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ECG Introductory tutorial

Bahri Teaching hospital

prepared by yusif elamin

thank you

ECG

introduction

Before Einthoven’s time, it was known that

electrical currents were produced by the beating of

the heart, but this phenomenon could not be measured

accurately without placing electrodes directly over the

heart.

Einthoven was born in Indonesia in the year 1860. His father who was a doctor, died when Einthoven

was still a child. His mother along with her children moved to Netherlands in 1870. He received a medical degree from the University of Utrecht in 1885. After that he went on to become a professor at University of

Leiden in 1886

before this guy

By the mid-19th century, galvanometers had been invented, and it was possible to see that nerves were indeed generating their own action potentials. These galvanometers exploited the then new technology of electromagnets. For example, Emil de Bois-Reymond built by hand a type of galvanometer with 24,000 turns around an iron plate. When the nerve fired action potentials, a metal needle suspended by the plate would deflect. These devices worked, but the needle movement was not fast enough to separate the 1 ms individual action potentials, and the machines occupied a lot of time to construct.

In the late 19th century, French scientist Gabriel Lippmann invented the capillary electrometer, which consisted of a test tube filled with mercury and capped with a layer of sulphuric acid. A wire was connected from the nerve to the mercury bath and the ground to the sulphuric acid. When the voltage of a nerve changed due to action potential firing, the shape of the meniscus between the mercury and sulphuric acid would change and could be observed underneath a microscope. A "liquid state amplifier," if you will. Capillary Electrometers were sensitive but, like the early galvanometers, also suffered from mechanical sloth (the meniscus did not change fast enough to isolate individual action potentials).

The amplifiers that gave us the first hint of the electrical impulses generated by neurons came from biological tissue itself! Scientists of the 18th and early 19th century used the contractions of muscles as "bioamplifiers" to indirectly measure neural firing. Using friction machines (spark generators), Leyden jars (primitive capacitors), or Voltaic Piles (the first batteries), electrical stimuli could be delivered to motor neurons that were still attached to muscles. The electrical stimulation would cause the nerve to fire action potentials (so people hypothesized), the muscle would then contract, and the force of contraction could be measured with a spring. With increasing electrical stimuli strength (thus more action potentials in the motor neurons), the muscle would contract with increasing force. This technique worked, but led to vigorous debates as to whether the neural tissue was actually generating its own action potentials at all, or whether the muscle contraction was just a direct result of electrical stimulation.

After Einthhoven

The original machine required cooling water for the powerful electromagnets.

It required 5 people to operate it and weighed around 600 lb. This device increased

the sensitivity of the standard galvanometer so that the electrical activity of the

heart could be measured despite the insulation of flesh and bones.

In 1902, on the cusp of the radio age and electronic revolution, Wilhelm Einhoven invented the most sensitive amplifier yet, the string galvanometer. This consisted of a gold coated glass string suspended between two high power electromagnets. Similar to the Astatic Galvanometer but more sensitive (as the electromagnets were actively powered), the string would oscillate when the nerve fired action potentials. A light could be presented on the string, and the movement of the shadow could be recorded on photographic film. Wilhelm used his string galvanometer to record the Electrocardiogram, for which he is famous.

  • Much of the terminology used in describing an EKG originated with Einthoven. His assignment of the letters P, Q, R, S and T to the various deflections is still used.
  • The term Einthoven’s triangle is named after him.
  • Einthoven went on to describe the electrocardiographic features of a number of cardiovascular disorders after his development of string galvanometer.
  • Later Einthoven studied the acoustics, particularly heart sounds which he researched with Dr P Battaerd.
  • He died in Leiden, Netherlands and is buried in the graveyard of the Reformed

Church at Haarlemmerstraatweg in Oegstgeest.

Objectives

Objectives

1. Describe How ECG Generated

2. Identfiy and measure ECG normal waveform

3.Practising a Systemic appoch to ECG

understanding how ecg tracing is generated

Vector

Electrocardiography is the recording of the electrical impulses that are generated

in the heart. These impulses initiate the contraction of cardiac muscles. The term

vector is used to describe these electrical impulses

ECG basics

The vector is a diagrammatic

way to show the strength and the direction of the electrical impulse. The vectors add up when they are going in the same direction and they get cancelled if they point in the opposite directions. But in case if they are at an angle to each other, they add or subtract energy and change their resultant direction of flow

Electrodes

Electrodes

Electrodes are the sensing devices that pick up the electrical activity occurring under it.

The SUM of electrical activity through the cardiac cells generated the ecg waveform

LEADs

  • The electrical activity of the heart is acptured through the twelve leads consisting of

six limb leads (I, II, III, aVR, aVL and aVF) and six chest leads (V1–V6).

  • Each lead is coposed of 2 electodes that are placed on the patient body. There are 10 electrodes

  • The limb leads consists of standard bipolar (I, II and III) and augmented (aVR, aVL and aVF) leads.
  • The bipolar leads were so named because they record the difference in electrical voltage between two extremities.

For example:

Lead I: Records the difference in voltage between the left arm and the right arm electrodes.

Lead II: The difference in voltage between the left leg and the right arm electrodes.

Lead III: The difference in voltage between the left leg and the left arm electrodes.

  • In augmented limb leads, the abbreviation ‘a’ refers to augmented; V to voltage; R, L and F to right arm, left arm and left foot (leg) respectively. They record the electrical voltage of corresponding extremity.

Remeber Direction of deflection

knowledge check !

ecg PAPER

ecg paper

normal ecg

normal ECg

1. Sinoatrial node (SA node)

2. Atrioventricular node (AV node)

3. Bundle of His.

4. Left bundle branch (LBB) and right bundle branch (RBB)

5. Purkinje fibers.

ELECTRICAL ACTIVITY

The conductive system of the heart consists of five specialized tissues.

RATES OF PACEMAKERS

1. SA node 60 – 100 bpm

2. Atrial cells 55 – 60 bpm

3. AV node 45 – 50 bpm

4. Bundle of His 40 – 45 bpm

5. Bundle branch 40 – 45 bpm

6. Purkinje cells 35 – 40 bpm

7. Myocardial cells 30 – 35 bpm

NORMAL SPREAD OF ELECTRICAL ACTIVITY IN THE HEART

Any disturbance in the sequence of stimulation of this specialized tissue leads to

rhythmic disturbances called arrhythmias or conduction abnormality called heart

block.

Step 2

Step 1

WAVES

Normal T wave characteristics

  • Upright in all leads except aVR and V1
  • Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm males, 8mm females)
  • Duration relates to QT interval

QRS

The Q Wave

A Q wave is any negative deflection that precedes an R wave

The Q wave represents the normal left-to-right depolarisation of the interventricular septum

Small ‘septal’ Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6)

Q waves in different leads

Small Q waves are normal in most leads

Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant

Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3)

Pathological Q Waves

Q waves are considered pathological if:

> 40 ms (1 mm) wide

> 2 mm deep

> 25% of depth of QRS complex

Seen in leads V1-3

Pathological Q waves usually indicate current or prior myocardial infarction.

Differential Diagnosis

Myocardial infarction

Cardiomyopathies — Hypertrophic (HCM), infiltrative myocardial disease

Rotation of the heart — Extreme clockwise or counter-clockwise rotation

Lead placement errors — e.g. upper limb leads placed on lower limbs

Loss of normal Q waves

The absence of small septal Q waves in leads V5-6 should be considered abnormal.

Absent Q waves in V5-6 is most commonly due to LBBB.

T wave abnormalities

Peakd T waves

ECG Peaked T waves hyperkalemia Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia

Hyperacute T waves (HATW)

Broad, asymmetrically peaked or ‘hyperacute’ T-waves (HATW) are seen in the early stages of ST-elevation MI (STEMI), and often precede the appearance of ST elevation and Q waves.They are also seen with Prinzmetal angina.

Inverted T waves

Inverted T waves are seen in the following conditions:

Normal finding in children

Persistent juvenile T wave pattern

Myocardial ischaemia and infarction (including Wellens Syndrome)

Bundle branch block

Ventricular hypertrophy (‘strain’ patterns)

Pulmonary embolism

Hypertrophic cardiomyopathy

Raised intracranial pressure

** T wave inversion in lead III is a normal variant. New T-wave inversion (compared with prior ECGs) is always abnormal. Pathological T wave inversion is usually symmetrical and deep (>3mm).

Biphasic T waves

There are two main causes of biphasic T waves:

Myocardial ischaemia

Hypokalaemia

The two waves go in opposite directions:

Biphasic T waves due to ischaemia – T waves go UP then DOWN

Biphasic T waves due to ischaemia

Biphasic T waves due to Hypokalaemia – T waves go DOWN then UP

1. Dominant R wave in V1

Causes of Dominant R wave in V1

Normal in children and young adults

Right Ventricular Hypertrophy (RVH)

Pulmonary Embolus

Persistence of infantile pattern

Left to right shunt

Right Bundle Branch Block (RBBB)

Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9)

Wolff-Parkinson-White (WPW) Type A

Incorrect lead placement (e.g. V1 and V3 reversed)

Dextrocardia

Hypertrophic cardiomyopathy

Dystrophy

Myotonic dystrophy

Duchenne Muscular dystrophy

. Dominant R wave in aVR

Poisoning with sodium-channel blocking drugs (e.g. TCAs)

Dextrocardia

Incorrect lead placement (left/right arm leads reversed)

Commonly elevated in ventricular tachycardia (VT)

2. Dominant R wave in aVR

Poisoning with sodium-channel blocking drugs (e.g. TCAs)

Dextrocardia

Incorrect lead placement (left/right arm leads reversed)

Commonly elevated in ventricular tachycardia (VT)

3. Poor R wave progression

Poor R wave progression is described with an R wave ≤ 3 mm inV3 and is caused by:

Prior anteroseptal MI

LVH

Inaccurate lead placement

May be a normal variant

In the normal ECG, there is a large S wave in V1 that progressively becomes smaller, to the point that almost no S wave is present in V6. A large slurred S wave is seen in leads I and V6 in the setting of a right bundle branch block.

The presence or absence of the S wave does not bear major clinical significance. Rarely is the morphology of the S wave discussed.

In the setting of a pulmonary embolism, a large S wave may be present in lead I

Knowledge check !

Knowledge check !

U wave - Osborne wave (J wave) Delta wave Epsilon Wave

other waves :

Prominent U waves

U waves are described as prominent if they are

>1-2mm or 25% of the height of the T wave.

Causes of prominent U waves

Prominent U waves most commonly found with:

Bradycardia

Severe hypokalaemia.

Drugs associated with prominent U waves:

Digoxin

inverted U waves

U-wave inversion is abnormal (in leads with upright T waves)

A negative U wave is highly specific for the presence of heart disease

Common causes of inverted U waves

Coronary artery disease

Hypertension

Valvular heart disease

Congenital heart disease

Cardiomyopathy

Hyperthyroidism

In patients presenting with chest pain, inverted U waves:

Are a very specific sign of myocardial ischaemia

May be the earliest marker of unstable angina and evolving myocardial infarction

Have been shown to predict a ≥ 75% stenosis of the LAD / LMCA and the presence of left ventricular dysfunction

U wave Overview

The U wave is a small (0.5 mm) deflection immediately following the T wave

U wave is usually in the same direction as the T wave.

U wave is best seen in leads V2 and V3.

Source of the U wave

The source of the U wave is unknown. Three common theories regarding its origin are:

Delayed repolarisation of Purkinje fibres

Prolonged repolarisation of mid-myocardial “M-cells”

After-potentials resulting from mechanical forces in the ventricular wall

Abnormalities of the U wave

Prominent U waves

Inverted U waves

systematic approach

Approach

Notes

Four Initial Features

Four Waves

Four Intervals

The ECG ‘Rule of Fours’

The FOUR INITIAL FEATURES to look for on an ECG

(1) History/ Clinical Picture

This is THE MOST IMPORTANT thing to look at on ANY ECG.

Remember, an ECG is just like any other test, a nd should always be interpreted in the clinical context,

perhaps even more so.

Simple things need to be recorded, like the name, age, time, patient symptoms (e.g. chest pain)

and other clinical features.

Also do a quick check for lead placement errors:

Limb leads: (a) check aVR for upside down P, QRS and T waves,

(b) aVL and aVR should generally be mirror images.

Chest leads: look for RS pattern in V1 – changing progressively to QR pattern in V6.

(2) Rate

The normal value is between 60-100/min. Lower than this is bradycardia, higher is tachycardia.

(3) Rhythm

Is the rhythm sinus or is it another rhythm? If so, what?

(4) Axis

The FOUR WAVES (or complexes) on an ECG

(1) P wave

Lead II is usually the best lead place to look at the P wave morphology.

Observe the P-wave morphology e.g. in particular P pulmonale or P mitrale.

(2) QRS complexes (or QRS “waves”)

Look in ALL leads for the presence of Q waves.

Observe the QRS amplitude and look for QRS progression through the chest leads.

(3) T waves

Look in ALL leads for T waves.

Look for T wave inversion, T wave concordance or discordance with QRS and the presence of T wave flattening.

(4) U waves

Are U waves present or not?

The FOUR INTERVALS (or segments) on an ECG

(1) PR interval

The PR interval is normally between 0.12-0.20 seconds (3-5 small squares).

A prolonged or changing (esp lengthening) PR interval indicates heart block. Shortened PR intervals can be because of WPW or LGL syndromes, or a junctional rhythm.

(2) QRS width (“QRS-interval”)

The QRS-interval is normally less than 0.12 seconds (3 small squares).

A widened QRS width indicates some sort of conduction defect with the left or right bundle branches.

(3) ST segment (“ST-interval”)

This is probably the most important thing to look at.

…then look at it a 2nd and 3rd time. Look for sloping (especially downsloping) or flattening of the ST segments.

(4) QT interval

The QT interval is the time from the start of the Q wave to the end of the T wave.

lets go ...

Rate Interpretation : 1) Large square method

RR

Useful as quick calculation for regular rhythms at regular rate

Rate Interpretation : 2) small square method

Useful for very fast regular rhythms, as likely to provide more accurate rate than large square method

Rate Interpretation : 3) R wave method

Useful for slow and/or irregular rhythms

Rate = Number of R waves (rhythm strip) X 6

The number of complexes (count R waves) on the rhythm strip gives the average rate over a ten-second period. This is multiplied by 6 (10 seconds x 6 = 1 minute) to give the average beats per minute (bpm)

Note:

  • Calculate atrial and ventricular rates separately if they are different (e.g. complete heart block)

  • The machine reading can also be used and is usually correct — however, it may occasionally be inaccurate in the presence of abnormal QRS/T-wave morphology, e.g. may count peaked T waves as QRS complexes or miss QRS complexes with reduced amplitude.

  • Other paper speeds: 50mm/sec

Mean Electrical Axis

axis

axis

Normal Or Left Axis Deviation

Normal Or Left Axis Deviation

Normal Or Left Axis Deviation

?

?

Rhythm

Is it Regular ?

Is it a sinus Rhythm ?

Now , Let's put it all together ...

let's practice what we learned so far ...

let's Practice !

answer the following ?

1. what is the rate?

2.what is the axis?

3. Is the rhythm sinus ? regular ?

7 step approach to ECG rhythm analysis

1. Rate

  • Tachycardia or bradycardia?

Normal rate is 60-100/min.

2. Pattern of QRS complexes

  • Regular or irregular?

If irregular is it regularly irregular or irregularly irregular?

3. QRS morphology

  • Narrow complex: sinus, atrial or junctional origin.
  • Wide complex: ventricular origin, or supraventricular with aberrant conduction.

4. P waves

  • Absent: sinus arrest, atrial fibrillation
  • Present: morphology and PR interval may suggest sinus, atrial, junctional or even retrograde from the ventricles.

5. Relationship between P waves and QRS complexes

  • AV association (may be difficult to distinguish from isorhythmic dissociation)
  • AV dissociation
  • complete: atrial and ventricular activity is always independent.
  • incomplete: intermittent capture.

6. Onset and termination

  • Abrupt: suggests re-entrant process.

Gradual: suggests increased automaticity.

7. Response to vagal manoeuvres

Sinus tachycardia, ectopic atrial tachydysrhythmia: gradual slowing during the vagal manoeuvre, but resumes on cessation.

AVNRT or AVRT: abrupt termination or no response.

Atrial fibrillation and atrial flutter: gradual slowing during the manoeuvre.

VT: no response.

answer the following ?

1. what is the rate?

2.what is the axis?

3. Is the rhythm sinus ? regular ?

Home work

Congratulation

we completed our introduction tutorial and we had the opportunity to :

1

2

3

start to adapt a systematic approach to ECG interpretation

understand how ECG tracing is generated .

identify the normal ECG waveform and related it to the cardiac cycle

Always practice ...

please

thank you

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