The whole ECG - a really basic ECG primer

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The following is a basic primer in interpretation of the ECG (EKG). It is intended solely for teaching purposes, and should not be relied upon in clinical decision making.

An Approach
ECGs can be very confusing, and there are dozens of different methods of interpretation. It's perhaps best if everyone works out their own individual approach, but here's just one approach you can build upon: 1. Sit back and look - identify the patterns, and write down what you see! 2. Go through the ECG systematically; 3. Correlate ECG and clinical findings, and if necessary, go back and do a complete rethink; 4. Try and invalidate your assessment --- look for holes! Of the above steps, the fourth seems counter-intuitive and unnecessary. In fact, it's the most important. As in all medicine, complacence is dangerous. Avoid it! Now, let's sketch out a systematic approach. Ours is: 1. 2. 3. 4. 5. 6. 7. Check the patient details - is the ECG correctly labelled? What is the rate? Is this sinus rhythm? If not, what is going on? What is the mean frontal plane QRS axis (You may wish at this stage to glance at the P and T wave axes too) Are the P waves normal (Good places to look are II and V1) What is the PR interval? Are the QRS complexes normal? Specifically, are there: significant Q waves? voltage criteria for LV hypertrophy? predominant R waves in V1? widened QRS complexes? Are the ST segments normal, depressed or elevated? Quantify abnormalities. Are the T waves normal? What is the QT interval? Are there abnormal U waves?

8. 9. 10.

Before we move through the systematic approach outlined above, we will outline a few basics. More advanced readers may wish to skip these basics, and move on to the systematic part of the tutorial.

How the ECG works
When cell membranes in the heart depolarise, voltages change and currents flow. Because a human can be regarded as a bag of salt water (with baad attitude), in other words, a volume conductor, changes in potential are transmitted throughout the body, and can be measured. When the heart depolarises, it's convenient (and fairly

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The whole ECG - a really basic ECG primer

accurate) to represent the electrical activity as a dipole --- a vector between two point charges. Remember that a vector has both a size (magnitude), and a direction. By looking at how the potential varies around the volume conductor, one can get an idea of the direction of the vector. This applies to all intra-cardiac events, so we can talk about a vector (or axis) for P waves, the QRS complex, T waves, and so on.

In the above picture, the schematic ECG lead on the right `sees' the (red) vector moving towards it, shown as a positive deflection in the ECG trace; the lead at 90 degrees to this sees nothing!
Various events

We assume some knowledge of heart anatomy. Note that the normal heart has, electrically speaking, only two chambers, an atrial and a ventricular `chamber'. Propagation of electrical activity spreads freely within atria and ventricles, but communication between these two chambers is limited to the AV node. Everyone knows that the P wave corresponds to atrial depolarisation, the QRS complex to ventricular depolarisation, and the T wave to repolarisation of the ventricle.

In order to be able to record myocardial activity, the electrocardiograph needs to be able to detect tiny changes in potential on the body surface. We are talking about signals that are often around 1mV, and may be smaller. In addition, we need some reference point to which we relate the potential changes.

The 12-lead ECG
Over the years, we have evolved several systems that go to make up the 12-lead ECG. These are: Bipolar leads: the reference point is on one limb, the `sensing' electrode (if you wish) is on another limb. The leads are termed I, II, and III.

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midclavicular line). then think dextrocardia.a really basic ECG primer http://www.The whole ECG . V1 in the fourth right interspace. but a better name is perhaps the `right orientated leads'). so effectively it's seeing the chambers of the heart. although "mirror image" changes will tend to be picked up in V1 and V2. and suggests that lead placement was incorrect. or some other strange congenital abnormality). and aVF points directly down (in a 'Southward' direction). in that the reference lead on the limb being sensed is disconnected from the other two. We can visualise the directions of the various leads --. II down towards the left which extend across the precordium. The V leads. AVL and I. V3 halfway in between V2 and V4.I points left. The other leads are arranged around the points of the compass --. III and AVF are inferior.anaesthetist.aVL about 30o more north of I. and most deflections in that lead are negative. V1 through V4 tend to look at the anterior aspect of the LV (some refer to V1 and V2 `septal'. aVR `looks' at the heart from up and right. 3 of 21 4/24/2013 7:49 PM .htm Unipolar leads: The reference point is several leads joined together. V4 at the apex (5th interspace. while II. These leads are conventionally augmented. (a net positive vector in AVR is unusual. about 60o south of I. as well as V5 and V6 are lateral. Changes in depolarisation in the posterior aspect of the heart are not directly seen in any of the conventional leads. If the leads were correctly sited. V2 4th left. It's usual to group the leads according to which part of the left ventricle (LV) they look at. and the sensing lead is on one limb. and V5 & V6 in the 5th interspace at the anterior and mid axillary lines respectively. and III off to the right of aVF.

150. the paper speed is usually 25mm/s. But always remember that in the heart. Always check the calibration voltage on the right of the ECG. Rates in between these numbers are easy to `interpolate'. the atria and ventricles. ten blocks usually correspond to 1 mV. and on the horizontal axis.anaesthetist. and paper speed. 50 2. and one method is as follows: 1. then the rate is 150. via normal conduction 4 of 21 4/24/2013 7:49 PM . Identify an R wave that falls on the marker of a `big block' 3. the two are linked in a convenient 1:1 ratio. If the number of big blocks is 1. that we are really looking at two rates --. if it's two.The whole ECG .a really basic ECG primer http://www. because we have two electrically `isolated' chambers. Remember the sequence: 300. Heart rate Knowing the paper speed.htm Paper ECG paper is traditionally divided into 1mm squares. Count the number of big blocks to the next R wave. and so on. the rate is 300. it's easy to work out heart rate. 100.the atrial and ventricular rates! It just so happens that in the normal heart. so one block is 0. 75. and should not be trusted. Note that we also have "big blocks" which are 5mm on their side. Vertically. The following image shows the normal 1mV calibration spike: Damping Note that if the calibration signal is not "squared off" then the ECG tracing is either over or (or 40ms). It's also very convenient to have a quick way of eyeballing the rate. 60.

Conventionally. or ischaemia. A sinus tachycardia then becomes any heart rate over 90. less than 50. always make sure that you are not mistaking atrial flutter with a 2:1 block for sinus tachycardia. vasodilator drugs.g. In disease states. including many hypotensive agents. including: hypothermia. FEVER myocarditis If the rate is almost exactly 150. Sinus arrhythmia is generally a good thing. and loss of this chaotic variation is of ominous prognostic significance.a rate of 85 in a highly trained athlete may represent a substantial tachycardia. called sinus arrhythmia. Sinus tachycardia Always consider pain as a possible cause of tachycardia.g. but otherwise normal individuals. this may not be the case. There's a long list.anaesthetist. and just before the onset of ventricular tachycardia (or fibrillation). 5 of 21 4/24/2013 7:49 PM . however: Any cause of adrenergic stimulation (including pain). structural SA node disease. atropine) anaemia. hypothyroidism.a really basic ECG primer http://www. pregnancy. vagolytic drugs (e. but it's probably more appropriate to re-adjust these limits to 50 -.htm down the AV node. especially if their resting rate is 32/minute! One should also beware of agressively trying to manage low rates in the presence of good perfusion and excellent organ function. marked intracranial hypertension.The whole ECG . Rhythm Sinus arrhythmia and heart rate variability There is normally a slight degree of chaotic variation in heart rate. Post myocardial infarction. a normal heart rate has been regarded as being between 60 and 100. thyrotoxicosis. Note that you have to look at the clinical context -. increased vagal tone (due to vagal stimulation or e.90/min. and even in uraemia. obstructive there's a long list of situations where sinus bradycardia occurs. Sinus bradycardia Apart from fit. drugs). hypovolaemia. and bradycardia. variability is lost! Absence of any sinus arrhythmia suggests an autonomic neuropathy. a metronome-like regularity of the heartbeat is associated with an increased likelihood of sudden death. beta blockade. A common error.

The conventional view of the pathogenesis of AF is that there are multiple re-entrant `wavelets' moving through the atrial muscle. rates of about 130 or more are common.The whole ECG . but recent evidence suggests that much AF actually arises from ectopic activity in the muscular cuff surrounding the pulmonary veins where they enter the left atrium. AF is thought to beget further AF through "electrical remodelling" --electrophysiological changes that are induced in atrial myocytes due to fast rates and the consequent calcium loading. and an atrial escape beat. where the SA node falters. it may find the His-Purkinje system not quite ready to receive an impulse. and a subsidiary pacemaker takes over: (Parenthetically. Commonly. Distinguish between an atrial extrasystole.htm Atrial extrasystoles These arise from ectopic atrial foci. Supraventricular tachyarrhythmias (SVT) Irregular SVT By far the commonest cause of irregular SVT is atrial fibrillation. and a degree of block may be seen.a really basic ECG primer writhing like a bag of worms. The atrium "fibrillates". Note that in the above tracing of AF. 6 of 21 4/24/2013 7:49 PM . where the atrial rate is in the region of 450 to 600/min. This is termed `aberration'. Don't let this put you off from indentifying the underlying rhythm). the ventricular response rate seems rather slow.anaesthetist. so subsequent beats of SA origin are not in synchrony with the previous sinus rhythm. the ectopic beat always arises at about the same time after the sinus beat! The ectopic beat usually discharges the SA node. so we suspect that AV block has been increased using pharmacological manipulation. and the atria really do not contract rhythmically at all. In uncontrolled AF. we didn't draw the P waves very well in the above strip. If the extrasystole occurs early on.

combined with tachycardia. There is often severe underlying disease (e. via an accessory pathway. A re-entrant circuit can be set up. The atrial rate is commonly 300/min. a slow and fast `pathway'. In the above ECG the clue is the rate. "Atrial flutter with variable block". and the heart may flip in and out of sinus rhythm. Other ratios are possible. the above image actually shows multifocal atrial tachycardia. The most well-characterised is the Wolff-Parkinson-White syndrome. there are generally two ways that electrical depolarisation can enter the AV node from the atrium. 2. congenital extra pathways between the atria and ventricles are common.anaesthetist. Note how there are at least three different P wave configurations! Regular SVT Atrial flutter is common. and causing depolarisation of the ventricles at fast rates (up to 200/min or even more). MAT has a poor prognosis.a really basic ECG primer http://www. or there may be runs of atrial fibrillation.htm Other causes of irregular SVT are: Frequent atrial extrasystoles. where there are three or more distinct atrial foci. discussed next. Probably the commonest cause of regular SVT is AV nodal re-entrant Reasonable (WHO) criteria for the WPW pattern on ECG are: 7 of 21 4/24/2013 7:49 PM . Accessory pathways Abnormal. and can perforate the electrically insulating fibrous ring that normally separates the atrial `chamber' and the ventricular one. due to repetitive discharges from an ectopic atrial focus. AV re-entrant tachycardia. ectopic atrial tachycardia.g. Here. Multifocal atrial tachycardia. resulting in a ventricular response rate of 150/min. This rhythm is often unstable. chronic obstructive airways disease).The whole ECG . A rate of 150 should always engender the suspicion of atrial flutter with 2:1 block. Although it looks like atrial fibrillation. and sometimes the ratio varies. and in the ICU setting. Other causes of regular SVT include: 1. and there is usually a 2:1 block. with impulses moving in a circular fashion.

3. up AV node. A few other hints: The baseline ECG is invaluable (may show WPW. 3.12s A delta wave QRS duration of 0. 4. If the P is after the QRS. 2. Accessory pathways are common. PR interval under 0. Ventricular extrasystoles Because these arise within an ectopic focus within the ventricular muscle. it's probably an ectopic atrial tachycardia.anaesthetist. Distinguishing causes of SVT A few pointers are in order. because the preceding beat influences the ectopic focus. bizarre. 2. and tachycardias. called orthodromic tachycardia). and unrelated to a preceding P wave. There is usually a constant relationship (timing) between the preceding sinus beat and a subsequent ventricular beat. It's useful if you can capture onset or termination of the arrhythmia. for example).a really basic ECG primer http://www. The important thing to look for is the P wave: 1. The WPW syndrome is a combination of the WPW the other way around (down accessory pathway.htm 1. It should be clear that the PR interval will therefore be short. causing collapse or even death. Note however that not everyone with an accessory pathway will conduct all of the time down that pathway. If the P is inscribed before the QRS.The whole ECG .12s (or more) A normal P-wave axis Because depolarisation moves `antegrade' from atria to ventricles. The tachycardias may be due to impulse conduction down via the AV node and back up the accessory pathway (commonest. and the QRS duration should be prolonged. and this is responsible for the slurred. initial delta wave. or even related to atrial fibrillation. the ventricle may be driven at rates in excess of 200/min. the QRS complex is wide. Symptomatic pathways are far less common. termed antidromic tachycardia). If the P is not seen (and probably lost within the QRS) it's likely to be AV nodal re-entrant tachycardia. 8 of 21 4/24/2013 7:49 PM . estimated to occur in one to three individuals in every thousand. consider orthodromic AV re-entrant tachycardia. as if the accessory pathway is able to conduct impulses at fast rates. This last cause is ominous. part of the ventricle depolarises prematurely.

we have a ventricular rhythm (a bit faster than one might expect. perhaps an accelerated idioventricular rhythm) with retrograde P waves. extrasystoles will tend to `squeeze in' during long RR intervals.a really basic ECG primer http://www. and is detected by noting the unvarying coupling between extrasystoles. and does its own merry thing. 9 of 21 4/24/2013 7:49 PM .. or was about to occur when the VE happened? Usually. note the fusion beats as the normal rhythm and parasystolic rhythm transiently coincide. but the subsequent atrial beat will occur on time. The atrial pacemaker is now reset! In the following rather complex tracing. and something else --..some of the P waves are followed by a normal looking `echo' beat as the impulse is conducted down back into the normal pathways). Because the intrinsic rate of an ectopic focus often tends to be What happens to the atrial beat that occurred. Some have called this the "rule of bigeminy". the ectopic focus is protected from other influences. the ventricular beat may be conducted retrogradely and capture the atrium (resulting in a P wave after the QRS. and be conducted normally. Rarely.anaesthetist. if the rate is varying. In addition. Fusion beat Occasionally. This is termed `parasystole'.htm The ventricular beat is not usually conducted back into the atria. This results in a `fusion beat'. this is blocked. which combines the morphology of a normal sinus beat and that of the extrasystole. Couplet Two VE's are termed a couplet. with an abnormal morphology as conduction through the atrium is retrograde). extrasystoles will tend to arise more commonly with slower rates. and the lack of coupling between the extrasystole and sinus beats! In the following trace.The whole ECG . a VE occurs just after a sinus beat has started to propagate into the His-Purkinje system. Parasystole Rarely.

The whole ECG . and there is dissociation between atria and ventricles --. clearly. resulting in a normally-shaped QRS complex and T wave. and are termed ventricular tachycardia (VT). Conventional wisdom has it that this results in chaotic.htm We've put in the above unusual ECG more as a mnemonic than for any other reason. If the patient is haemostable. The ectopic focus is therefore modulated by the normal rhythm. There is also a capture beat later on. and agonize later.Brugada's approach may have merit --. one should apply synchronised DC countershock. and usually occurs at about the same interval from the normal events. then one may have more time. Parasystole is can explore a web-based version of his algorithm here. Sustained VT (more than about 30 beats) often degenerates into ventricular fibrillation. There is usually severe underlying myocardial that occurs during the relative refractory period of the myocardial fibres. the rate is slowish (under about 150). and the person will survive. If unsynchronised DC countershock is applied within 30s of the onset of VF. When in doubt. Apart from the regular fast rate and wide complexes.a QRS complex which is something in between the VT morphology and normal morphology. and SVT with aberration is tricky. VF is a dire emergency. there is an approximately 97% chance that sinus rhythm will be restored. Survival decreases exponentially thereafter. A variety of algorithms have been proposed . This is especially the case if the patient is haemodynamically unstable. Even more characteristic of VT is the presence of a fusion beat at the start of the trace --. resulting in death. we have a few more clues . It is often precipitated by a critically timed extrasystole.a really basic ECG primer http://www.the P waves occur at any time in relation to the QRS complexes. We want you to remember that even with extrasystoles. Ventricular flutter 10 of 21 4/24/2013 7:49 PM .. unco-ordinated wavelets of depolarisation moving through the ventricular mass. the atrial rate is different from the ventricular rate. Ventricular fibrillation This is a chaotic ventricular rhythm that rapidly results in death. VT vs SVT+aberration Distinguishing between VT.. where the P wave has managed to sneak through and transiently take over. The above strip shows several `characteristic' features of VT. Ventricular tachycardia Three or more ventricular extrasystoles are a bad sign. with every minute of delay.anaesthetist. there is flow of information from the normal rhythm to the ectopic focus.

You won't see it often (or for long). We can talk about the `axis' of any ECG depolarisation.The whole ECG . Do the same for AVF. Estimate the overall deflection (positive or negative. but most people when they are talking 'axis' are referring to the mean frontal plane QRS axis. You can work out that ± 180o is 'West'. There is a number of ways of determining this. but +90o is South. 3. instead of North as it would be in a Cartesian system. and that minus 90o is 'North'. Plot the vector on a system of axes. People tend to faff quite a lot about QRS axis deviations. and estimate the angle. but the following method has the merit of simplicity: 1.g. and usually degerates into ventricular fibrillation. Marked right axis deviation (e. Axis The peculiar system we use in electrocardiography is non-Cartesian. the most likely `diagnosis' is left 11 of 21 4/24/2013 7:49 PM .anaesthetist. and how much) of the QRS in standard lead I. Left axis deviation is not uncommon in inferior myocardial but they are a fairly blunt-edged tool. and rather arbitrary! We measure the direction of vectors in degrees. 2.htm Ventricular 'flutter' is a bizarre sine-wave like rhythm. and if this is absent. +150o) may signify significant `right-sided' heart disease. thus: Note in the above picture that the (abnormal) axis illustrated is negative ("towards the left") because AVF is negative. and zero is indeed facing `East'.a really basic ECG primer http://www.

11 seconds in duration. *{Footnote: One reader pointed out that an axis of -135o could just as well be regarded as being `markedly to the right'. It is commonly seen in congenital heart disease. another good place to look. causing a negative deflection. and sometimes in severe chronic obstructive airway disease.. a widened bifid one. depolarisation of the right atrium results in an initial positive deflection. This is a reasonable argument. Schamroth gives a super mnemonic --. It's convenient at this point to discuss blocks. (There are several other cause of left or right axis deviation. even up to -30o (especially Ebstein's anomaly).5mm tall..} The P wave Normal atrial activation is over in about 0. The normal P wave in V1 is thus biphasic. If the T wave axis is more than about 45 to 60o different from the QRS axis.10s. for example depolarisation via accessory pathways). followed by a vector away from V1 into the left atrium.htm anterior hemiblock. moving right with chronic obstructive disease. left atrial enlargement: In V1. and may be of value.The whole ECG . One can also spot an ectopic atrial focus low down in the atrium (`coronary sinus rhythm') due to the `northern' shift in axis. to the start of the very first r or q wave)."the T-wave axis moves away from the `region of mischief'". The normal axis is about +40 to +60o. where the P shouldn't be more than 2. The T wave axis is much neglected. often due to tricuspid regurgitation! (Observed by Sodi-Pallares). A P wave originating in the left atrium often has a `dome and dart' configuration. dextrocardia. A good place to look at P waves is in Even the P-wave axis is of use. The PR interval (and PR segment) The PR interval extends from the start of the P wave to the very start of the QRS complex (that is. It's easy to work out the corresponding abnormalities with left or right atrial enlargement: There are a few other tips: A qR in V1 suggests right atrial enlargement. starting in the right atrium.20 seconds). A tall P wave (3 blocks or more) signifies right atrial enlargement. A normal value is 3 to 5 `little blocks' (0. -135o)*. and 0.12 to 0.a really basic ECG primer http://www. Where the axis is up and to the left (eg. 12 of 21 4/24/2013 7:49 PM . The axis may move left with congenital heart disease. there is probably RA enlargement! (Tranchesi). If the overall QRS amplitude in V1 is under a third of the overall QRS amplitude in V2.anaesthetist. this is termed a "north west axis". this is abnormal.

anaesthetist. An impulse that was expected to arise in the SA node is delayed in its exit from the node.The whole ECG . Clearly a bad thing. say. or progressive (The Wenckebach phenomenon. Type II second degree block). *{ Footnote: Thanks to the reader who pointed out the typo} 3. requiring temporary or even permanent pacing. 2.this is otherwise known as Mobitz Type I second degree heart block)*. a subsidiary pacemaker will (we hope) take over. This is manifest by a prolonged PR interval.a really basic ECG primer http://www. Second degree block: Conduction intermittently fails AV node. or blocked completely. in the atrium. 13 of 21 4/24/2013 7:49 PM . as no electrical activity is seen. If the SA node is blocked.htm SA node block This is a diagnosis of deduction. This may be in a constant ratio (more ominous. administration of atropine. or ventricle! AV nodal blocks There are three "degrees" of AV nodal block: 1. First degree block: simply slowed conduction. A second degree SA block can be `diagnosed' if the heart rate suddenly doubles in response to. characterised by progressively increasing PR interval culminating in a dropped beat --. Third degree block: There is complete dissociation of atria and ventricles.

so we have R'. depolarisation moves from the chamber outwards. thickening of the ventricle may result in increased voltages seen on the surface ECG. in the normal myocardium. amplitude must be diminished. A simplistic explanation of these prominent Q waves is that an appropriately placed lead "sees through" the dead tissue. from an ECG point of view. (The fancy name for this sudden downstroke is the `intrinsicoid deflection').g. Left ventricular systolic overload/hypertrophy (LVH) The absence of LVH on ECG means nothing. Note that we refer to a second deflection in the same direction by adding a prime.a really basic ECG primer http://www. and the most conspicuous of these is Q waves. It's easy to imagine that if muscle is lost.anaesthetist. which in the `septal leads' (V1 and V2) is a positive deflection.g. often termed the ventricular activation time. as the features are insensitive. In right orientated leads. the septum depolarises before other parts of the left ventricle. This observation is of relevance. Q waves . Hypertrophy and chamber enlargement Because of the thin-walled nature of the atria. An upward deflection is an R.small deflections are reflected using lower case. and in lateral leads (e.04s. If however they are 14 of 21 4/24/2013 7:49 PM .myocardial infarction Many people who have had a prior MI will have an ECG that appears normal. this normal depolarisation is seen as a Q wave! Another feature of previous MI is loss of R wave amplitude. and larger deflections UPPER CASE. V6) the duration should not exceed 0. a normal VAT is 0. We might thus refer to an rSR' There may however be typical features of previous MI.htm The QRS complex The nomenclature is mildly arcane --. V6) is seen as a small q. Conversely. lateral.The whole ECG . and visualises the normal depolarisation of the viable myocardial wall directly opposite the infarcted area. or whatever. one cannot talk about "atrial hypertrophy" but only about enlargement. This is seen as a small initial vector.02s. One can get some idea of the site of infarction from the lead in which abnormalities are seen . Normally. and on the left (e. and we can then discuss "ventricular hypertrophy". or anterior. An initial downwards deflection is a Q (or q). We can estimate this from the surface ECG by looking at the time from the onset of the QRS to the sudden downstroke of the QRS. any negative deflection after this is an S. where the septum cannot depolarise normally. R''. (Having a pre-infarction ECG for comparison is invaluable). the lateral (septal) q is conspicuously missing. Because. as in conditions such as left bundle branch block. Something of some importance is the time it takes the ventricle to depolarise.inferior. S' and so on.

Increased VAT in V1 left-sided RS or rS complexes. Enormous R waves may be seen in left-sided leads. RV hypertrophy A number of ECG abnormalities have been associated with right ventricular hypertrophy. where septal q waves in the lateral leads are often diminished or absent.htm present. These include: right axis deviation. with the sum of the S in V1 and the R in V5 or V6 over 35mm indicating hypertrophy. LV diastolic overload Features of LVH may be present (as above).a really basic ECG primer http://www. LVH is very likely. Unlike systolic overload (where the T waves are often inverted). or a tiny q). In contrast to systolic overload. T waves are usually upright. they are very insensitive in e. especially with aortic or mitral regurgitation. 15 of 21 4/24/2013 7:49 PM . or RS complexes in the mid-precordial leads. Inverted U waves in V4-6 suggest either systolic or diastolic LV overload. a small r.g. very symmetrical. Useful are: R in I over 15mm R in AVL over 11mm Sum of all QRS voltages under 175mm (!) T wave axis changes can be predicted knowing Schamroth's rule .com/icu/organs/heart/ecg/index. and somewhat pointed. partial or complete RBBB. A host of other criteria have been proposed. suggesting left atrial enlargement). A `little something' in V1 (an initial slur of the QRS. Systolic overload results in increased QRS deflections. Because the criteria were formulated on white males.The whole ECG . (In the above picture. black women. in diastolic overload. A tall R wave (bigger than the S) in V1.anaesthetist. prominent lateral Qs are noted. also note the predominantly negative deflection of the P wave in V1.

V6).12s or greater (some would say. RBBB is sometimes seen in normal people. cardiomyopathy. or may reflect congenital heart disease (e. Duchenne muscular dystrophy. >= 0. 2. The tiny q waves normally seen in the left-sided leads are absent. consider the following differential: posterior myocardial infarction RV hypertrophy Right bundle branch block Wolff-Parkinson-White syndrome (with an appropriately placed accessory pathway) Other rare causes such as dextrocardia. (And likewise for the normal tiny r in V1).com/icu/organs/heart/ecg/index. but useful. there is usually a prominent S in the lateral leads (I.12s or more. There must be evidence of abnormal septal depolarization. Tall R' in V1. In addition. although there are other causes: RBBB Diagnostic criteria for right bundle branch block are somewhat empiric. and so on and.htm Whenever you see a tall R in V1. of course. QRS duration 0. 3. incorrect lead placement! Bundle branch blocks A broadened QRS complex suggests a bundle branch block. or even acute right heart strain.14). Here they are: 1. V5.The whole ECG . No RBBB can be present. LBBB Diagnose this as follows: 1. ischaemic heart disease. atrial septal defect).anaesthetist. QRS duration is 0. 16 of 21 4/24/2013 7:49 PM . 2.g.a really basic ECG primer http://www.

but is much more worrying when associated with other abnormalities (such as PR interval prolongation or RBBB). the VAT is prolonged. and tall.anaesthetist. and nonspecific T wave abnormalities.htm In addition. or some types of congenital heart disease or accessory pathways). In addition. with QT prolongation. Suspect it if there is left axis deviation (past -45o) without another cause (such as inferior myocardial infarction. and finally ventricular fibrillation occurs. a long VAT. QRS prolongation.The whole ECG . and several other minor changes. notched R waves are seen in the lateral leads (RR' waves). Other features of LAHB include an initial QRS vector which is down and to the right. the most common finding is a prominent J wave. There is usually a notched QS complex in V1 and V2. blocks. LAHB may indicate underlying heart disease. there may be delayed VAT . ventricular extrasystoles. Eventually. The diagnosis of left posterior hemiblock is mentioned only to be avoided! The ST segment The junction between QRS and ST Hypothermia Besides sinus 17 of 21 4/24/2013 7:49 PM .a really basic ECG primer http://www. below 30oC. Fascicular blocks Left anterior hemiblock (LAHB) is interruption of the thin anterosuperior division of the left bundle.

anaesthetist. Exercise testing to elicit ischaemia is also not very sensitive in detecting this common and V2. Established acute myocardial infarction We now lay great emphasis on ST segment elevation in diagnosing acute MI (In the past. S we'll see a tall R (corresponding to a Q). Acute myocardial infarction --. that a significant proportion of people having an acute MI will have a normal ECG.the `hyperacute phase' There are four main features of early myocardial infarction (as per Schamroth): 1.ST changes One should always remember that more than a quarter of people presenting with an acute myocardial infarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edged tool in the detection of coronary artery disease.htm Ischaemic heart disease .a really basic ECG primer http://www. early on). The features of `full blown' MI may be: 1. prominent Q waves. Remember our previous warning. 4. Posterior MI The trick in diagnosing this is to realise that posterior wall changes will be mirrored in the leads opposite to the lesion --. 3. elevated ST segments. ST depression. 2. 2. these are often absent. 3. widened T waves (The ST segment often merges with these) Note that Q waves are not seen early on. Q waves were remarked on. Inverted `arrowhead' T waves. and upright arrowhead T waves: Right ventricular infarction 18 of 21 4/24/2013 7:49 PM . but as noted above. so do not rely on any of these features to exclude MI.The whole ECG . increased VAT increased R wave amplitude (!) ST elevation which is sloped upwards! Tall.

Angina and stress testing The most important component of an effort ECG that indicates the presence of coronary artery disease is where exercise reproduces the patient's chest discomfort or pain. Other findings may be: ST segment depression (It is customary to apply the Sheffield criteria.V3. Another suggestive feature is lack of ST depression in V1 with evidence of MI in the inferior leads (look for ST depression in V2 under 50% of the ST elevation in AVF).1mV) ST depression 0.htm This occurs in about 1/3 of patients with inferior MI. but is often missed.a really basic ECG primer http://www. There may be no ECG changes. This disorder is thought to be related to vascular spasm. Other morphological abnormalities 'Early repolarisation' This is common --. and angiography shows coronaries without a significant burden of atheroma. 1mm (0. Failure of the blood pressure to rise with exercise (an ominous finding).08s after the J point. Non-ST elevation MI There are no reliable correlates of "subendocardial" or non-ST elevation MI.anaesthetist. often with a prominent J wave. as otherwise one might inappropriately suspect serious underlying heart disease. failure of suppression of ventricular ectopy. T-wave changes that suggest ischaemia are a very sudden junction between the ST segment and the T wave.The whole ECG . or even ST segment depression and/or T wave Sensitivity can be improved by looking at V4R --.V4. that is. It's important to relate the ECG to the clinical context. ST segment elevation T-wave changes (which may be rather nonspecific) Development of inverted U waves. as always. which. It has been remarked upon in athletes. particularly. and the diagnosis is based on the combination of clinical and laboratory criteria (troponin elevation being important). T waves T wave abnormalities are common and often rather nonspecific.ST segment elevation is conspicuous. although subtle. It would be distinctly unusual in the absence of inferior MI. Many other morphological abnormalities have been described with this disorder. is said to be specific for the presence of ischaemia! Did you notice the ST segment depression in our section on voltage and timing. above? Prinzmetal's angina The simple (and possibly even correct) explanation of why you see ST segment elevation with this variant form of angina is that the predominant area of ischaemia is epicardial. but put the lead on the right side of the chest! Look for ST elevation which is higher than that in V1 -. or (especially) development of ectopy in the recovery period. and very symmetrical T 19 of 21 4/24/2013 7:49 PM .

The whole ECG .and hyper-kalaemia. it is common to apply a correction. as may be seen in poisoning with tricyclic antidepressants. Be particularly concerned if the value is over 0. A normal value is about 0. heart blocks (first degree. U waves become prominent (this may be falsely interpreted as QT prolongation). Other cause have been reported.39s ±0. including hypothermia.anaesthetist. Because QT varies with rate. and toxicity from a variety of other drugs (quinidine. acute myocardial infarction (!). usually using Bazett's formula: QTc = QTmeasured --------------------SQRT (RR interval) SQRT refers to the square root.QT This is the time from onset of QRS to end of T wave. and there may even be first or second degree AV block. LAHB). 20 of 21 4/24/2013 7:49 PM .htm waves. amiodarone. the QRS complexes broaden and become bizarre.a really basic ECG primer http://www. We should all know the features of hypo. and increased VAT . Later. A variety of ST changes may be seen. and hypertrophic cardiomyopathy. A variety of changes may be seen with Hyperkalaemia Initial features are tall "tented" T waves. hypocalcaemia. etc). erythromycin. despite the continuation of sinus rhythm. U waves Hypokalaemia The T waves flatten. Atrial and ventricular extrasystoles are common. Symmetrical deep T-wave changes most prominent in V3 and V4 suggest ischaemia in the territory of the left anterior descending artery (LAD T0-waves). the P waves disappear. intracranial haemorrhage and so on. Several syndromes Myocarditis Common findings are tachycardia. procainamide. head injury. For features of hypokalaemia. and the patient dies from ventricular arrhythmia or cardiac standstill. Measures . see below .04s (slightly larger values are acceptable in women). sotalol. including those of myopericarditis. the ST segment almost vanishes.5. congenital QT syndromes. and finally.

Electrical alternans Here. but at slower rates usually signifies severe heart disease. The `classical' S1Q3T3 syndrome occurs in under 10%..htm Myopericarditis Pericarditis is usually associated with a degree of contiguous myocarditis..tall one beat.The whole ECG . and a brilliant physician. Date of First Publication: 2003/7/4 Date of Last Update: 2006/07/24 Web page author: Click here 21 of 21 4/24/2013 7:49 PM . with their "reverse tick" conformation. ISBN 0-632-02411-9). published by Blackwell Scientific. Other features may be those of right atrial enlargement. 1990. but merely the presence of digitalis. to boot. There is also usually sinus tachycardia. accuracy and depth. but the QRS amplitude alternates --. shorter the next (and so on. Bibliography and sources A good general reference is Leo Schamroth's An Introduction to Electrocardiography. there is no rhythm disturbance. basic approach to the ECG. With toxicity. this is said to be of little significance. A site we've encountered which shows promise is Learn The ECG.). RBBB and atrial tachyarrhythmias. practically any arrhythmia can be seen. ECG abnormalities are not common. There may also be T wave inversion. Pericardial effusion The most common finding here is simply diminished amplitude of the ECG deflections. The major manifestation is widespread ST segment elevation. Digoxin effect ST segment changes are pretty characteristic. although certain arrhythmias are highly RV hypertrophy or ischaemia. the presence of both increased irritability and AV nodal block (such as paroxysmal atrial tachycardia with a 2:1 AV nodal block).a really basic ECG primer http://www. At fast rates.. These changes are not indicative of toxicity. It has the merits of clarity. Pulmonary thromboembolism Apart from sinus tachycardia. or pericardial effusion. for example. and sometimes one sees electrical alternans . It's free. Leo was one of the truly great men of electrocardiography. (7th Ed. and T wave abnormalities are common. interactive and provides a reasonable.

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