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Bahri Teaching hospital
prepared by yusif elamin
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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
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.
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.
Church at Haarlemmerstraatweg in Oegstgeest.
1. Describe How ECG Generated
2. Identfiy and measure ECG normal waveform
3.Practising a Systemic appoch to ECG
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
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
six limb leads (I, II, III, aVR, aVL and aVF) and six chest leads (V1–V6).
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.
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.
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
Any disturbance in the sequence of stimulation of this specialized tissue leads to
rhythmic disturbances called arrhythmias or conduction abnormality called heart
block.
Normal T wave characteristics
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
U wave - Osborne wave (J wave) Delta wave Epsilon Wave
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
Four Initial Features
Four Waves
Four Intervals
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.
RR
Useful as quick calculation for regular rhythms at regular rate
Useful for very fast regular rhythms, as likely to provide more accurate rate than large square 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:
Normal Or Left Axis Deviation
Normal Or Left Axis Deviation
Normal Or Left Axis Deviation
?
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
Normal rate is 60-100/min.
2. Pattern of QRS complexes
If irregular is it regularly irregular or irregularly irregular?
3. QRS morphology
4. P waves
5. Relationship between P waves and QRS complexes
6. Onset and termination
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 ?
we completed our introduction tutorial and we had the opportunity to :
please
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