ECG scribbles 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: Sit back and look - identify the patterns, and write down what you see! 1. Go through the ECG systematically; 2. Correlate ECG and clinical findings, and if necessary, go back and do a complete rethink; 3. Try and invalidate your assessment --- look for holes! 4. 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: Check the patient details - is the ECG correctly labelled? 1. What is the rate? 2. Is this sinus rhythm? If not, what is going on? 3. What is the mean frontal plane QRS axis (You may wish at this stage to glance at the P and T wave axes too) 4. Are the P waves normal (Good places to look are II and V1) 5. What is the PR interval ? 6. Are the QRS complexes normal? Specifically, are there: significant Q waves? voltage criteria for LV hypertrophy? predominant R waves in V1? widened QRS complexes? 7. Are the ST segments normal, depressed or elevated? Quantify abnormalities. 8. Are the T waves normal? What is the QT interval? 9. Are there abnormal U waves? 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 Easy ECG Screening Tool The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm 1 of 21 4/24/2013 7:49 PM
21

# The Whole ECG - A Really Basic ECG Primer

Feb 09, 2016

## Documents

rumgod

Basic ECG Primer

#### t waves normal

Welcome message from author
Transcript

ECG scribblesThe following is a basic primer in interpretation of the ECG (EKG). It is intended solely for teachingpurposes, 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 perhapsbest if everyone works out their own individual approach, but here's just one approach you can buildupon:

Sit back and look - identify the patterns, and write down what yousee!

1.

Go through the ECG systematically;2.Correlate ECG and clinical findings, and if necessary, go backand do a complete rethink;

3.

Try and invalidate your assessment --- look for holes!4.

Of the above steps, the fourth seems counter-intuitive and unnecessary. In fact, it's the mostimportant. As in all medicine, complacence is dangerous. Avoid it!

Now, let's sketch out a systematic approach. Ours is:

Check the patient details - is the ECG correctly labelled?1.What is the rate?2.Is this sinus rhythm? If not, what is going on?3.What is the mean frontal plane QRS axis (You may wish at this stage to glance at the P and Twave axes too)

4.

Are the P waves normal (Good places to look are II and V1)5.What is the PR interval?6.Are the QRS complexes normal? Specifically, are there:

significant Q waves?voltage criteria for LV hypertrophy?predominant R waves in V1?widened QRS complexes?

7.

Are the ST segments normal, depressed or elevated? Quantify abnormalities.8.Are the T waves normal? What is the QT interval?9.Are there abnormal U waves?10.

Before we move through the systematic approach outlined above, we will outline a few basics. Moreadvanced 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 beregarded as a bag of salt water (with baad attitude), in other words, a volume conductor, changes in potential aretransmitted throughout the body, and can be measured. When the heart depolarises, it's convenient (and fairly

Easy ECG Screening Tool

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

1 of 21 4/24/2013 7:49 PM

accurate) to represent the electrical activity as a dipole --- a vector between two point charges. Remember thata vector has both a size (magnitude), and a direction

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 spreadsfreely within atria and ventricles, but communication between these two chambers is limited to the AVnode. Everyone knows that the P wave corresponds to atrial depolarisation, the QRS complex toventricular depolarisation, and the T wave to repolarisation of the ventricle.

The ECG (EKG)

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

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 onanother limb. The leads are termed I, II, and III.

. By looking at how the potential varies around the volumeconductor, one can get an idea of the direction of the vector. This applies to all intra-cardiac events, so we cantalk about a vector (or axis) for P waves, the QRS complex, T waves, and so on.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

2 of 21 4/24/2013 7:49 PM

Unipolar leads: The reference point is several leads joined together, and the sensing lead is onone limb. These leads are conventionally augmented, in that the reference lead on the limb beingsensed is disconnected from the other two.

The V leads, which extend across the precordium, V1 in the fourth right interspace, V2 4th left,V4 at the apex (5th interspace, midclavicular line), V3 halfway in between V2 and V4, and V5 &V6 in the 5th interspace at the anterior and mid axillary lines respectively.

We can visualise the directions of the various leads --- I points left, and aVF points directly down (in a'Southward' direction). The other leads are arranged around the points of the compass --- aVL about30o more north of I, II down towards the left foot, about 60o south of I, and III off to the right ofaVF. aVR `looks' at the heart from up and right, so effectively it's seeing the chambers of the heart, andmost deflections in that lead are negative.

(a net positive vector in AVR is unusual, and suggests that lead placement was incorrect. If the leadswere correctly sited, then think dextrocardia, or some other strange congenital abnormality).

It's usual to group the leads according to which part of the left ventricle (LV) they look at. AVL and I,as well as V5 and V6 are lateral, while II, III and AVF are inferior. V1 through V4 tend to look at theanterior aspect of the LV (some refer to V1 and V2 `septal', but a better name is perhaps the `rightorientated leads'). Changes in depolarisation in the posterior aspect of the heart are not directly seen inany of the conventional leads, although "mirror image" changes will tend to be picked up in V1 andV2.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

3 of 21 4/24/2013 7:49 PM

Paper

ECG paper is traditionally divided into 1mm squares. Vertically, ten blocks usually correspond to 1mV, and on the horizontal axis, the paper speed is usually 25mm/s, so one block is 0.04s (or 40ms).Note that we also have "big blocks" which are 5mm on their side.

Always check the calibration voltage on the right of the ECG, and paper speed. The following imageshows the normal 1mV calibration spike:

Damping

Note that if the calibration signal is not "squared off" then the ECG tracing is either over or under-damped, and should not be trusted.

Heart rate

Knowing the paper speed, it's easy to work out heart rate. It's also very convenient to have a quick wayof eyeballing the rate, and one method is as follows:

Remember the sequence: 300, 150, 100, 75, 60, 501.Identify an R wave that falls on the marker of a `big block'2.Count the number of big blocks to the next R wave.3.

If the number of big blocks is 1, the rate is 300, if it's two, then the rate is 150, and so on. Rates inbetween these numbers are easy to `interpolate'.

But always remember that in the heart, because we have two electrically `isolated' chambers, the atriaand ventricles, that we are really looking at two rates --- the atrial and ventricular rates! It just sohappens that in the normal heart, the two are linked in a convenient 1:1 ratio, via normal conduction

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

4 of 21 4/24/2013 7:49 PM

down the AV node. In disease states, this may not be the case.

Conventionally, a normal heart rate has been regarded as being between 60 and 100, but it's probablymore appropriate to re-adjust these limits to 50 -- 90/min. A sinus tachycardia then becomes any heartrate over 90, and bradycardia, less than 50. Note that you have to look at the clinical context -- a rate of85 in a highly trained athlete may represent a substantial tachycardia, especially if their resting rate is32/minute! One should also beware of agressively trying to manage low rates in the presence of goodperfusion and excellent organ function.

Apart from fit, but otherwise normal individuals, there's a long list of situations where sinusbradycardia occurs, including:

hypothermia;increased vagal tone (due to vagal stimulation or e.g. drugs);hypothyroidism;beta blockade;marked intracranial hypertension;obstructive jaundice, and even in uraemia;structural SA node disease, or ischaemia.

Sinus tachycardia

Always consider pain as a possible cause of tachycardia. There's a long list, however:

Any cause of adrenergic stimulation (including pain);thyrotoxicosis;hypovolaemia;vagolytic drugs (e.g. atropine)anaemia, pregnancy;vasodilator drugs, including many hypotensive agents;FEVERmyocarditis

If the rate is almost exactly 150, always make sure that you are not mistaking atrial flutter with a 2:1block for sinus tachycardia. A common error.

Rhythm

Sinus arrhythmia and heart rate variability

There is normally a slight degree of chaotic variation in heart rate, called sinus arrhythmia. Sinusarrhythmia is generally a good thing, and loss of this chaotic variation is of ominous prognosticsignificance. Post myocardial infarction, a metronome-like regularity of the heartbeat is associated withan increased likelihood of sudden death, and just before the onset of ventricular tachycardia (orfibrillation), variability is lost! Absence of any sinus arrhythmia suggests an autonomic neuropathy.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

5 of 21 4/24/2013 7:49 PM

Atrial extrasystoles

These arise from ectopic atrial foci. Commonly, the ectopic beat always arises at about the same timeafter the sinus beat!

The ectopic beat usually discharges the SA node, so subsequent beats of SA origin are not insynchrony with the previous sinus rhythm.

If the extrasystole occurs early on, it may find the His-Purkinje system not quite ready to receive animpulse, and a degree of block may be seen. This is termed `aberration'.

Distinguish between an atrial extrasystole, and an atrial escape beat, where the SA node falters, and asubsidiary pacemaker takes over:

(Parenthetically, we didn't draw the P waves very well in the above strip. Don't let this put you off from indentifying theunderlying rhythm).

Supraventricular tachyarrhythmias (SVT)

Irregular SVT

By far the commonest cause of irregular SVT is atrial fibrillation, where the atrial rate is in the regionof 450 to 600/min, and the atria really do not contract rhythmically at all. The atrium "fibrillates",writhing like a bag of worms. The conventional view of the pathogenesis of AF is that there aremultiple re-entrant `wavelets' moving through the atrial muscle, but recent evidence suggests thatmuch AF actually arises from ectopic activity in the muscular cuff surrounding the pulmonary veinswhere 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 consequentcalcium loading.

Note that in the above tracing of AF, the ventricular response rate seems rather slow, so we suspectthat AV block has been increased using pharmacological manipulation. In uncontrolled AF, rates ofabout 130 or more are common.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

6 of 21 4/24/2013 7:49 PM

Other causes of irregular SVT are:

Frequent atrial extrasystoles;Multifocal atrial tachycardia, where there are three or more distinct atrial foci, combined withtachycardia. There is often severe underlying disease (e.g. chronic obstructive airways disease),and in the ICU setting, MAT has a poor prognosis."Atrial flutter with variable block".

Although it looks like atrial fibrillation, the above image actually shows multifocal atrial tachycardia.Note how there are at least three different P wave configurations!

Regular SVT

Atrial flutter is common. The atrial rate is commonly 300/min, and there is usually a 2:1 block, resultingin a ventricular response rate of 150/min. Other ratios are possible, and sometimes the ratio varies.This rhythm is often unstable, and the heart may flip in and out of sinus rhythm, or there may be runsof atrial fibrillation.

In the above ECG the clue is the rate. A rate of 150 should always engender the suspicion of atrialflutter with 2:1 block.

Probably the commonest cause of regular SVT is AV nodal re-entrant tachycardia. Here, there aregenerally two ways that electrical depolarisation can enter the AV node from the atrium, a slow and fast`pathway'. A re-entrant circuit can be set up, with impulses moving in a circular fashion, and causingdepolarisation of the ventricles at fast rates (up to 200/min or even more).

Other causes of regular SVT include:

ectopic atrial tachycardia, due to repetitive discharges from an ectopic atrial focus;1.AV re-entrant tachycardia, via an accessory pathway, discussed next.2.

Accessory pathways

Abnormal, congenital extra pathways between the atria and ventricles are common, and can perforatethe electrically insulating fibrous ring that normally separates the atrial `chamber' and the ventricularone. The most well-characterised is the Wolff-Parkinson-White syndrome. Reasonable (WHO) criteriafor the WPW pattern on ECG are:

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

7 of 21 4/24/2013 7:49 PM

PR interval under 0.12s1.A delta wave2.QRS duration of 0.12s (or more)3.A normal P-wave axis4.

Because depolarisation moves `antegrade' from atria to ventricles, part of the ventricle depolarisesprematurely, and this is responsible for the slurred, initial delta wave. It should be clear that the PRinterval will therefore be short, and the QRS duration should be prolonged. Note however that noteveryone with an accessory pathway will conduct all of the time down that pathway. Accessorypathways are common, estimated to occur in one to three individuals in every thousand. Symptomaticpathways are far less common.

The WPW syndrome is a combination of the WPW pattern, and tachycardias. The tachycardias may bedue to impulse conduction down via the AV node and back up the accessory pathway (commonest,called orthodromic tachycardia), the other way around (down accessory pathway, up AV node, termedantidromic tachycardia), or even related to atrial fibrillation. This last cause is ominous, as if theaccessory pathway is able to conduct impulses at fast rates, the ventricle may be driven at rates inexcess of 200/min, causing collapse or even death.

Distinguishing causes of SVT

A few pointers are in order. The important thing to look for is the P wave:

If the P is inscribed before the QRS, it's probably an ectopic atrial tachycardia;1.If the P is after the QRS, consider orthodromic AV re-entrant tachycardia;2.If the P is not seen (and probably lost within the QRS) it's likely to be AV nodal re-entranttachycardia.

3.

A few other hints:

The baseline ECG is invaluable (may show WPW, for example);It's useful if you can capture onset or termination of the arrhythmia.

Ventricular extrasystoles

Because these arise within an ectopic focus within the ventricular muscle, the QRS complex is wide,bizarre, and unrelated to a preceding P wave. There is usually a constant relationship (timing) betweenthe preceding sinus beat and a subsequent ventricular beat, because the preceding beat influences theectopic focus.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

8 of 21 4/24/2013 7:49 PM

The ventricular beat is not usually conducted back into the atria. What happens to the atrial beat thatoccurred, or was about to occur when the VE happened? Usually, this is blocked, but the subsequentatrial beat will occur on time, and be conducted normally.

Rarely, the ventricular beat may be conducted retrogradely and capture the atrium (resulting in a Pwave after the QRS, with an abnormal morphology as conduction through the atrium is retrograde).The atrial pacemaker is now reset! In the following rather complex tracing, we have a ventricularrhythm (a bit faster than one might expect, perhaps an accelerated idioventricular rhythm) withretrograde P waves, 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 slow-ish, extrasystoles will tend to arisemore commonly with slower rates. In addition, if the rate is varying, extrasystoles will tend to `squeezein' during long RR intervals. Some have called this the "rule of bigeminy".

Couplet

Two VE's are termed a couplet.

Fusion beat

Occasionally, a VE occurs just after a sinus beat has started to propagate into the His-Purkinje system.This results in a `fusion beat', which combines the morphology of a normal sinus beat and that of theextrasystole.

Parasystole

Rarely, the ectopic focus is protected from other influences, and does its own merry thing. This istermed `parasystole', and is detected by noting the unvarying coupling between extrasystoles, and thelack of coupling between the extrasystole and sinus beats! In the following trace, note the fusion beatsas the normal rhythm and parasystolic rhythm transiently coincide...

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

9 of 21 4/24/2013 7:49 PM

We've put in the above unusual ECG more as a mnemonic than for any other reason. We want you toremember that even with extrasystoles, there is flow of information from the normal rhythm to theectopic focus. The ectopic focus is therefore modulated by the normal rhythm, and usually occurs atabout the same interval from the normal events. Parasystole is unusual.

Ventricular tachycardia

Three or more ventricular extrasystoles are a bad sign, and are termed ventricular tachycardia (VT).There is usually severe underlying myocardial disease. Sustained VT (more than about 30 beats) oftendegenerates into ventricular fibrillation, resulting in death.

The above strip shows several `characteristic' features of VT. Apart from the regular fast rate and widecomplexes, we have a few more clues ... clearly, the atrial rate is different from the ventricular rate, andthere is dissociation between atria and ventricles --- the P waves occur at any time in relation to theQRS complexes. Even more characteristic of VT is the presence of a fusion beat at the start of thetrace --- a QRS complex which is something in between the VT morphology and normal morphology.There is also a capture beat later on, where the P wave has managed to sneak through and transientlytake over, resulting in a normally-shaped QRS complex and T wave.

VT vs SVT+aberration

Distinguishing between VT, and SVT with aberration is tricky. When in doubt, one should applysynchronised DC countershock, and agonize later. This is especially the case if the patient ishaemodynamically unstable. If the patient is haemostable, the rate is slowish (under about 150), thenone may have more time. A variety of algorithms have been proposed - Brugada's approach may havemerit --- you can explore a web-based version of his algorithm here.

Ventricular fibrillation

This is a chaotic ventricular rhythm that rapidly results in death. It is often precipitated by a criticallytimed extrasystole, that occurs during the relative refractory period of the myocardial fibres.Conventional wisdom has it that this results in chaotic, unco-ordinated wavelets of depolarisationmoving through the ventricular mass.

VF is a dire emergency. If unsynchronised DC countershock is applied within 30s of the onset of VF,there is an approximately 97% chance that sinus rhythm will be restored, and the person will survive.Survival decreases exponentially thereafter, with every minute of delay.

Ventricular flutter

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

10 of 21 4/24/2013 7:49 PM

Ventricular 'flutter' is a bizarre sine-wave like rhythm, and usually degerates into ventricular fibrillation.You won't see it often (or for long).

Axis

The peculiar system we use in electrocardiography is non-Cartesian, and rather arbitrary! We measurethe direction of vectors in degrees, and zero is indeed facing `East', but +90o is South, instead of Northas it would be in a Cartesian system. You can work out that ± 180o is 'West', and that minus 90o is'North'.

We can talk about the `axis' of any ECG depolarisation, but most people when they are talking 'axis'are referring to the mean frontal plane QRS axis. There is a number of ways of determining this, but thefollowing method has the merit of simplicity:

Estimate the overall deflection (positive or negative, and how much) of the QRS in standard leadI;

1.

Do the same for AVF;2.Plot the vector on a system of axes, and estimate the angle, thus:3.

Note in the above picture that the (abnormal) axis illustrated is negative ("towards the left") becauseAVF is negative.

People tend to faff quite a lot about QRS axis deviations, but they are a fairly blunt-edged tool. Markedright axis deviation (e.g. +150o) may signify significant `right-sided' heart disease. Left axis deviation isnot uncommon in inferior myocardial infarction, and if this is absent, the most likely `diagnosis' is left

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

11 of 21 4/24/2013 7:49 PM

anterior hemiblock. (There are several other cause of left or right axis deviation, for exampledepolarisation via accessory pathways).

Where the axis is up and to the left (eg. -135o)*, this is termed a "north west axis". It is commonly seenin congenital heart disease, dextrocardia, and sometimes in severe chronic obstructive airway disease.

The T wave axis is much neglected, and may be of value. If the T wave axis is more than about 45 to60o different from the QRS axis, this is abnormal. Schamroth gives a super mnemonic --- "the T-waveaxis moves away from the `region of mischief'".

Even the P-wave axis is of use. The normal axis is about +40 to +60o, moving right with chronicobstructive disease. The axis may move left with congenital heart disease, even up to -30o (especiallyEbstein's anomaly). One can also spot an ectopic atrial focus low down in the atrium (`coronary sinusrhythm') due to the `northern' shift in axis.

*{Footnote: One reader pointed out that an axis of -135o could just as well be regarded as being `markedly to the right'. This

is a reasonable argument.}

The P wave

Normal atrial activation is over in about 0.10s, starting in the right atrium. A good place to look at Pwaves is in II, where the P shouldn't be more than 2.5mm tall, and 0.11 seconds in duration.

A tall P wave (3 blocks or more) signifies right atrial enlargement, a widened bifid one, left atrialenlargement:

In V1, another good place to look, depolarisation of the right atrium results in an initial positivedeflection, followed by a vector away from V1 into the left atrium, causing a negative deflection. Thenormal P wave in V1 is thus biphasic. It's easy to work out the corresponding abnormalities with leftor right atrial enlargement:

There are a few other tips:

A qR in V1 suggests right atrial enlargement, often due to tricuspid regurgitation! (Observed bySodi-Pallares).If the overall QRS amplitude in V1 is under a third of the overall QRS amplitude in V2, there isprobably RA enlargement! (Tranchesi).A P wave originating in the left atrium often has a `dome and dart' configuration.

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, tothe start of the very first r or q wave). A normal value is 3 to 5 `little blocks' (0.12 to 0.20 seconds). It'sconvenient at this point to discuss blocks...

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

12 of 21 4/24/2013 7:49 PM

SA node block

This is a diagnosis of deduction, as no electrical activity is seen. An impulse that was expected to arisein the SA node is delayed in its exit from the node, or blocked completely. A second degree SA blockcan be `diagnosed' if the heart rate suddenly doubles in response to, say, administration of atropine. Ifthe SA node is blocked, a subsidiary pacemaker will (we hope) take over, in the atrium, AV node, orventricle!

AV nodal blocks

There are three "degrees" of AV nodal block:

First degree block:1.

simply slowed conduction. This is manifest by a prolonged PR interval;

Second degree block:2.

Conduction intermittently fails completely. This may be in a constant ratio (more ominous, Type IIsecond degree block), or progressive (The Wenckebach phenomenon, characterised by progressivelyincreasing PR interval culminating in a dropped beat --- this is otherwise known as Mobitz Type Isecond degree heart block)*.

*{Footnote: Thanks to the reader who pointed out the typo}

Third degree block:3.

There is complete dissociation of atria and ventricles.

Clearly a bad thing, requiring temporary or even permanent pacing.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

13 of 21 4/24/2013 7:49 PM

The QRS complex

The nomenclature is mildly arcane --- small deflections are reflected using lower case, and largerdeflections UPPER CASE. An initial downwards deflection is a Q (or q), any negative deflection afterthis is an S. An upward deflection is an R. Note that we refer to a second deflection in the samedirection by adding a prime, so we have R', R'', S' and so on. We might thus refer to an rSR'morphology, or whatever.

Normally, the septum depolarises before other parts of the left ventricle. This is seen as a small initialvector, which in the `septal leads' (V1 and V2) is a positive deflection, and in lateral leads (e.g. V6) isseen as a small q. This observation is of relevance, as in conditions such as left bundle branch block,where the septum cannot depolarise normally, the lateral (septal) q is conspicuously missing.

Something of some importance is the time it takes the ventricle to depolarise, often termed theventricular activation time. We can estimate this from the surface ECG by looking at the time from theonset of the QRS to the sudden downstroke of the QRS. (The fancy name for this sudden downstrokeis the `intrinsicoid deflection'). In right orientated leads, a normal VAT is 0.02s, and on the left (e.g. V6)the duration should not exceed 0.04s.

Q waves - myocardial infarction

Many people who have had a prior MI will have an ECGthat appears normal. There may however be typical featuresof previous MI, and the most conspicuous of these is Qwaves. A simplistic explanation of these prominent Q wavesis that an appropriately placed lead "sees through" the deadtissue, and visualises the normal depolarisation of the viablemyocardial wall directly opposite the infarcted area.Because, in the normal myocardium, depolarisation movesfrom the chamber outwards, this normal depolarisation isseen as a Q wave!

Another feature of previous MI is loss of R wave amplitude.It's easy to imagine that if muscle is lost, amplitude must bediminished. (Having a pre-infarction ECG for comparisonis invaluable).

One can get some idea of the site of infarction from the lead in which abnormalities are seen - inferior,lateral, or anterior.

Hypertrophy and chamber enlargement

Because of the thin-walled nature of the atria, from an ECG point of view, one cannot talk about"atrial hypertrophy" but only about enlargement. Conversely, thickening of the ventricle may result inincreased voltages seen on the surface ECG, and we can then discuss "ventricular hypertrophy".

The absence of LVH on ECG means nothing, as the features are insensitive. If however they are

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

14 of 21 4/24/2013 7:49 PM

present, LVH is very likely. Because the criteria were formulated on white males, they are veryinsensitive in e.g. black women.

Systolic overload results in increased QRS deflections, with the sum of the S in V1 and the R in V5 orV6 over 35mm indicating hypertrophy. (In the above picture, also note the predominantly negativedeflection of the P wave in V1, suggesting left atrial enlargement). A host of other criteria have beenproposed. Useful are:

R in I over 15mmR in AVL over 11mmSum of all QRS voltages under 175mm (!)

T wave axis changes can be predicted knowing Schamroth's rule .

Features of LVH may be present (as above). Enormous R waves may be seen in left-sided leads,especially with aortic or mitral regurgitation. In contrast to systolic overload, where septal q waves inthe lateral leads are often diminished or absent, in diastolic overload, prominent lateral Qs are noted.Unlike systolic overload (where the T waves are often inverted), T waves are usually upright, verysymmetrical, and somewhat pointed.

Inverted U waves in V4-6 suggest either systolic or diastolic LV overload.

RV hypertrophy

A number of ECG abnormalities have been associated with right ventricular hypertrophy. Theseinclude:

right axis deviation;A tall R wave (bigger than the S) in V1;A `little something' in V1 (an initial slur of the QRS, a small r, or a tiny q).Increased VAT in V1left-sided RS or rS complexes, partial or complete RBBB, or RS complexes in the mid-precordialleads.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

15 of 21 4/24/2013 7:49 PM

Whenever you see a tall R in V1, consider the following differential:

posterior myocardial infarctionRV hypertrophyRight bundle branch blockWolff-Parkinson-White syndrome (with an appropriately placed accessory pathway)Other rare causes such as dextrocardia, Duchenne muscular dystrophy, and so onand, of course, incorrect lead placement!

Bundle branch blocks

A broadened QRS complex suggests a bundle branch block, although there are other causes:

RBBB

Diagnostic criteria for right bundle branch block are somewhat empiric, but useful. Here they are:

Tall R' in V1;1.QRS duration 0.12s or greater (some would say, >= 0.14);2.

In addition, there is usually a prominent S in the lateral leads (I, V5, V6).

RBBB is sometimes seen in normal people, or may reflect congenital heart disease (e.g. atrial septaldefect), ischaemic heart disease, cardiomyopathy, or even acute right heart strain.

LBBB

Diagnose this as follows:

No RBBB can be present;1.QRS duration is 0.12s or more;2.There must be evidence of abnormal septal depolarization. The tiny q waves normally seen inthe left-sided leads are absent. (And likewise for the normal tiny r in V1).

3.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

16 of 21 4/24/2013 7:49 PM

In addition, the VAT is prolonged, and tall, notched R waves are seen in the lateral leads (RR' waves).There is usually a notched QS complex in V1 and V2.

Fascicular blocks

Left anterior hemiblock (LAHB) is interruption of the thin anterosuperior division of the left bundle.Suspect it if there is left axis deviation (past -45o) without another cause (such as inferior myocardialinfarction, or some types of congenital heart disease or accessory pathways).

Other features of LAHB include an initial QRS vector which is down and to the right, a long VAT, andseveral other minor changes.

LAHB may indicate underlying heart disease, but is much more worrying when associated with otherabnormalities (such as PR interval prolongation or RBBB).

The diagnosis of left posterior hemiblock is mentioned only to be avoided!

The ST segment

The junction between QRS and ST

Hypothermia

Besides sinus bradycardia, the most common finding is a prominent J wave.

In addition, there may be delayed VAT , QRS prolongation, and nonspecific T wave abnormalities,with QT prolongation. Eventually, blocks, ventricular extrasystoles, and finally ventricular fibrillationoccurs, below 30oC.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

17 of 21 4/24/2013 7:49 PM

Ischaemic heart disease - ST changes

One should always remember that more than a quarter of people presenting with an acute myocardialinfarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edgedtool in the detection of coronary artery disease. Exercise testing to elicit ischaemia is also not verysensitive in detecting this common disease.

Acute myocardial infarction --- the `hyperacute phase'

There are four main features of early myocardial infarction (as per Schamroth):

increased VAT1.increased R wave amplitude (!)2.ST elevation which is sloped upwards!3.Tall, widened T waves (The ST segment often merges with these)4.

Note that Q waves are not seen early on.

Established acute myocardial infarction

We now lay great emphasis on ST segment elevation in diagnosingacute MI (In the past, Q waves were remarked on, but as notedabove, these are often absent, early on). The features of `full blown'MI may be:

prominent Q waves;1.elevated ST segments;2.Inverted `arrowhead' T waves.3.

Remember our previous warning, that a significant proportion ofpeople having an acute MI will have a normal ECG, so do not relyon any of these features to exclude MI.

Posterior MI

The trick in diagnosing this is to realise that posterior wall changes will be mirrored in the leadsopposite to the lesion --- V1 and V2. S we'll see a tall R (corresponding to a Q), ST depression, andupright arrowhead T waves:

Right ventricular infarction

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

18 of 21 4/24/2013 7:49 PM

This occurs in about 1/3 of patients with inferior MI, but is often missed. It would be distinctlyunusual in the absence of inferior MI. Sensitivity can be improved by looking at V4R --- V4, but putthe lead on the right side of the chest! Look for ST elevation which is higher than that in V1 -- 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).

Non-ST elevation MI

There are no reliable correlates of "subendocardial" or non-ST elevation MI, and the diagnosis isbased on the combination of clinical and laboratory criteria (troponin elevation being important).There may be no ECG changes, or even ST segment depression and/or T wave abnormalities.

Angina and stress testing

The most important component of an effort ECG that indicates the presence of coronary arterydisease 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, that is, 1mm (0.1mV) STdepression 0.08s after the J point;failure of suppression of ventricular ectopy, or (especially) development of ectopy in the recoveryperiod;Failure of the blood pressure to rise with exercise (an ominous finding);ST segment elevationT-wave changes (which may be rather nonspecific)Development of inverted U waves, which, although subtle, is said to be specific for the presenceof 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 thisvariant form of angina is that the predominant area of ischaemia is epicardial. This disorder is thoughtto be related to vascular spasm, and angiography shows coronaries without a significant burden ofatheroma. Many other morphological abnormalities have been described with this disorder.

Other morphological abnormalities

'Early repolarisation'

This is common --- ST segment elevation is conspicuous, often with a prominent J wave. It has beenremarked upon in athletes, particularly. It's important to relate the ECG to the clinical context, asalways, as otherwise one might inappropriately suspect serious underlying heart disease.

T waves

T wave abnormalities are common and often rather nonspecific. T-wave changes that suggestischaemia are a very sudden junction between the ST segment and the T wave, and very symmetrical T

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

19 of 21 4/24/2013 7:49 PM

waves. A variety of changes may be seen with cardiomyopathies, intracranial haemorrhage and so on.Symmetrical deep T-wave changes most prominent in V3 and V4 suggest ischaemia in the territory ofthe left anterior descending artery (LAD T0-waves). We should all know the features of hypo- andhyper-kalaemia.

Hyperkalaemia

Initial features are tall "tented" T waves. Later, despite the continuation of sinus rhythm, the P wavesdisappear, and finally, the QRS complexes broaden and become bizarre, the ST segment almostvanishes, and the patient dies from ventricular arrhythmia or cardiac standstill.

For features of hypokalaemia, see below .

Measures - QT

This is the time from onset of QRS to end of T wave. Because QT varies with rate, it is common toapply a correction, usually using Bazett's formula:

QTc = QTmeasured

---------------------

SQRT (RR interval)

SQRT refers to the square root. A normal value is about 0.39s ±0.04s (slightly larger values areacceptable in women). Be particularly concerned if the value is over 0.5, as may be seen in poisoningwith tricyclic antidepressants, congenital QT syndromes, hypocalcaemia, and toxicity from a variety ofother drugs (quinidine, procainamide, amiodarone, sotalol, erythromycin, etc). Other cause have beenreported, including hypothermia, head injury, acute myocardial infarction (!), and hypertrophiccardiomyopathy.

U waves

Hypokalaemia

The T waves flatten, U waves become prominent (this may be falsely interpreted as QT prolongation),and there may even be first or second degree AV block.

Several syndromes

Myocarditis

Common findings are tachycardia, heart blocks (first degree, LAHB), and increased VAT . A variety ofST changes may be seen, including those of myopericarditis. Atrial and ventricular extrasystoles arecommon.

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

20 of 21 4/24/2013 7:49 PM

Myopericarditis

Pericarditis is usually associated with a degree of contiguous myocarditis. The major manifestation iswidespread ST segment elevation.

There is also usually sinus tachycardia, and T wave abnormalities are common.

Pericardial effusion

The most common finding here is simply diminished amplitude of the ECG deflections. There mayalso be T wave inversion, and sometimes one sees electrical alternans .

Pulmonary thromboembolism

Apart from sinus tachycardia, ECG abnormalities are not common. The `classical' S1Q3T3 syndromeoccurs in under 10%. Other features may be those of right atrial enlargement, RV hypertrophy orischaemia, RBBB and atrial tachyarrhythmias.

Digoxin effect

ST segment changes are pretty characteristic, with their "reverse tick" conformation. These changes arenot indicative of toxicity, but merely the presence of digitalis. With toxicity, practically any arrhythmiacan be seen, although certain arrhythmias are highly suggestive, for example, the presence of bothincreased irritability and AV nodal block (such as paroxysmal atrial tachycardia with a 2:1 AV nodalblock).

Electrical alternans

Here, there is no rhythm disturbance, but the QRS amplitude alternates --- tall one beat, shorter thenext (and so on...). At fast rates, this is said to be of little significance, but at slower rates usuallysignifies severe heart disease, or pericardial effusion.

Bibliography and sources

A good general reference is Leo Schamroth's An Introduction to Electrocardiography, published byBlackwell Scientific. (7th Ed., 1990, ISBN 0-632-02411-9). It has the merits of clarity, accuracy anddepth. Leo was one of the truly great men of electrocardiography, and a brilliant physician, to boot.

A site we've encountered which shows promise is Learn The ECG. It's free, interactive and provides areasonable, basic approach to the ECG.

Date of First Publication: 2003/7/4 Date of Last Update: 2006/07/24 Web page author: Click here

The whole ECG - a really basic ECG primer http://www.anaesthetist.com/icu/organs/heart/ecg/index.htm

21 of 21 4/24/2013 7:49 PM

Related Documents
##### Pocket ECG
Category: Documents
##### ECG Interpretation
Category: Documents
##### ECG= MWAFI====
Category: Documents
##### ECG Basica
Category: Documents
##### Ecg pediátrico
Category: Documents
##### ECG Miscelaneous
Category: Health & Medicine
##### ECG Syllabus
Category: Documents
##### ECG Infarction
Category: Health & Medicine
##### ECG Normal
Category: Documents
##### Overview ecg
Category: Health & Medicine
##### ECG Cardiff and Vale ECG Department Electrocardiogram (ECG)....
Category: Documents
##### Cables Ecg
Category: Documents