Describe electrical activity in the myocardium
The myocardium is a large mass of muscle undergoing electrical changes; all cells are more or less transmitting an AP at the same time.
This generates a large changing electrical field which can be detected by electrodes on the body surface.
This is the electrocardiogram (ECG)
Electrodes outside of the cell 'see' a different signal to those inside.
What do the electrodes outside of cells record?
They record only CHANGES in membrane potential (there is no recording/no electrical activity when membrane potential is constant).
The electrodes on the skin therefore 'see ' 2 signals with each systole: one on depolarisation (at the beginning of the AP) and one on repolarization (at the end of the AP).
So one AP generates 2 signals.
Describe in general terms the pattern of spread of excitation over the normal heart
An action potential is generated by the pacemaker cells in the SAN (1) and electrical activity spreads over the surface of the heart to the AV node, where there is a delay of ~120ms (2).
After the delay the excitation spreads down the septum through the specialised Purkinje fibres of the left and right bundle of His branches (3) then out over the ventricular myocardium, from inside --> outside (endocardial --> epicardial surface) and then spreads upwards until all ventricular cells are depolarised (4/5)
Describe the pattern of repolarization
After ~280ms, cells be in to repolarise.
Repolarization spreads in the opposite direction over the ventricle to depolarisation (epicardial --> endocardial surface) - as the heart depolarises, it twists and contracts so repolarisation happens in the opposite direction.
Discuss the term Electrode 'View'
What an electrode 'sees' depends on its position relative to the spread of activity - depending on its position, it will see something different.
What are the rules governing the sign of the signal recorded by a positive recording electrode when depolarisation and repolarisation spread towards and away from that electrode?
Depolarisation moving towards an electrode creates an UPWARD going signal 'blip'.
Depolarisation moving away from an electrode creates a DOWNWARD signal 'blip'.
Repolarisation moving towards an electrode creates a DOWNWARD going signal 'blip'.
Repolarisation moving away from an electrode creates an UPWARD signal 'blip'.
Signal also depends on:
- How much muscle is depolarising (large amount of muscle = large signal)
- How directly towards the electrode the excitation is moving (direct/straight spread = large signal, the more indirect the spread of activity (at an angle), the smaller the signal).
Explain the P wave formation
Atrial depolarisation will produce a small upward deflection
(small because little muscle is depolarising, upwards because depolarisation is moving towards the view - towards the electrode).
Why is there is a constant line after the P wave?
Indicates the period the electrical activity is delayed at the AV node (no blips as no change in electrical activity)
Explain the Q wave formation
Excitation spreads about halfway down the septum, then out across the acid of the heart, producing a small downward deflection
(downward because depolarisation is moving away, small because depolarisation is moving away at an angle - not direct)
Describe the R wave formation
Depolarisation spreads through the ventricular muscle along an axis slightly to the left of the septum.
Produces a large upward deflection - upward because depolarisation moving toward view, large because lots of muscle is involved and the signal is moving directly towards the electrode.
Describe the S wave formation
Depolarisation spreads upwards to the base of the ventricles (near the valves).
This produces a small downward deflection (downward because depolarisation is moving away from the view, small because the depolarisation is not moving directly away - moving away at an angle).
Why is there a straight line after the S wave?
Period between depolarisation and repolarisation where there is no change in electrical activity so no signals.
Ventricular contraction (~280ms)
Explain the T wave formation
Repolarisation begins on the epicardial surface.
This spreads through the ventricular myocardium in the opposite way to depolarisation (from epicardium to endocardium).
Produces a small upward deflection (upward because repolarisation is moving away from view, medium because timing in different cells is dispersed).
Put all the different wave formations together
P wave - atrial depolarisation
Q wave - septal depolarisation spreading to ventricle
R wave - main ventricular depolarisation
S wave - end ventricular depolarisation
T wave - ventricular repolarisation
Why isn't there a wave for Atrial Repolarisation?
Atrial repolarisation got lost in the QRS complex (atrial cells repolarise at the same time as ventricular depolarisation).
Describe how the QRS Complex will change if the viewing electrode is moved around a circle with the heart at its centre.
As the electrode position moved around the heart, the directions and amplitude of the waves change predictably.
An electrode viewing the R wave head on will see a large upward deflection.
An electrode viewing the R wave from sideways on will see no signal
An electrode viewing the R end on sees a large downward signal.
Be able to place electrodes correctly to record (12-lead electrode)
Limb leads: one on each limb (only 3 are recording - right lower limb is neutral).
The limb leads provide a vertical heart of the heart.
6 chest leads provide a horizontal view of the heart:
V1- 4th intercostal space to the right of the sternum
V2 - 4th intercostal space to the left of the sternum
V3 - directly between the leads V2 and V4
V4 - 5th intercostal space at midclavicular line
V5 - level with V4 at left anterior axillary line.
V6 - level with V5 at left mid axillary line (directly under the midpoint of the armpit).
What is a "lead" and why do we compare multiple leads?
A "lead" is an electrical view of the heart (a particular electrode position).
By comparing multiple leads (looking at the heart from different angles) we can localise abnormalities and detect changes in electrical axis
What are differential amplifiers and why are they used?
Used because cellular signals are very small.
Differential amplifiers have one positive and one negative electrode but they are converted to one view.
Amplifiers take the signal coming in on the negative input and invert it, add it to the signal from the positive input before amplifying the total. [(1/n +P)a].
This produces a single electrode view.
Describe the Single Electrode View at Lead II
Positive electrode bottom left.
Negative electrode top left is converted to equivalent positive of negative bottom left.
Put the two together - two views from BOTTOM LEFT - same direction.
2 positives combined = 1 output.
Lead II views the heart towards the apex
Describe the Single Electrode View at Lead I
Positive electrode top left
Negative electrode top right is converted to equivalent positive of negative --> bottom left
Put the two together - single electrode view looking from LEFT SIDE.
Describe the Single Electrode View at Lead III
Positive bottom left
Negative top left is converted to equivalent positive - bottom right.
Put the two together - single electrode view looking at the heart FROM THE BOTTOM (straight up)
Describe the Single Electrode View at AVR
Looking at the heart from top right
Describe the Single Electrode View at AVL
Looking at the heart from top left
Describe the Single Electrode View at AVF
Looking at the heart from the bottom (view between Lead III and Lead II) +90 degrees from bottom.
Discuss the Rate of an ECG
Usually Lead II - a rhythm strip is used.
All ECG machine run at a standard rate (time scale is always the same)
Each large square is equivalent to 0.2s i.e. 300 squares/min
Calculate HR by 300 / (no. of squares in R-R interval)
For irregular rhythms, it is important to use a larger interval than one R-R interval.
For example multiplying the number of beats in 10 seconds by 6 (count the number of QRS complexes in 30 squares and multiply by 10)
What abnormalities would you identify in Atrial Fibrillation?
The P wave reflects atrial depolarisation and if the muscles are not contracting in a coordinated way (atrial fibrillin ation), the P wave will be absent.
Individual atrial muscle ifbres are contracting independently and there are only small depolarisation waves of varying strength - irregular fibrillation
There is no regular stimulus reaching the AV node but the ventricles still contract - other pacemaker cells take over so heart is still beating.
Depolarisations of different strengths reach the AV node. Some of these are capable of producing a depolarisation of nodal cells which is transmitted down the bundle of His to cause depolarisation and contraction of the ventricles.
QRS complexes are irregularly spaced - indicate irregular rate.
What abnormalities are there in a ventricular ectopic beat?
Ventricular cells gain pacemaker activity, causing ventricular contraction before the underlying rhythm would normally depolarise the ventricles.
The resulting ECG often appears wider and taller than that seen with the underlying rhythm.
Ventricular ectopic beats may occur every other beat, every third beat, every fourth best etc or in groups such as couplets, triplets etc. The example shown is a ventricular ectopic beat every other beat.
What abnormalities are there in Ventricular Fibrillation
Uncoordinated contraction of the ventricular myocardium causes it to quiver rather than contract properly.
What is the P-R interval normally?
Normally 3-5 small squares (0.12-0.2s)
What is Heart Block?
A communication problem between the atria and ventricles
What abnormalities are seen First Degree Heart Block?
The P-R interval is elongated/prolonged
There is a conduction delay but all electrical signals reach the ventricles.
What abnormalities are seen in Second Degree Heart Block Type I?
The P-R interval is erratic.
It follows a pattern of the P-R interval elongating until eventually a QRS complex is dropped (absent completely - there is a missed beat).
The system is then reset. Some but not all atrial beats get through to the ventricles.
What abnormalities are seen Second Degree Heart Block Type II?
Electrical excitation sometimes fails to pass through the AV node of Bundle of His.
Electrical conduction usually has a constant P-R interval but not all atrial contractions are followed by ventricular contraction.
There may 2 P waves for every QRS complex or 3...etc.
Sometimes the extra P wave is bounced back or superimposed on the T wave...
This is dangerous and can disintegrate entirely into complete (third degree) heart block.
Pacemaker may need to be inserted.
What abnormalities are seen in Third Degree (Complete) oHeart Block?
Atrial contractions are normal but no electrical conduction is conveyed to the ventricles.
The ventricles then generate their own signal through an ectopic pacemaker.
These beats are usually small. Regularly spaced P waves but P waves and QRS complexes bear no relation to each other.
How does a Bundle Branch Block change the ECG trace?
A Bundle Branch Block lengthens and changes the shape of the QRS complex.
There are many variations depending on the location of the block.
If there is abnormal conduction through either the right or left bundle branches, there will be a delay in the depolarisation of part of the ventricular muscle. The extra time causes the widening of the QRS complex.
Blocks of both bundle branches has the same effect as block of the His bundle and causes complete (third degree) heart block.
Explain about Left Axis Deviation
When the LV hypertrophies, it exerts more influence on the QRS complex than the RV.
Hence the axis may swing to the left and QRS complex becomes predominantly negative in Lead III.
Although left acid deviation can be due to excess influence of an enlarged left ventricle, in fact this axis change is usually due to a conduction defect rather than to increased bulk of the left ventricular muscle.
Explain about Right Axis Deviation
If the RV hypertrophies (more muscle), it has more effect on the QRS complex than the LV and the average depolarisation wave - the axis - will shift towards the right.
The deflection in Lead I becomes negative (predominantly downward) because depolarisation is spreading away from it and the deflection in Lead III becomes more positive (predominantly upward) because depolarisation is spreading towards it.
Right Axis Deviation is associated mainly with pulmonary conditions that put a strain on the the right side of the heart and congenital heart disorders.
Describe in outline the ECG changes associated with the acute phase of MI and myocardial ischaemia during exercise.
Features of MIs:
- S-T elevation
- Pathological Q-waves
- Inverted T waves
Localising the damage: the view with the most prominent abnormality could help you identify which part of the heart is affected and how badly including which coronary artery is blocked and whether the whole thickness of the ventricular wall is affected.
Pathological Q waves (more than 0.04s - 1small square wide, 2 mm deep). Present in full thickness myocardial infarction. Remain after other changes resolve so could indicate a previous MI.
On the following diagram label the structures involved in conduction of excitation over the ventricles
Bundle of His
Left Bundle Branch (posterior)
Left Bundle Branch (anterior)
Right Bundle Branch
What is R-R interval?
- From peak to peak of R-waves
- Shorter interval --> Faster heart rate
What is the QRS complex?
- Start of Q wave to end of S-wave
- Wider QRS complexes are associated with ventricular depolarisations that are not initiated by the normal conductance mechanism
What is the P-R interval?
Start of P wave to start of Q wave
Longer P-R intervals indicate slow conduction from the atria to the ventricle (1st degree heart block)
What is the ST segment?
- End of S-wave to start of T-wave
- The ST segment should be isoelectric. If it is raised or depressed this indicates myocardial infarction or ischaemia
What is the Q-T interval?
Start of Q wave to end of T wave
it is related to the duration of the action potential.
A prolonged Q-T interval suggests prolonged repolarisation of the ventricles. This can lead to arrhythmias as occur in long QT syndrome but this very rare.
Many drugs have been found to interact with a class of K+ channel, increasing AP duration, resulting in long QT and predisposing the individual to arrhythmias.
Long QT syndrome can result in sudden fainting brought on by stress or exercise.
The QT interval gets shorter with increasing heart rate and to assess this accurately it needs to be corrected for heart rate.
How might you get the fibrillating ventricle back into near normal activity?
With a defibrillator; this discharges a high voltage field which depolarise the whole heart allowing an organised rhythm to emerge.
What changes do you think you would see on the ECG trace of an individual with severe hyperkalaemia (serum K+ of more 7.0mmol/L or more) or hypokalaemia?