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THE BASICS   ECG stands for electrocardiogram. It is a method of measuring the efficiency of the conducting system of the heart.

P represents depolarisation of the atria QRS represents depolarisation of the ventricles T represents repolarisation of the ventricles There is no wave for repolarisation of the atria because this is covered up by the depolarisation of the ventricles. It is quite normal for no q wave to be present.

ECG paper Each large square represents 0.2s (200milliseconds) and each small square represents 40ms (5 small squares per large square).   1 big square is 0.5cm 1 small square is 1mm Five large squares represent 1 second. There are 300 large squares per minute. So, if a QRS occurs once every large square, the HR is 300.min. However, if they occur once only 4 squares, the heart rate is 300/4 = 75bpm. When you work this out, you say you are doing the R-R interval.

Segments and intervals

Segment This term is used to refer to a part of the ECG between the end of one wave and the start of the next. The two main segments are the PR segment and the ST segment. Intervals This term is more ambiguous and refers to various stretches of the ECG:  PR Interval – this is from the beginning of the P wave, until the beginning of the QRS complex. It measures the time taken for excitation to spread from the SA node (all the way through the AV node, and various bundles) to the ventricular muscle.     Normal interval – 0.12-0.2s – i.e. it should be between 3-5 little squares. QT interval – this is from the beginnings of the QRS complex until the end of the t wave. QRS duration – this tells us the amount of time it took the signal to spread throughout the ventricles. Normal interval – 0.12s (i.e. about 3 little squares) – however various conditions can cause a lengthened QRS duration. Practicalities Normally you take a „12-lead ECG‟. This term is confusing because the word „lead‟ has two meanings.

and thus 12 graphs can be produced.  To try and avoid confusion here I will refer to the physical connections as „electrodes‟ It is important to attach your electrodes in the right place so they you get signals that can be properly interpreted. It can mean the physical electrical cable that you use to connect the reader with the patient. If they don‟t have an upper limb. this calibration signal should be seen on the print out: Taking a reading     The patient should be laid down and relaxed (to prevent muscle tremors which may cause interference) Now connect the electrodes Calibrate the machine Make the recording! Placing your electrodes You should connect the electrodes in the following order:        V1 – 4 IC space on the right sternal edge V2– 4 IC space on the left sternal edge V4– 5 intercostal space at the midclavicular line. Thus it is important that the reader is calibrated correctly so we can interpret the wave height.  So a ‟12-lead ECG‟ has 12 of these lines along which conductivity is measure d. However. The electrode is Red – “red right” RL – right leg – the electrode is black. At the start of each ECG trace. there are only 10 physical electrodes and „leads‟ that you attach to the patient‟s body. V3 – place this half way between II and IV so that it sits on the 5 rib.    The electrode is yellow – “lemon left” RA – right arm. Calibrating the machine The height of the waves can be important in defining certain conditions. LA – should be connected to the left arm – it can be done anywhere on the arm. or. th th th th th th .at the apex beat. V6–mid axillary line at the 5 intercostals space V5 – anterior axillary line at the 5 intercostal space. A signal of 1mV should cause the graph to rise 1cm (2 large squares). along which electrical conductivity is measured. but use your common sense – for example if they have a tremor don‟t place it at the extremity. you should try to still place the electrode distally to the shoulder joint on the stub (if they have one – they will pretty much always have something there!). more correctly it refers to an „imaginary line‟ between two ECG electrodes.

Bipolar limb leads Lead Lead I Lead II Lead III From RA (-) RA (-) LA (-) To LA(+) LL (+) LF (+) Plane Lateral Inferior Inferior Viewing t Lateral wall of le Diaphragmatic Diaphragmatic You might wonder how the LA can operate as both a negative and a positive electrode simultaneously. so it is relatively more positive than the Right arm. Each type of lead basically measures the conductivity of the heart in a different plane. Bipolar limb leads – these comprise of a positive electrode and a single negative electrode. there won‟t be ST elevation in 7-9. bipolar (limb) leads. you have to take 4-6 off and put them on the back. If there is posterior MI. Well so do I! I guess these voltages are relative. and thus looking at the diaphragmatic surface. 5 IC space. and thus this allows us to see the activity of different parts of the heart.posterior axillary line. through which the conductivity of the heart are measured. Augmented Unipolar Limb leads Lead aVR From LA+LL (-) To RA (+) Plane Lateral (reversed) Viewing the… Right atrium* . which consists mainly of the left ventricle.  LL – left leg – the electrode is green (spleen! – just means put it on the left ankle – put it over a bony prominence!) LA – left arm – the lead is yellow – lemon left! Note that the colouring scheme of leads varies.    7. chest unipolar leads and augmented unipolar leads. If there is just anterior ischaemia. left hand side 8 – between 7 & 9 9 – left spinal edge at the 5 IC space th th Leads There are three types of lead. Also note that the „inferior‟ plane leads are viewing the heart from below. this is to look if there is just anterior ischaemia (don‟t thrombolise) or if there is posterior MI. Unipolar leads – these utilise a single positive electrode. and then use a combination of other electrodes to represent a negative electrode. whilst still being more negative than the left leg. In cases of massive posterior MI there will be marked anterior ST depression. there will be ST elevation in the posterior leads.

Lead V1 V2 V3 V4 Plane Septal Septal Anterior Anterior Viewing the… Septal wall of ventricles Septal wall of ventricles Anterior surface* Anterior surface* .Left Unipolar chest leads These account for the other 6 leads of the 12-lead ECG.aVL aVF RA+LL (-) RA+ LA (-) LA (+) LL (+) Lateral Inferior Lateral wall of left ventricle Diaphragmatic surface *although the view is pretty non-specific Some people find Einthoven‟s triangle helpful in understanding the leads: (sorry about the captions in Dutch but I‟m sure you can understand!) Just thought of a little trick to remember which goes where: aVF . Each of the electrodes is positive.Right aVL .Foot aVR .

but the wave produced is the average of this. and a negative one. This creates a nice positive R wave in lead II. aVR however has its positive and negative electrodes the other way around. and this is because it is a NEUTRAL electrode. A normal cardiac axis will cause a positive signal in all 3 of these leads – because between them these leads measure the lateral (right to left) and inferior dimensions – and the signal is travelling laterally and inferiorly! The deflection is greatest in lead II because this lead measure both laterally and inferiorly. there is a positive line when the signal travels towards a particular lead. it means the signal is negative and moving away from the lead. When the depolarisation wave is moving at right angles to the lead. When the R wave is greater than the S wave. this means the signal is generally positive. Therefore. and thus there is a negative signal produced in this lead. From here. then R and S waves will be of equal size. You can determine the direction of the cardiac axis (to check if it is normal or not) by looking at leads I-III. Imagine looking at the heart from the front. This direction of spread of the signal is known as the cardiac axis. and so the signal travels against this lead. when the signal travels away from a lead. Graph Production When the graph is drawn. and thus not utilised in the measurements themselves.V5 V6 Lateral Lateral Lateral wall of left ventricle Lateral wall of left ventricle *note that this consists mainly of the right ventricle You may notice that the Right Leg electrode is not mentioned. and therefore moving towards the lead. . Depolarisation spreads throughout the heart in many directions at once. When the S wave is greater than the R wave. they head along lead II. the waves of depolarisation generally spread through the heart from 11 o‟clock to 5 o‟clock.

. The general rule is that V1 and V2 have a negative QRS. and points away from any lead where the S is larger than the R. right axis deviation is often a result of right ventricular hypertrophy (due to pulmonary disease) but in left axis deviation the most likely cause is NOT hypertrophy. however. and V5 and V6 have a positive QRS The point where R and S waves are equal indicates the site of the septum . the overall flow of charge. It is associated mainly with pulmonary conditions that put a strain on the heart. they prompt you to look for other things. and thus you only have an approximation – thus this is why it is useful to have several leads! Where R and S are of equal size. We call this left axis deviation. V3 and V4 have roughly equal sized R and S waves. The overall direction of charge is now from 1-7 o‟ is called the transition point. the lead I signal will become very weak. QRS in the V leads    V1 and V2 – look at the right ventricle V3 and V4 – look at the septum V5 and V6 – look at the left ventricle There is more muscle on the left than the right – therefore the ECG trace is biased towards the left of the heart. is away from these leads – thus leading to a negative QRS. This alters the signal. and to some extent at the septum. This axis shift is called right axis deviation. Left ventricular hypertrophy can also cause an axis deviation. and lead III will now have the tallest QRS (not lead II). whilst leads II and III will become negative. This is often a result of a conduction defect rather than left ventricular hypertrophy.However. then the transition pointwill not appear in lead V3/V4. Looking at these allows you to determine of there is right ventricular hypertrophy – because if there is. the cardiac axis is at 90‟ to that particular lead. This means that for leads looking at the right of the heart. However. Also remember. and therefore extra signal strength on the right side of the heart. because there is extra muscle. but a conduction blockage. but instead may appear in V5/V6. in right ventricular hypertrophy the cardiac axis becomes displaced. as the enlarged ventricle shifts the septum to the left. Deviations in the cardiac axis may not themselves be significant – they can occur in normal people (often if they are very tall. such that lead I will display a negative QRS. Basically. or very thin or fat). In this. the cardiac axis points to any where the R is larger than the S. it is unlikely that it will point directly towards any of the leads.

This is usually lead II or V1. there are 2 or 3 p waves. Second degree Heart block This is where there is an intermittent absence of QRS complexes – and thus an indication that there is a blockage somewhere between the AV nodes and the ventricles. . acute rheumatic carditis. All the waves will still be present. and a fairly constant PR interval. 1 big square. The PR interval the time taken for the depolarisation to spread from the SA node to the ventricular muscle.2s.Conduction Problems Always remember the pattern of conduction: SA node ≫ AV node ≫ His Bundle ≫ bundle branches When looking at conduction problems.e. then we call it first degree block. digoxin toxicity or electrolyte disturbance. but every now and again there is an absent QRS (pictured above). you are best to look at whichever lead shows p waves most clearly.2s – i. There are three types of this:  Mobitz type 2 phenomenon – this is where there is a regular rhythm. basically for every QRS. This should not be greater than 0. First degree heart block is not in itself very important – it can be a sign of coronary artery disease. there will just be a gap between the p wave and QRS complex. First degree Heart block If the PR interval is greater than 0.

and the cycle begins again. The ventricles are still excited by their own internal „ectopic pacemaker‟ system! Thus the definition of complete heart block is:  P wave ~90/min (more p waves than QRS complexes) . then a shortened PR interval and normal QRS. Wenckebach phenomenon (aka Mobitz type 1) – progressive lengthening of the PR interval followed by an absence of the QRS. The cycle is variable in length. and the R-R interval shortens with the lengthening of the PR interval  2:1 and 3:1 conduction – there is one normal cycle. then two cycles without a QRS (3:1) – pictured below Causes     Acute – MI Chronic – heart disease (CHD) Mobitz type 2 and Weckenbech don‟t require and specific treatment X:1 block may require a pacemaker (temporary or permanent). especially if the ventricular rate is slow Third degree Heart block – complete heart block This occurs when atrial contraction is normal. but no beats are conducted to the ventricles. then one cycle with an absent QRS (2:1) or there is one normal cycle.

>3 little squares) . this is still the case. and is often transient Chronic – often due to fibrosis around the Bundle of His. however they should still get a pacemaker because this situation can change at any time If the number of atrial and ventricular complexes is equal then we call it AV dissociation. And in bundle branch block. or bundle branch block of both branches Always indicates underlying disease – more often fibrosis then ischaemia Consider temporary or permanent pacemaker More info about complete heart block:   Patients with AV block can be haemodynamically stable. Thus.    o   QRS ~36/min Variable PR intervals No relationship between P wave and QRS complexes. and not AV block Bundle Branch Block If the wave of depolarisation can reach the intraventricular septum. then the PR interval will usually be normal. and thus thus duration of the QRS is lengthened. in bundle branch block there is:   Normal PR interval Lengthened QRS duration (greater than 120ms . However. Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles QRS will generally be broad (~160ms – as opposed to a maximum of 120ms in a normal heart – 4 little squares as opposed to 3 little squares) Right axis deviation Escape rhythms present (more on these later) Causes:    o MI – it will occur acutely. but both are present. the time taken for depolarisation to spread throughout the ventricles is altered because of the block.

left ventricular depolarisation continues as normal. It often indicates right sided heart disease. You can use the word WillaM to try and remember this one! Causes    Ischaemic disease – if the patient has had recent chest pain. you should look at the P waves and the PR interval – and the P waves will still be related to the PR interval. William has „LL) in the middle for left.Thus to differentiate this from complete heart block. In RBBB this still happens. this does not cause abnormalities of the ECG. But after this has happened. the depolarisation of the septum occurs from right to left. So. then the right ventricle does not depolarise at the same time as the left. Right Bundle Branch Block (RBBB) In many people. This creates a distinctive pattern on the ECG:  V1 – creates an „M‟ shaped QRS – because the R wave is positive. S is negative (and R1 is also positive). . and V6 makes a “W” Important – the QRS complexes will also be wide – greater than 120ms The axis of any BBB can be either normal. Aortic stenosis If the patient is asymptomatic. then no treatment is needed But how do you know which side is which?! – well. The QRS sign. LBBB is likely to indicated MI. LAD or RAD. then another up („R‟)  V6 – creates a „W‟ shaped QRS – because the R wave is negative. In the normal heart. and physiology behind LBBB is pretty much the exact opposite of that in RBBB. NB – the William and marrow signs are not always that great. It is most commonly normal. but because the RBB is blocked. and thus thrombolysis should be considered. There is no specific treatment – and it may often be caused by an atrial septal defect Left Bundle Branch Block (LBBB) Usually indicates left sided heart disease. and causes a second R wave (R1). the right ventricle then depolarises. and Marrow has RR in the middle for right! You could also try the sentence – William left his Marrow – if this helps you remember the words and better. and S is positive (and R1 is also negative) You can try to remember this with the word MarroW – because V1 makes an M. so the sign is opposite. and produces a normal R and a normal S wave. This is also known as an „RSR‟ pattern – there is an up („R‟) then a down („S‟).

the right fascicle. You can have a sinus tachycardia. Treatment    A new bifascicular block in a patient with acute MI needs emergency pacemaker placement A bifascicular block with RBBB and LAH is as stable condition that can go unchanged for years. You will need to look at old ECG‟s to establish how long it has been there A bifascicular block with RBBB and LPH should be considered for pacemaker therapy. So there is one on the right and two on the left. sinus bradycardia. sometimes called LPH – left posterior hemiblock). the left anterior fascicle and the left posterior fascicle. These three fascicles are. the patient should be referred for emergency pacemaker. sometimes called LAH – left anterior hemiblock) or left posterior fascicular block (LPFB. or junctional rhythm). If the pattern is new or may only see the „M‟ in lead V1 LBBB – you may only see the „W‟ in lead V6 Bifascicular block This refers to any situation in which two of the three main fascicles of the His/Purkinje system are blocked. the region around the AV node (known as nodal. Note – both LPH and LAH can cause left axis deviation Rhythms Rhythms can originate in 3 places in the heart – the SA node.  Usually it refers to RBBB with either left anterior fascicular block (LAFB. or the ventricular muscle Sinus Rhythm This basically means that the rhythm of the heart is being controlled by the SA node – i.e. and also sinus arrhythmias.  Some people consider LBBB a bifascicular block because technically LBBB occurs above the bifurcation of the LAF and the LFP. The way to tell if it is „sinus‟ or not is   There is one P wave per QRS There is a constant PR interval Sinus arrhythmia . this is the „normal‟ way the rhythm of the heart. and thus both are blocked.  RBBB .

hypothermia. and so the T wave is an abnormal shape. Thus. junctional region.Sinus tachycardia Associated with. sinus rhythm is a supraventricular rhythm. exercise. as is junctional rhythm. o Unless! – there is also a right or left BBB. or atrial muscle. fear. On the ECG you can see atrial escape where there is: . Repolarisation is also abnormal. and some part of the atrium starts the depolarisation instead. thyrotoxicosis Sinus bradycardia Associated with. myxoedema. These will produce:  Normal QRS complexes – because the part of the heart producing the QRS is not in the ventricles . and thus the QRS us abnormal. no matter if the producing part of the heart was the SA node. It occurs when the normal depolarisation of the SA node has not the conduction will still pass through the ventricles as if it was produced normally. seen immediately after MI Supraventricular rhythms This is any rhythm that originates outside of the ventricles. pain. via the bundle of His. and left and right bundle branches. and spreads to the ventricles in the normal manner. in which case the QRS may be wide Ventricular rhythms – the bradycardias The spread of the electrical charge in this case is abnormal. athletic training. haemorrhage. There will be:  Wide QRS complexes Atrial escape This is a supraventricular rhythm. fainting attacks.

Accelerated idioventricualr rhythm Normally. except that where an escape beat occurs later than expected. and not a result of a bundle block. Note there is no wave before the escape in this instance – because in this case the escape is a result of the SA node failing to fire (and the junctional escape also failing to kick in). but it has been generated by the ventricles. an extrasystole occurs earlier than expected. However. whereas in branch block. the ventricular rhythm is slower than that of the SV node. although you may see it without complete heart block.   An abnormal p wave . normal rhythm is not restored. Note that in this type of escape. normal rhythm is restored afterwards. as well as abnormal T waves Extrasystoles These basically have the same appearance as their corresponding escape beats. there is a rhythm of around 75pm.because the excitation has begun somewhere away from the SA node Normal QRS Normal beats after the abnormal one Junctional escape    No p waves Normal QRS Slightly slower rate (~75bpm max) Ventricular escape Most commonly seen in complete heart block. in this particular instance. You should not confuse it with ventricular tachycardia – which requires a heart rate of over 120bpm  There are widened QRS complexes. and it may occur as a one off instance. . This is often benign and need not be treated (although it is also associated with MI).

the rhythm is roughly sinus rhythm In atrial tachycardia. the rhythm is fast Atrial flutter    Rate >250bpm No flat lines between P waves („saw tooth p waves‟) Often associated block – remember the AV node cannot pass on rhythms of greater than about 125bpm. then atrioventricular block occurs.  When tachycardias occur intermittently they are called „paroxysmal‟. then it is 3:1 block. The tachycardias These are the result of foci either in the atria or in the junctional ( AV node) region depolarising quickly. the ventricular rate will be 125. SUPRAVENTRIUCLAR TACHYCARDIAS Atrial tachycardia      o o Atria depolarise >150bpm P waves superimposed on the t wave of the preceding beat QRS complexes are the same shape as normal The AV node cannot conduct faster than 200bpm. Normal QRS  Atrial extrasystole – Normal QRS. To identify the origin of the tachycardia you have to look at the p wave. thus if there is an atrial rate of 250. Differentiating from 2 In 1 and 2 st nd nd degree heart block: degree heart block. if the rate of atrial depolarisation is faster than this. . Junctional extrasystole – absent or misplaced P wave – because the depolarisation travels towards the atria and the ventricles. not just away from the atria and towards the ventricles like a normal beat. not followed by QRS complexes. and 2:1 block will be present. even if they look like T waves. where there are some p waves.  P waves may be difficult to discern from T waves – however you can tell if they are p waves because they occur regularly. normal looking beat – apart from it occurred earlier than expected. If the rate ventricular rate is 100. and the atrial rate is 300. In the example below you can‟t see t waves – they are all p waves.

Thus. Applying the pressure basically reduces the frequency of QRS complexes.Junctional (nodal) tachycardia    Due to an area around the AV node causing depolarisation – results in p waves very close to the QRS.and are sometimes called atrioventricular nodal re-entry tachycardias (AVNRE). . and increase the time of conduction across the AV node. resulting in wide and abnormal QRS complexes. This will reduce the frequency of discharge of the SA node. by applying pressure to the carotid sinus you can:    Reduce the rate of some arrhythmias Completely stop some arrhythmias It will have NO EFFECT ON VENTRICULAR TACHYCARDIAS – thus is can help you differentiate. This causes an abnormal spread of charge through the ventricles. Basically – there are probably no p waves. but a normal. or no p waves visible. QRS is normal – because like all supraventricular arrhythmias the ventricles are still activated in the normal way. and allows the underlying atrial arrhythmia to become more visible. Carotid sinus pressure By applying pressure to the carotid sinus you can stimulate the AV and SA nodes via vagal stimulation. VENTRICULAR TACHYCARDIAS These are caused by a foci in the ventricles discharging at a high frequency. regular QRS These are usually due to small re-entry circuits around the AV node.

Atrial fibrillation      No p waves – just an irregular baseline Irregular QRS – between 75-190bpm Normal shape QRS – because conduction through the AV node is normal In V1 the trace resembles atrial flutter Normal T waves . it is most likely AF with BBB FIBRILLATION This occurs when individual muscle fibres contract of their own accord. Left axis deviation normally means ventricular in origin If the QRS‟s are irregular. from VT  o  o o o o o Remember the clinical state of the patient: If they have just had an MI it is most likely to be VT An isolated incidence of broad complex tachycardia is more difficult to differentiate: Look very carefully for p waves (only present in BBB not VT) Compare the tachycardia to the patient‟s normal rhythm (if possible) – if the QRS is the same shape in both then it is BBB with supra-v tachycardia If the QRS is >160ms (4 small squares) then it is most likely ventricular.     QRS is broad T waves difficult to identify No p waves Regular QRS (~200bpm) REMEMBER – you also see wide and abnormal QRS complexes in bundle branch block Differentiating BBB with supraventricular tachycardia. So far all the rhythms we have looked at have involvedsynchronous muscle contraction.

When this occurs. no P. and back into the atria. This occurs in about 0. and is discussed in more detail in the Atrial Fibrillation article Ventricular fibrillation   No discernable pattern – no QRS. very high!) The vast majority of patients will be asymptomatic. Findings in an asymptomatic individual:      Sinus rhythm Right axis deviation Short PR interval Short QRS complex Delta wave – this is a short upstroke that occurs just before the QRS. It basically looks like the upstroke of the R wave is a bit bent – it starts off with a low gradient. This sudden death can occur when there isparoxysmal tachycardia.e. . and then increases to its normal gradient. in some people there exists anaccessory pathway through which conduction is able to travel.6% of those with WPW. Conduction is able to travel through this accessory pathway. However.Atrial fibrillation is a particularly common arrhythmia. sometimes called a re-entry circuit. the signal from the atria. This is usually on the left side of the heart. but there is a risk of sudden death. and is not delayed by the AV node. travels down through the accessory pathway. and then back up the bundle of His.     The accessory pathway is known as the bundle of kent. and thus there is pre-excitation of the ventricles. no T Patient is very likely to lose consciousness – thus the diagnosis is easy! WOLFF-PARKINSON-WHITE SYNDROME (WPW syndrome) In normal people the only route from the atria to the ventricles is through the AV bundle. This sets of a loop of depolarisation. The incidence of WPW syndrome is between 1-3% of the general population (i.

Q waves – these show the spread of depolarisation of the ventricles travelling in the horizontal plane. QRS complexes are broad – because pacemakers usually stimulate the right ventricle – and thus the depolarisation is ventricular in origin.Findings during re-entry tachycardia:   No p waves tachycardia PACEMAKER You should probably know what an ECG looks like when a pacemaker is present:    Occasional P waves. thus they are often not present. When pathological Q waves are present (basically big Q waves . Lead III is a good one to look at Q waves. because the charge travels equally in both directions and cancels itself out overall. then this is basically a sign that part of the heart tissue is dead – because it is no longer „cancelling out‟ the opposite side of the heart. not related to QRS QRS is preceded by a big spike – which is the pacemaker stimulus. and they are often normally present here.see MI notes for definition). .

thus lead I which measures laterally from right to left now gets a negative signal because the signal is going from left to right. except>100bpm Seen in All leads (best to look at the rhythm strip) All leads (best to look at the rhythm strip) All leads (best to look at the rhythm strip) Lead I Pathology Sinus Tachycardia Could just be someone has done some exercise! Could be some sort of respiratory problem This is normal in young fit people Sinus bradycardia Same as above except<60bpm Right ventricular hypertrophy Negative QRS Because the cardiac axis has shifted from 11-5 o‟clock to 1-7 o‟clock. Right ventricular hypertrophy Taller QRS Lead III – becomes taller than lead II Because lead III measures vertically but also slightly left to right.Abnormality Sinus rhythm (not an abnormality I know!) ECG sign regular p waves. and not an increased bulk of left ventricular tissue. Lead II. . negative leads II and lead III QRS Equally sized R and S now seen in V5/V6 Leads I-III Left axis deviation – this is often the results of a conduction defect. This axis shift is called right axis deviation. and each p wave is followed by a QRS. Left Ventricular Hypertrophy Transition point moved to the left – equal sized R and S (normally seen in V3/V4) Small lead I QRS. This axis shift is called right axis deviation. and this is pretty much the exact direction of the new shifted axis. measuring from right arm to left leg is no longer lined up as well. 60-100bpm Same as above.

this not only transmits a signal throughout the rest of the ventricles to depolarise them This is an AV node block Can be caused by CAD. The QRS can be regular or irregular. Often associated block. usually benign and generally doesn‟t require specific treatment. It can be very difficult to see t waves – what looks like a T wave will probably just be a p wave. The p waves occur at very regular intervals. There will be afibrillating baseline due to uncoordinated activity. 100 or 75 bpm due to various blocks. or no QRS visible. Alcohol excess 6. or an SA node block. Thyrotoxicosis (hyperthyroidism) 3. Sepsis 4. some? Rhythm strip As well as no p waves.e. Caused by a foci of the atria (outside of the SA node) depolarising quickly Due to a „re-entry‟ loop.2s (one big square) 1 degree heart block st Allover – best in I or V1 This can be an AV node block (nearly Progressive lengthening of the PR interval followed by absent QRS. acute rheumatic carditis. normal QRS P waves very close to QRS. digoxin toxicity.Wencebach nd Atrial tachycardia Junctional tachycardia >150bpm. QRS is normal PR interval >0. . can be caused by CHD or acute MI. Ischaemic heart disease 2. in which case Atrial Flutter Tachycardia Can‟t tell if T/P waves are present – rhythm is too fast (250bpm). PE Generally Note that AF can also co-exist with complete heart block. Irregularly Irregular.g. then cycle repeats. there are QRS complexes at a lower rate than the p waves Rhythm strip Lead where p waves are most easily visible – you should use drugs to slow down the heart rate to see what is going on Any where p waves are best seen Anywhere the QRS will be regular! There will be saw tooth p waves that occur at 300bpm. irregular QRS (but QRS is normal shape) Might look messy! E. The causes of atrial fibrillation are: 1. Cycles are variable in Anywhere always). p waves superimposed over t waves of preceding beat. but the QRS complexes will only be at 150. there is an area of depolarisation near the AV node. the rhythm will be irregularly irregular. Valvular heart disease 5. i. or electrolyte disturbance It is NOT an medical emergency 2 degree heart block Mobitz type 1 .Atrial fibrillation Absent P waves – just anirregular baseline.

but it ismost commonly normal Anywhere Best in II and V1 May require a pacemaker. The rhythm of the ventricles is the escape rhythm. However. from which there is often no escape rhythm. RBBB – right bundle branch block These are infra-Hisian blocks. ECG may appear normal. the time taken for the depolarisation to spread throughout the ventricles is longer – thus QRS complex duration is lengthened. The two R waves indicate the depolarisation of the right and left sides of the heart at different times (the right depolarises after the left). and be broad (>120ms). It can progress to complete heart block. Can be caused by CHD or MI 2:1 and 3:1 conduction This is the ratio of P:QRS Complete (third degree) heart block 90 P waves/min. the wave of depolarisation can still reach the IV septum. In the acute setting it may be caused by MI RBBB – may indicate right sided disease. You can remember the pattern with the word MarroW – there is M in V1. and thus this needs treatment! the definitive treatment is an implanted pacemaker.Mobitz type 2 length. but can present with: Dizziness / light-headedness / syncope This can be an SA node block. This always indicates underlying disease – the disease is often fibrosisrather than ischaemia. or far more commonly infra-Hisian block(distal block). QRS will often have an abnormal shape. then the PR interval will be normal – and it is. This creates a distinctive pattern: V1 – there is an M shaped QRS – this is sometimes called an RSR pattern V6 – there is a W shaped QRS Wide QRS (120ms) LBBB – left bundle branch block V1 – there is an W shaped QRS V6 – there is a M shaped QRS Wide QRS (>120ms) The axis can be deviated either way in BBB‟s. and the „rr‟ tells you it is on the . only about 38 QRS/min. particularly if the rate is slow This is an AV node block. Atrial activity will be completely normal. the P-P intervals will be regular. but this conductivity does not pass into the ventricles. R-R interval shortens with lengthening of PR interval Absent QRS every now and again Anywhere - It is usually symptomless. as will the R-R intervals – they are just not in time with each other. However. and not relationship between the P waves and the QRS complexes. and W in v6. but it can occur in MI.In some people there may be2 R waves. In bundle branch blockages.

dilated cardiomyopathy. fainting.inverted) Normal QRS Some normal beats after Junctional escape the abnormal one Anywhere This occurs when the SA node fails to depolarise. thyrotoxicosis Examples include: Ventricular rhythms (aka escape rhythms) Atrial escape Abnormal p wave (e. Instead. and it is often caused by an atrial septal defect. Causes: Aortic stenosis. exercise. seen immediately after MI Associated with. myxedema (hypothyroidism). acute MI.g. haemorrhage.right! There is NOT specific treatment. and in more severe cases. athletic training. heart failure. some other part of the atrium depolarises and sends the signal to the ventricles. fear. hypothermia. Remember the pattern withWillaM. Associated with. In the acute setting it may be caused by MI LBBB – often indicates left sided heart disease. CAD Symptoms: Syncope. pain. Those with syncope and / or heart failure will usually be treated Sinus bradycardia Normal rhythm <60bpm Anywhere with a pacemaker. Wide QRS complexes Anywhere Sinus rhythms LBBB RBBB Sinus Tachycardia Supraventricular rhythms Normal rhythm >100bpm This is any rhythm that originates outside the ventricle Anywhere .

No p waves Normal QRS Slightly slow rate (max 75bpm) The escape occurs somewhere at the AV junction. The resulting bradycardia reduces cardiac outputand can cause symptoms similar to other bradycardias such as: Dizziness Light-headedness Syncope Hypotension Usually the bradycardia can be tolerated as long as it is above 50bpm Ventricular escape Accelerated idioventricular rhythm . thus the AV node starts the beat instead. It occurs when the rate of depolarisation of the SA node falls below the rate of the AV node.

Usually benign and does not need to be treated. followed by long gap. Wide QRS Rhythm of about 75bpm No p waves Abnormal T waves Don‟t confuse this with ventricular tachycardia – which requires a HR of >125pbm.Two types: Many p waves per QRS (complete heart block) Occasional missing p wave. Otherwise it looks very similar. The QRS complexes are the same as those of sinus rhythm. then normal rhythm Somewhere along the line the p waves isn‟t getting conducted to the ventricles. Also associated with MI Extrasystoles (aka ectopics) These are easy – they are the same as ventricular escapes. and thus the ventricles depolarise at their normal escape rate. and then a ventricular QRS. except that where in escapes the escape beat comes after a pause in the rhythm. but there are usually abnormal p waves that tend to come immediately before or immediately after the . in extrasystole. there is an abnormal beat earlier than expected.

In a full thickness infarctionthen there are pathological Q waves. usually from the left atria to the left ventricle allows direct transition of the signal. The differentiation between full /thickness and non full thickness is pretty much the same as ST elevation / non-ST elevation Can be difficult to differentiate from BBB. This causes a sloping ST segment that has a „reversed tick‟ look. no p waves. and has QRS >160ms ST elevation MI (STEMI) ST elevation >2mm in 2+ chest leads OR >1mm in 2+ limb leads. tall R waves ST elevation ST elevation II. thus the tall R waves are the opposite of Q waves (remember Q waves are negative). short QRS ? Supraventricular tachycardia Ventricular fibrillation Patient is very likely to lose consciousness – thus the diagnosis is easy! Accessory pathway. but in a non-full thickness MI then there is only T wave inversion. This occurs because digoxin blocks the na/K pump. (similarly. which increases intracellular Ca2+ concentrations. aVF (theinferior leads) V2-5 – the anterior leads V1-V3 The ST elevation in these leads is often accompanied by ST depression in the antero-lateral leads – V1-V6. III. and ST depression occurs in place of ST elevation Both factors. hence the shortened PR interval. most patients are symptomless and live with no problems. no T Delta waves present. and thus reduced pump activity) Wolff-Parkinson-White SYndrome The digoxin effect Depression of ST. no QRS. rate >200bpm Narrow QRS No discernable pattern. short PR interval. BBB has p waves. VT is more likely scenario after MI. inverted T waves widespread . It has a risk of mortality as it can cause re-entry tachycardia. and a QRS generally 120-160ms. Posterior MI is unusual! The changes that occur are opposite to the changes of other type of MI. are usually permanent. however. The presence of Q waves implies a full thickness infarction. and possibly in lead I and aVL This will also cause deep q waves. bypassing the AV node. pathological Q waves occur several days after initial MI NSTEMI Ventricular tachycardia Pathological Q waves only Wide QRS. Inferior MI (probably the right coronary artery) Anterior MI (probably the left anterior descending) Posterior MI ST depression. ischaemia causes reduced production of ATP. right axis deviation. T-wave inversion (after several hours) Pathological Q waves (24 hours +) T wave inversion occurs within a few hours of MI. no P. if they occur. T waves difficult to identify. and T wave inversion.QRS.

Pericarditis T wave inversion (rare: also ST elevation) Widespread P pulmonale Tall . but also caused by drugs Hyperkalaemia Left ventricular hypertrophy Pacemaker Wide. not The large spike is pacemaker stimulus.QRS complexes broad Axis deviation Lead I + + Lead II + Either Axis Normal LAD RAD . then there is a risk of sudden cardiac death. hence the name „Mitrale‟ T waves with t peaks Prolonged QT ? If ST elevation does occur. related to QRS. wide QRS S wave in V1 or V2 >35mm AND R wave in V5 or V6 >35mm R in aVF >20mm R in aVL >11mm Any chest lead >45mm R in lead I >12mm ? Occasional P waves. is the QT interval as it would be at 60bpm. broad – looks like an „M‟. tall. the elevation in MI tends to be confined to a certain area. „tented‟ T ? Can lead to VF and AF waves. also. it is widespread Seen in cor pulmonale. p wave height >2mm in lead II Lead II Bifid P waves („P-Mitrale‟) Bi-phasic T waves Prolonged QT interval P waves with two peaks. QRS The QRS‟s are wide because the precede by large stimulus originates in the ventricles spike. small or absent p waves. but in pericarditis.It can be congenital. if this is long.peaked T waves. shortened/absent ST segment. or pretty muchanything that causes right atrial enlargement (or hypertrophy) – such astricuspid stenosis or pulmonary hypertension Left ventricular hypertrophy Can occur as a result of MI The corrected QT. then the ST waves will appear „saddle shaped‟ thus helping you to differentiate it from MI.

it could be due to incorrect limb lead placement.aVR should always be negative! If it is positive. Thus. Carotid sinus pressure By applying pressure to the carotid sinus you can stimulate the AV and SA nodes via vagal stimulation. This will reduce the frequency of discharge of the SA node. . or artificial pacing. due to the pacemaker wire . and increase the time of conduction across the AV node.this enters the heart at the apex. dextrocardia. Applying the pressure basically reduces the frequency of QRS complexes. and allows the underlying atrial arrhythmia to become more is called north-west axis. by applying pressure to the carotid sinus you can:    Reduce the rate of some arrhythmias Completely stop some arrhythmias It will have NO EFFECT ON VENTRICULAR TACHYCARDIAS – thus is can help you differentiate.