OMDURMAN TEACHING HOSPITAL DR ALI ADAM ALHADIS UNIT

ECG
Presented by Dr Osman Alzubair

What is an electrocardiogram?
A recording of the changing potentials of the electrical field imparted by the heart.

What's the point?

Fundamental part of CVS assessment. Heart rhythm (Arrhythmias)

E.g. SR cf AF, bradycardia, tachycardia E.g. Ischaemia, infarction E.g. LVH E.g. oK

Heart Injury

Heart structure

Metabolic disorders

Principles of ECG I
Myocardial cells
Contraction

due to Depolarisation Relaxation due to Repolarisation

The electrical changes associated with de- and repolarisation are recorded and form the ECG

Principles of ECG II
Depolarisation towards positive electrode results in upward deflection, away from electrode deflection downward Size of deflection reflects volume of depolarised muscle

Conduction system of Heart

SA node
Natural pacemaker Initiates atrial depolarisation

AV node

Propagation of impulse to ventricles Conducting tissues of ventricles

His-Purkinje system

Formation of ECG

Lead placement chest leads

Lead placement chest leads

Chest leads (Anterior leads)

V1-V6

View heart in horizontal plane

Lead placement - limb leads

Lead placement - limb leads

Limb Leads
I, II, III aVL, aVF, aVR

View heart in a vertical plane

Anatomical Relationship
Lead II, III, aVF V1-V6 I, aVL, V5-V6 Heart surface Inferior Anterior Lateral

TECHNICAL ASPECTS

Technical aspects I
ECG recorded on standard paper
Paper speed 25mm/s Paper

 

1 Large square = 5mm = 0.2s 1 Small square = 1mm = 0.04s

Technical Aspects II
Electrical aspect is measured in Millivolts Machines are calibrated
Amplitude 1mV moves stylus 1cm vertically 0.1mV = 1mm = 1 small square

Technical Aspects III

Amplitude of wave form is influenced by
Myocardial

mass e.g. LVH Thickness of intervening tissue Distance between electrode and myocardium Net vector of depolarisation

Technical Aspects IV
Low amplitude
Obesity COPD Pericardial Fluid Hypothyroidism

High amplitude
Thin patient Left Ventricular Hypertrophy (LVH)

P Wave
The SA node lies high in the wall of the right atrium and initiates atrial depolarisation producing the P wave. Its amplitude rarely exceeds two and a half small squares (0.25mG). Its duration should not exceed three small squares (0.12s) Positive in leads I and II Best seen in leads II and VI

PR interval
The PR segment represents the time in which electrical impulse is conducted through the AV node, the bundle of His, the bundle branches and the Purkinje fibres The PR interval is the time between the onset of atrial depolarisation and the onset of ventricular depolarisation. It is measured from the beginning of the P to the first deflection of the QRS complex Its duration is 3 to 5 small squares (0.12-0.20s)

QRS Complex
Represents the electrical forces generated by ventricular depolarisation The duration should not exceed two and a half small squares (0.10s) The left side of the septum depolarised first and the impulse then spread towards the right, lead V I lies immediately to the right of the septum and thus registers an initial positive deflection (R wave) while the first deflection inscribed is negative (septal Q wave) in the lateral leads (lead I, aVL, V5 and V6) These non pathological Q waves are <2 small squares deep and <1 small square wide and should be <25% of the amplitude of the corresponding R wave

QRS Complex
Depolarisation of the right and left ventricles produces opposing electrical vectors but the left ventricle has larger muscle mass and its depolarisation dominates the ECG In the precordial leads, QRS complex morphology changes depending on whether the depolarisation forces are moving towards or away from a lead:  Towards electrode-upward deflection (Positive)  Away from electrode-downward deflection (Negative)  When the wave of depolarisation is at right angles to the lead Equiphasic deflection is produced.

QRS Complex IIM

Wave of depolarisation

ST Segment
The QRS complex terminates at the J point or ST junction ST Segment lies between the J point and the beginning of the T wave Represents the period between the end of ventricular depolarisation and the beginning of repolarisation

ST segment

TP segment

J point

T wave
Represents ventricular repolarisation Maybe inverted aVR, lead III and lead VI Isolated T wave inversion lead V2 is abnormal T wave inversion in two or more of the right precordial leads is known as persistent juvenile pattern (common in black people) The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the corresponding R wave; T wave amplitude rarely exceeds 10mm

QT interval
Is measured from the beginning of the QRS complex to the end of the T wave Represents the total time taken for depolarisation and repolarisation of the ventricle Lengthens as the heart rate slows thus when measuring the QT interval, the rate must be taken in account QT interval should be 0.35-0.45s and should not be more than half of the interval between adjacent R waves ( R-R interval) QT interval corrected for the heart rate (QTc) QTc= QT / R-R (seconds)

U wave
U wave is a small deflection following the T wave Most prominent in V2 to V4 Results from repolarisation of the mid myocardial cells (those between the endocardium and the epicardium and the His-Purkinje system Maybe found in athletes and are associated with hypokalemia and hypercalcaemia

Normal ECG

HEART RATE

Heart Rate
Tachycardia (fast) Bradycardia (slow) HR>100 beats/min HR<60 beats/min

1 large square = 0.2 seconds 5 large squares = 1 second 300 large squares = 1 minute

How to calculate heart rate

How to calculate heart rate

R-R = 2 large squares i.e. 300 / 2 = 150/ min

How to calculate heart rate

R-R = 2 large squares i.e. 300 / 2 = 150/ min

R-R = 6 large squares i.e. 300/6= 50/min

HEART RHYTHM

Rhythm
Use a rhythm strip, Lead II commonly used

Sinus Rhythm
Normal cardiac rhythm P wave precedes every QRS P wave upright in leads I and II HR 60min< RATE < 100 min Rhythm originates in the SA node and conducts to ventricles

Sinus Arrthymia
Common in healthy individuals Beat-Beat variation in R-R interval with respiration (constant PR interval) Rate Increases with Inspiration Vagally mediated
Increased

volume of blood returns to heart in Inspiration.

Heart Rate II
Irregular Rhythm
Heart

rate calculated from rhythm strip I.e. lead II 1 second to record 2.5cm 10 seconds to record 25cm

Count number of intervals between QRS complexes X 10

Atrial Fibrillation-What is the rate?

CARDIAC AXIS

Cardiac Axis
The average direction of spread of the depolarisation wave through the ventricles as measured from a zero reference point

Cardiac Axis-Vertical Plane

Cardiac Axis II
Vertical plane = limb leads. Zero reference point = lead I Normal range
-30 to + 90 aVL-aVF

Axis above Negative Axis below Positive

Cardiac Axis III

Normal cardiac axis 11 o clock- 5 o clock. Right Axis Deviation (RAD)

Axis beyond +90

Left Axis Deviation (LAD)

Axis beyond 30

How to measure axis?

Normal I II III or RAD LAD

What is the axis?

Introduction
ECG used to assess patients with suspected ischaemic heart disease. ECG must be interpreted in light of the clinical history. ECG has limitations. 20% of patients with an AMI have a normal ECG.

ECG Terminology

R wave ST segment TP segment

Q wave

S wave

J point

Acute Myocardial Infarction (AMI)

Rapid initiation of treatment improves prognosis. Commonest ECG finding ST elevation. pseudo infarct patterns also seen. First trace is often normal. Serial ECGs show evolving changes.

Hyperacute T Waves
Earliest sign is an increase in T wave amplitude. T wave pointed. Most evident in anterior chest leads. Changes are usually only present for 5-30 minutes. ST segment change follows.

Hyperacute T waves

ST Segment
ST segment elevation occurs within the first few hours of symptom onset. Degree of ST elevation varies. ST elevation>1mm in 2 contiguous limb leads or >2mm in 2 contiguous chest leads is an indication for thrombolysis.

ST Elevation

Q Waves
As AMI evolves pathological Q waves develop. Loss of viable myocardium beneath the recording electrode. May develop within 1-2 hours. Q waves act as a permanent marker of myocardial necrosis.

Pathological Q Waves

Resolution of changes
ST segment elevation diminishes. T waves invert. ST segment elevation can take weeks to diminish. T wave inversion may persist for many months.

Evolution of AMI

Normal

Peaked T wave

Degree of ST segment elevation Q wave formation and loss of R wave

T wave inversion

Reciprocal ST depression
ST depression in leads remote from the infarct site. Reciprocal changes are highly sensitive marker of AMI.
70% inferior MI 30% anterior MI

Pathogenesis is uncertain
mirror image change (electrical phenomenon) Extension of infarct

Reciprocal ST changes

Localisation of site
Distribution of ECG changes indicate site of arterial disease. Anterior and inferior aspects of the heart are the commonest sites of infarction.
RCA LAD Cx

Inferior Anteroseptal Lateral

II, III, aVF V1-V4 1, aVL, V5, V6

Right ventricular infarct

Often missed on standard 12 lead ECG. Associated with 40% of inferior AMI. ECG
Inferior

ST elevation ST elevation V1

Right sided leads in all patients with inferior MI.

Right Ventricular infarct

Lead V4R is the most useful lead. ST elevation in right ventricular infarction can be short lived. Associated with HYPOtension.

Right Ventricular infarct

Posterior MI
Indication for thrombolysis. Infarct of posterobasal wall of left ventricle. Often missed on standard 12 lead ECG. Indirect changes
ST

depression V1-V3

Dominant R wave V1. Reversed changes in lead V1-V3.

Posterior Leads
V7-V9

Shows ST elevation in patients with posterior MI.

Posterior Myocardial Infarction

Differential diagnosis of ST elevation

Pericarditis
LV

Aneurysm LBBB Head Injury e.g. SAH

ST elevation must be taken in the context of the clinical history.

Heart block
Atrioventricular block. For 1st-degree block, conduction is slowed without skipped beats. All normal P waves are followed by QRS complexes, but the PR interval is longer than normal (> 0.2 sec).

Heart block
Second degree heart block; Mobitz type I 2nd-degree atrioventricular block. The PR interval progressively lengthens with each beat until the atrial impulse is not conducted and the QRS complex is dropped (Wenckebach phenomenon); AV nodal conduction resumes with the next beat, and the sequence is repeated.

Heart block
Mobitz type II 2nd-degree atrioventricular block. The PR interval remains constant. Beats are intermittently nonconducted, and QRS complexes dropped, usually in a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave.

Heart block:
Third-degree atrioventricular block. There is no electrical communication between the atria and ventricles and no relationship between P waves and QRS complexes (AV dissociation). Cardiac function is maintained by an escape junctional or ventricular pacemaker

Bundle branch block and fascicular block

The bundle of His divides into the right and left bundle branches. The left bundle branch then splits into anterior and posterior hemifascicles. Conduction blocks in any of these structures produce characteristic electrocardiographic changes.

Right bunddle branch block:

Conditions associated with right bundle branch block x Rheumatic heart disease x Cor pulmonale/right ventricular hypertrophy x Myocarditis or cardiomyopathy x Ischaemic heart disease x Degenerative disease of the conduction system x Pulmonary embolus x Congenital heart diseasefor example, in atrial septal defects

Right bundle branch block:

Left bundle branch block

Left bundle branch block is most commonly caused by: coronary artery disease, hypertensive heart disease, or dilated cardiomyopathy. It is unusual for left bundle branch block to exist in the absence of organic disease.

Left bundle branch block:

arrythmias

Supraventricular tachycardia
A supraventricular tachycardia (SVT) is a rapid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node

Ventricular Tachycard (VT)

Ventricular tachycardia occurs when electrical impulses originating from the ventricles cause rapid ventricular depolarization (140-250 beats per minute). Since the impulse originates from the ventricles, the QRS complexes are wide and bizarre. Ventricular impulses can be sometimes conducted backwards to the atria. in which case, P-waves may be inverted. Otherwise, regular normal P waves (60-100 beats per minute) may be present but not associated with QRS complexes (AV dissociation).

Ventricular Fibrillation

Ventricular Fibrillation
Ventricular fibrillation occurs when parts of the ventricles depolarize repeatedly in an erratic, uncoordinated manner. The EKG in ventricular fibrillation shows random, apparently unrelated waves. Usually, there is no recognizable QRS complex.

Ventricular Fibrillation

Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White syndrome is characterized by the presence of an accessory atrioventicular pathway located between the wall of the right or left atria and the ventricles, known as the Bundle of Kent. This pathway allows the impulse to bypass the AV node and activate the ventricles prematurely. Consequently, an initial slur to the QRS complex, known as a delta wave may be observed. The QRS complexes are wide, more than 0.11 sec, indicating that the impulse did not travel through the normal conducting system. The PR is shortened, to less than 0.12 sec, because the delay at the AV node is bypassed

Wolff-Parkinson-White Syndrome