ECG Cellular and molecular events in the heart are associated with characteristic electrical changes millions of cells

s undergoing the same change almost simultaneously generates a biologically large electrical field flux in these field can be detected by electrodes placed on the body and graphically displayed as what is known as the ECG Individual cells fire an AP during systole with a characteristic waveform lasting ~250300ms External electrodes can see the depolarisation and repolarisation and give an indirect signal recording of the fluctuating electrical field around the body it does not record static potentials So for one AP firing, an electrode would record two spikes one for the de- and one for re-polarisation Since the AP spreads over the heart as a wave, not all cells are stimulated at exactly the same time therefore the resulting ECG is a result of both the changes in membrane potential and the spread of AP across the heart The AP is conducted from cell to cell via junctions through the intercalated discs It is triggered at the SA node when the pacemaker potential reaches threshold and the wave of depolarisation spreads over the atria It also reaches the AV node, where it is delayed for ~120ms after which the AV node fires and the AP passes along the Bundle of His within the ventricular septum As it spreads over the myocardium, it progresses from the endocardial to epicardial surface, propagating through the thickness of the ventricles It then progresses upwards through the muscle towards the base of the ventricles, to complete the myocardial depolarisation By now, no part of the myocardium has finished depolarising so nothing happens for 250ms until repolarisation occurs Depolarisation begins on the endocardial surface The heart twists itself to wring out, generating internal tensions During repolarisation, the heart relaxes in reverse to contraction from the outside in to avoid damaging itself from mechanical stresses This occurs because epicardial cells have a shorter AP than endocardial cells What the electrode sees is different depending on where the electrode is relative to the movement of electrical activity There are simple rules to predict the signal given an electrode position Depolarisation moving towards electrode = upwards deflection Depolarisation moving away from electrode = downwards deflection Repolarisation moving towards electrode = downwards deflection Repolarisation moving away from electrode = upwards deflection The amplitude depends on how much muscle is active and how directly towards or away from the electrode the wave of activity is moving

Consider an electrode looking up at the apex of the heart Atrial depolarisation causes a small upwards deflection AP moving towards apex, not much muscle contraction in the atria = P wave AV node retains the signal for ~120ms = PQ interval Excitation spreads halfway down the septum and out across the heart = Q spike downwards deflection as movement is slightly away from apex Depolarisation of the ventricle, spreading across the entire myocardium on an axis just left of the septum produces a large upwards spike = R spike The depolarisation spreads up to the base of the ventricles, away from the apex = S spike Nothing then happens for 250ms so the reading is flat until repolarisation This occurs, moving inwards and away from the apex so there is an upwards deflection = T wave, since the repolarisation is dispersed over time the wave is of lower amplitude P atrial depolarisation Q septal depolarisation across upper ventricles PQ interval = AV delay R main ventricular depolarisation S end of ventricular depolarisation T ventricular repolarisation ST interval = duration of systole The atrial repolarisation occurs during the QRS complex and is not detected As the electrode moves, the recorded signal also changes as relative position is different So it is important to know where the viewing angle is in order to interpret an ECG reading In a 12-lead reading, different views allow detection and location of abnormalities For each lead, at least two connections are required to the body to create a circuit There are two connections but only one viewpoint The two connections are connected to an amplifier, which inverts the signal from the negative electrode and adds it to the signal from the positive electrode this is amplified and produces a deflection on the ECG The negative electrode looks at the heart from the opposite position to the positive so it is virtually flipped and this has the same effect as physically moving it Leads I-III and the AV leads view the heart in the vertical (coronal) plane Lead I and AVL look at the left ventricle Leads II, III and AVF look at the inferior border AVR looks at the right atrium Lead I positive on left shoulder, negative on right shoulder Negative is flipped, now looking up from apex Viewpoint is in between the two negatives looking from the left side Lead II positive looking up at apex, negative on right shoulder Flipping moves negative to apex view, same as positive Viewpoint is apex view Lead III Positive looking from apex, negative looking from left shoulder

Negative flipped to lower right Viewpoint is from underneath the heart Augmented leads three connections (two negative, one positive) Here both negatives need to be inverted and added to the actual positive to give a single viewpoint AVR right shoulder positive, left arm and lower left view negative AVL left shoulder positive, right arm and lower right view negative AVF lower left view positive, right and left shoulder negative In addition to these there are six unipolar chest leads, numbered V1 to V6, which are placed in an array across the chest to view the heart on the horizontal (transverse) plane These leads look across the ventricles V1 4th IC right of the sternum V2 4th IC left of the sternum V3 midway between 2 and 4 V4 5th IC left (apex position, mid-clavicular line) V5 between 4 and 6, anterior axillary line V6 6th IC left, axillary line The QRS complex differs in shape depending on which lead is looked at Examining ECGs needs to be thorough to spot abnormalities Examine every part and aspect of the recording Actively seek out possible abnormalities Rate 300sq/min (1 large sq=0.2s), heart rate = 300/interval between two R spikes Rhythm regular or irregular, look for presence of P wave Axis perpendicular to lead with the smallest, most equiphasic deflection (AVL) P wave look for its presence and characteristics - accentuated in RA strain, prolonged or notched in LA strain, absent in atrial fibrillation PR interval - note its timing to look for heart block where normal is ~120ms (primary = prolonged PQ interval, secondary = dropped sync, complete = no sync) QRS complex orientation depends on the cardiac axis, normal duration of 0.12s and is prolonged in bundle block QT interval length of systole should be ~300ms T wave Pathological waveforms Q wave wider than 0.04s (1 square) and more than 2mm deep This is present in full-thickness MI, where the dead tissue creates an electrical window through which distant atrial activity can be seen ST elevation and inverted T waves can also be seen in patients with MI Describe in general terms and draw the changes in membrane potential of cardiac pacemaker and ventricular myocardium during systole

Cardiac pacemaker potential has a triangular waveform with a rapid upstroke and downstroke this is preceded by a gradual spontaneous depolarisation towards threshold Myocardial potential initially resembles an axonal potential, but after depolarisation calcium channels open and maintain this state for ~250-300ms before it repolarises, giving an approximately trapezial waveform Describe in general terms the pattern of spread of excitation over the normal heart, from the SA to AV nodes and through the ventricles A potential is initiated in the SA node, from where it spreads over the atria before reaching the AV node here it is delayed for ~120ms before it passes via the Bundle of His into the ventricular septum Excitation spreads over the ventricles outwards and down towards the apex, across the thickness of the heart from endocardium to epicardium, completing coverage by proceeding up towards the base of the ventricles in the terminal branch bundles Define the terms depolarisation and repolarisation Depolarisation is a change in the membrane potential towards a positive charge, and repolarisation is a return to normal resting levels, negative relative to the outside of the cell Describe the signal recorded by an extracellular electrode placed near a cell during systole A single electrode would record the change in the electrical charge one deflection each for depolarisation and repolarisation with a latent period in between since it does not record standing charges State the rules governing the sign of the signal recorded by a positive electrode when depolarisation and repolarisation spreads towards and away from that electrode A positive electrode gives an upwards deflection when depolarisation moves towards or repolarisation moves away from it, a downwards deflection is given when depolarisation is away or repolarisation towards The amplitude is governed by how directly towards or away the excitation is moving and how large the field is as in how much cardiac muscle is electrically excited Describe the form of the signal recorded by a single electrode viewing the heart from the apex, labelling PQRST and identifying the signals associated with atrial depolarisation, ventricular depolarisation and ventricular repolarisation A small upwards deflection, the P wave, precedes the QRS complex by roughly 120ms due to AV node delay

The QRS complex is a slight downwards, followed by a large upwards then downwards deflection caused by the lateral, outwards then upwards spread of excitation across the ventricles via the Purkinje fibres The T wave is an upwards deflection caused by repolarisation moving in a wave away from the apex Describe how the QRS complex will change if the viewing electrode is moved in a circle with the heart at the centre The R spike will change in amplitude and orientation most obviously if the electrode is moved largest upwards in the apex view Moving around the heart around the inferior and right border, then over the atria back down to the apex would cause a reduction in amplitude and then a flip to downwards deflection, largest when looking from over the right atrium When the viewing angle is perpendicular to the cardiac axis, there is no deflection as the spread of excitation is parallel to the plane of view not moving towards or away from the electrode Place positive and negative electrodes correctly to record leads I, II, III, AVR, AVL, AVF and V1-V6, stating the single electrode views for the multipolar leads Lead I: Positive LS, Negative RS, VP = left lateral surface Lead II: Positive APX, Negative RS, VP = apex, left lateral surface Lead III: Positive APX, Negative LS, VP = inferior surface AVR: Positive RS, Negative LS/LL, VP = right shoulder AVL: Positive LS, Negative RS/LL, VP = left shoulder AVF: Positive LL, Negative RS/LS, VP = perineum V1: 4th IC, right sternal V2: 4th IC, left sternal V3: Between 2 and 4 V4: 5th IC, left mid-clavicular line V5: Between 4 and 6 V6: 6th IC, left axillary line Describe the ECG appearance of ventricular ectopic beats, atrial and ventricular fibrillation and the three types of heart block Ventricular ectopic beats show bizarre enlarged QRS complexes without preceding P Atrial fibrillation displays with absent P waves and irregular QRS there may be flutter of the baseline Ventricular fibrillation shows rapid, irregular and bizarre RS spikes Primary heart block has normal rhythm but a prolonged PR interval Secondary has QRS only after every 3rd, 4th or 5th P wave or showing the Wenkebach phenomenon cyclic gradual elongation of PR interval until a beat is dropped Complete heart block shows no correlation between P and QRS, with slow ventricular rate

Describe the ECG changes associated with acute MI and myocardial ischaemia during exercise Acute MI presents with several ECG abnormalities - ST elevation with T inversion in leads facing the infarct and accentuated Q waves, wider than 0.04 seconds and deeper than 2mm Myocardial ischaemia creates ST depression and symmetrical T wave inversion