini

2. When the rhythm is two normal beats followed by a APB Atrial trigemini

3. When two APBs in a row Atrial couplet

1

2

3

Arrhythmias

none• Rate?

• Regularity? irregularly irregular

none

wide, if recognizable

• P waves?

• PR interval? none

• QRS duration?

Ventricular Fibrillation

ECG RULES

• Professor Chamberlains 10 rules of a normal

ECG, a foundation to ECG interpretation used all over the

world to this date.

http://www.ambulancetechnicianstudy.co.uk/10Rules/Title.gif

RULE 1

PR interval should be 120 to 200 milliseconds or 3 to 5 little squares

RULE 2

The width of the QRS complex should not exceed 110 ms, less than 3 little squares

RULE 3

The QRS complex should be dominantly upright in

leads I and II

http://www.ambulancetechnicianstudy.co.uk/10Rules/Image3.gif

RULE 4

QRS and T waves tend to have the same

general direction in the limb leads


RULE 5

All waves are negative in lead aVR


RULE 6

The R wave must grow from V1 to at least V4

The S wave must grow from V1 to at least V3

and disappear in V6


RULE 7

The ST segment should start isoelectric

except in V1 and V2 where it may be elevated


RULE 8

The P waves should be upright in I, II, and V2 to V6


RULE 9

There should be no Q wave or only a small q less

than 0.04 seconds in width in I, II, V2 to V6


RULE 10

The T wave must be upright in I, II, V2 to V6


ecg fundamentals

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