how the ecg works

8/7/2019 How the ECG works

1/18

How the ECG worksWhen cell membranes in the heart depolarise, voltages change and currentsflow. Because a human can be regarded as a bag of salt water (with baadattitude), in other words, a volume conductor, changes in potential aretransmitted throughout the body, and can be measured. When the heartdepolarises, it's convenient (and fairly accurate) to represent the electricalactivity as a dipole --- a vector between two point charges. Remember that avector has both a size (magnitude), and a direction. By looking at how thepotential varies around the volume conductor, one can get an idea of thedirection of the vector. This applies to all intra-cardiac events, so we can talkabout 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 eventsWe assume some knowledge of heart anatomy. Note that the normal hearthas, electrically speaking, only two chambers, an atrial and a ventricular`chamber'. Propagation of electrical activity spreads freely within atria andventricles, but communication between these two chambers is limited to theAV node. Everyone knows that the P wave corresponds to atrialdepolarisation, the QRS complex to ventricular depolarisation, and the Twave 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 tiny changes in potential on the body surface. Weare talking about signals that are often around 1mV, and may be smaller. Inaddition, we need some reference point to which we relate the potentialchanges.

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.

Unipolar leads: The reference point is several leads joined together,and the sensing lead is on one limb. These leads are conventionallyaugmented, in that the reference lead on the limb being sensed isdisconnected from the other two.

The V leads, which extend across the precordium, V1 in the fourthright interspace, V2 4th left, V4 at the apex (5th interspace,


2/18

midclavicular line), V3 halfway in between V2 and V4, and V5 & V6 inthe 5th interspace at the anterior and mid axillary lines respectively.

We can visualise the directions of the various leads --- I points left, and aVFpoints directly down (in a 'Southward' direction). The other leads arearranged around the points of the compass --- aVL about 30o 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, and most deflections in that lead are negative.

(a net positive vector in AVR is unusual, and suggests that lead placementwas incorrect. If the leads were correctly sited, then think dextrocardia, orsome 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 AVFare inferior. V1 through V4 tend to look at the anterior 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 in any of the conventional leads, although "mirrorimage" changes will tend to be picked up in V1 and V2.

Paper

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

Always check the calibration voltage on the right of the ECG, and paperspeed. The following image shows the normal 1mV calibration spike:

Damping

Note that if the calibration signal is not "squared off" then the ECG tracing iseither 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 way of eyeballing the rate, and one method is asfollows:

1. Remember the sequence: 300, 150, 100, 75, 60, 502. Identify an R wave that falls on the marker of a `big block'3. Count the number of big blocks to the next R wave.

If the number of big blocks is 1, the rate is 300, if it's two, then the rate is150, and so on. Rates in between these numbers are easy to `interpolate'.


3/18

But always remember that in the heart, because we have two electrically`isolated' chambers, the atria and ventricles, that we are really looking attwo rates --- the atrial and ventricular rates! It just so happens that in thenormal heart, the two are linked in a convenient 1:1 ratio, via normalconduction down the AV node. In disease states, this may not be the case.

Conventionally, a normal heart rate has been regarded as being between 60and 100, but it's probably more appropriate to re-adjust these limits to 50 --

90/min. A sinus tachycardia then becomes any heart rate over 90, andbradycardia, less than 50. Note that you have to look at the clinical context-- a rate of 85 in a highly trained athlete may represent a substantialtachycardia, especially if their resting rate is 32/minute! One should alsobeware of agressively trying to manage low rates in the presence of goodperfusion and excellent organ function.

Sinus bradycardia

Apart from fit, but otherwise normal individuals, there's a long list ofsituations where sinus bradycardia 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; FEVER myocarditis

If the rate is almost exactly 150, always make sure that you are notmistaking atrial flutter with a 2:1 block for sinus tachycardia. A commonerror.

Rhythm

Sinus arrhythmia and heart rate variability


4/18

There is normallya slight degree of chaotic variation in heart rate, calledsinus arrhythmia. Sinus arrhythmia is generally a good thing, and loss of thischaotic variation is of ominous prognostic significance. Post myocardialinfarction, a metronome-like regularity of the heartbeat is associated with anincreased likelihood of sudden death, and just before the onset of ventriculartachycardia (or fibrillation), variability islost! Absence of any sinus arrhythmia suggestsan autonomic neuropathy.

Atrial extrasystoles

These arise from ectopic atrial foci. Commonly, the ectopic beat alwaysarises at about the same time after the sinus beat!

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

If the extrasystole occurs early on, it may find the His-Purkinje system notquite ready to receive an impulse, and a degree of block may be seen. Thisis termed `aberration'.

Distinguish between an atrial extrasystole,and an atrial escape beat, where the SAnode falters, and a subsidiary pacemakertakes over:

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

Supraventricular tachyarrhythmias (SVT)

Irregular SVT

By far the commonest cause of irregular SVT is atrial fibrillation, where theatrial rate is in the region of 450 to 600/min, and the atria really do notcontract rhythmically at all. The atrium "fibrillates", writhing like a bag ofworms. The conventional view of the pathogenesis of AF is that there aremultiple re-entrant `wavelets' moving through the atrial muscle, but recentevidence suggests that much AF actually arises from ectopic activity in themuscular cuff surrounding the pulmonary veins where they enter the leftatrium. AF is thought to beget further AF through "electrical remodelling" ---

electrophysiological changes that are induced in atrial myocytes due to fastrates and the consequent calcium loading.

Note that in the above tracing of AF, the ventricular response rate seemsrather slow, so we suspect that AV block has been increased usingpharmacological manipulation. In uncontrolled AF, rates of about 130 ormore are common.

Other causes of irregular SVT are:


5/18

Frequent atrial extrasystoles; Multifocal atrial tachycardia, where there are three or more distinctatrial foci, combined with tachycardia. There is often severe underlyingdisease (e.g. chronic obstructive airways disease), and in the ICUsetting, 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 Pwave configurations!

Regular SVT

Atrial flutter is common. The atrial rate iscommonly 300/min, and there is usually a 2:1block, resulting in a ventricular response rate of150/min. Other ratios are possible, and sometimesthe ratio varies. This rhythm is often unstable, andthe heart may flip in and out of sinus rhythm, or there may be runs of atrialfibrillation.

In the above ECG the clue is the rate. A rate of 150 should always engenderthe suspicion of atrial flutter with 2:1 block.

Probably the commonest cause of regular SVT is AV nodal re-entranttachycardia. Here, there are generally two ways that electricaldepolarisation 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 acircular fashion, and causing depolarisation of the ventricles at fast rates (upto 200/min or even more).

Other causes of regular SVT include:

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

Accessory pathways

Abnormal, congenital extra pathways between the atria and ventricles arecommon, and can perforate the electrically insulating fibrous ring that

normally separates the atrial `chamber' and the ventricular one. The mostwell-characterised is the Wolff-Parkinson-White syndrome. Reasonable(WHO) criteria for the WPW pattern on ECG are:

1. PR interval under 0.12s2. A delta wave3. QRS duration of 0.12s (or more)4. A normal P-wave axis

Because depolarisation moves `antegrade'from atria to ventricles, part of the ventricle


6/18

depolarises prematurely, and this is responsible for the slurred, initial deltawave. It should be clear that the PR interval will therefore be short, and theQRS duration should be prolonged. Note however that not everyone with anaccessory pathway will conduct all of the time down that pathway.Accessory pathways are common, estimated to occur in one to threeindividuals in every thousand. Symptomatic pathways are far less common.

The WPW syndrome is a combination of the WPW pattern, and tachycardias.

The tachycardias may be due to impulse conduction down via the AV nodeand back up the accessory pathway (commonest, called orthodromictachycardia), the other way around (down accessory pathway, up AV node,termed antidromic tachycardia), or even related to atrial fibrillation. This lastcause is ominous, as if the accessory pathway is able to conduct impulses atfast rates, the ventricle may be driven at rates in excess of 200/min, causingcollapse or even death.

Distinguishing causes of SVT

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

1. If the P is inscribed before the QRS, it's probably an ectopic atrialtachycardia;2. If the P is after the QRS, consider orthodromic AV re-entranttachycardia;3. If the P is not seen (and probably lost within the QRS) it's likely tobe AV nodal re-entrant tachycardia.

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 withinthe ventricular muscle, the QRS complex is wide,bizarre, and unrelated to a preceding P wave. Thereis usually a constant relationship (timing) betweenthe preceding sinus beat and a subsequentventricular beat, because the preceding beatinfluences the ectopic focus.

The ventricular beat is not usually conducted back into the atria. Whathappens to the atrial beat that occurred, or was about to occur when the VEhappened? Usually, this is blocked, but the subsequent atrial beat will occuron time, and be conducted normally.

Rarely, the ventricular beat may be conducted retrogradely and capture theatrium (resulting in a P wave after the QRS, with an abnormal morphology asconduction through the atrium is retrograde). The atrial pacemaker is nowreset! In the following rather complex tracing, we have a ventricular rhythm(a bit faster than one might expect, perhaps an accelerated idioventricularrhythm) with retrograde P waves, and something else --- some of the P


7/18

waves are followed by a normal looking `echo' beat as the impulse isconducted down back into the normal pathways).

Because the intrinsic rate of an ectopicfocus often tends to be slow-ish,extrasystoles will tend to arise more

commonly with slower rates. In addition, ifthe rate is varying, extrasystoles will tend to `squeeze in' during long RRintervals. 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 propagateinto the His-Purkinje system. This results in a `fusion beat', which combinesthe morphology of a normal sinus beat and that of the extrasystole.

Parasystole

Rarely, the ectopic focus is protectedfrom other influences, and does itsown merry thing. This is termed`parasystole', and is detected bynoting the unvarying coupling between extrasystoles, and the lack ofcoupling between the extrasystole and sinus beats! In the following trace,note the fusion beats as the normal rhythm and parasystolic rhythmtransiently coincide...

We've put in the above unusual ECG more as a mnemonic than for any otherreason. We want you to remember that even with extrasystoles, there is flowof information from the normal rhythm to the ectopic focus. The ectopicfocus 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 ventricularextrasystoles are a bad sign,and are termed ventricular

tachycardia (VT). There is usually severe underlying myocardial disease.Sustained VT (more than about 30 beats) often degenerates into ventricularfibrillation, resulting in death.

The above strip shows several `characteristic' features of VT. Apart from theregular fast rate and wide complexes, we have a few more clues ... clearly,the atrial rate is different from the ventricular rate, and there is dissociationbetween atria and ventricles --- the P waves occur at any time in relation tothe QRS complexes. Even more characteristic of VT is the presence of afusion beat at the start of the trace --- a QRS complex which is something inbetween the VT morphology and normal morphology. There is also a capture


8/18

beat later on, where the P wave has managed to sneak through andtransiently take over, resulting in a normally-shaped QRS complex and Twave.

VT vs SVT+aberration

Distinguishing between VT, and SVT with aberration is tricky. When in doubt,one should apply synchronised DC countershock, and agonize later. This isespecially the case if the patient is haemodynamically unstable. If the

patient is haemostable, the rate is slowish (under about 150), then one mayhave more time. A variety of algorithms have been proposed - Brugada'sapproach may have merit --- you can explore a web-based version of hisalgorithm here.

Ventricular fibrillation

This is a chaotic ventricular rhythm that rapidly results in death. It is oftenprecipitated by a critically timed extrasystole, that occurs during the relativerefractory period of the myocardial fibres. Conventional wisdom has it thatthis results in chaotic, unco-ordinated wavelets of depolarisation movingthrough the ventricular mass.

VF is a dire emergency. If unsynchronised DC countershock is applied within30s of the onset of VF, there is an approximately 97% chance that sinusrhythm will be restored, and the person will survive. Survival decreasesexponentially thereafter, with everyminute of delay.

Ventricular flutter

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

AxisThe peculiar system we use in electrocardiography is non-Cartesian, andrather arbitrary! We measure the direction of vectors in degrees, and zero isindeed facing `East', but +90o is South, instead of North as it would be in aCartesian system. You can work out that 180o is 'West', and that minus 90o

is 'North'.

We can talk about the `axis' of any ECGdepolarisation, but most people when they are talking'axis' are referring to the mean frontal plane QRS axis.
http://www.anaesthetist.com/icu/organs/heart/ecg/wctnotes.htmhttp://www.anaesthetist.com/icu/organs/heart/ecg/wctnotes.htm


9/18

There is a number of ways of determining this, but the following method hasthe merit of simplicity:

1. Estimate the overall deflection (positive or negative, and howmuch) of the QRS in standard lead I;2. Do the same for AVF;3. Plot the vector on a system of axes, and estimate the angle, thus:

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

People tend to faff quite a lot about QRS axis deviations, but they are a fairlyblunt-edged tool. Marked right axis deviation (e.g. +150o) may signifysignificant `right-sided' heart disease. Left axis deviation is not uncommonin inferior myocardial infarction, and if this is absent, the most likely`diagnosis' is left anterior hemiblock. (There are several other cause of leftor right axis deviation, for example depolarisation via accessory pathways).

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

The T wave axis is much neglected, and may be of value. If the T wave axisis more than about 45 to 60o different from the QRS axis, this is abnormal.Schamroth gives a super mnemonic --- "the T-wave axis moves away fromthe `region of mischief'".

Even the P-wave axis is of use. The normal axis is about +40 to +60o,

moving right with chronic obstructive disease. The axis may move left withcongenital heart disease, even up to -30o (especially Ebstein's anomaly).One can also spot an ectopic atrial focus low down in the atrium (`coronarysinus rhythm') due to the `northern' shift in axis.

*{Footnote: One reader pointed out that an axis of -135o could just as well be regarded asbeing `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 P waves is in II, where the P shouldn't be more than2.5mm tall, and 0.11 seconds in duration.

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

In V1, another good place to look,depolarisation of the right

atrium results in an initial positive


10/18

deflection, followed by a vector away from V1 into the left atrium, causing anegative deflection. The normal P wave in V1 is thus biphasic. It's easy towork out the corresponding abnormalities with left or right atrialenlargement:

There are a few other tips:

A qR in V1 suggests right atrial enlargement, often due to tricuspid

regurgitation! (Observed by Sodi-Pallares). If the overall QRS amplitude in V1 is under a third of the overall QRSamplitude in V2, there is probably 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 theQRS complex (that is, to the start of the very first r orq wave). A normal

value is 3 to 5 `little blocks' (0.12 to 0.20 seconds). It's convenient at thispoint to discuss blocks...

SA node block

This is a diagnosis of deduction, as no electrical activity is seen. An impulsethat was expected to arise in the SA node is delayed in its exit from thenode, or blocked completely. A second degree SA block can be `diagnosed' ifthe heart rate suddenly doubles in response to, say, administration ofatropine. If the SA node is blocked, a subsidiary pacemaker will (we hope)take over, in the atrium, AV node, or ventricle!

AV nodal blocks

There are three "degrees" of AV nodal block:

1. First degree block:

simply slowed conduction. This ismanifest by a prolonged PRinterval;

2. Second degree block:

Conduction intermittently fails completely. This may be in a constant ratio(more ominous, Type II second degree block), or progressive (TheWenckebach phenomenon, characterised by progressively increasing PRinterval culminating in a dropped beat --- this is otherwise known asMobitz Type I second degree heart block)*.


11/18

*{Footnote: Thanks to the reader who pointed

out the typo}

3. Third degree block:

There is complete dissociation of atria and ventricles.

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

The QRS complex

The nomenclature is mildly arcane --- small deflections are reflected usinglower case, and larger deflections UPPER CASE. An initial downwardsdeflection is a Q (or q), any negative deflection after this is an S. An upwarddeflection 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 thusrefer to an rSR' morphology, or whatever.

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

Something of some importance is the time it takes the ventricle todepolarise, often termed the ventricular activation time. We can estimatethis from the surface ECG by looking at the time from the onset of the QRS

to the sudden downstroke of the QRS. (The fancy name for this suddendownstroke is the `intrinsicoid deflection'). In right orientated leads, anormal VAT is 0.02s, and on the left (e.g. V6) the duration should not exceed0.04s.

Q waves - myocardial infarction

Many people who have had a prior MI will have an ECG that appearsnormal. There may however be typical features of previous MI, and the


12/18

most conspicuous of these is Q waves. A simplistic explanation of theseprominent Q waves is that an appropriately placed lead "sees through" thedead tissue, and visualises the normal depolarisation of the viablemyocardial wall directly opposite the infarcted area. Because, in thenormal myocardium, depolarisation moves from the chamber outwards,this normal depolarisation is seen as a Q wave!

Another feature of previous MI is loss of R wave amplitude. It's easy toimagine that if muscle is lost, amplitude must be diminished. (Having apre-infarction ECG for comparison is invaluable).

One can get some idea of the site of infarction from the lead in whichabnormalities 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".

Left ventricular systolic overload/hypertrophy (LVH)

The absence of LVH on ECG means nothing, as thefeatures are insensitive. If however they are present,LVH is very likely. Because the criteria wereformulated on white males, they are veryinsensitivein e.g. black women.

Systolic overload results in increased QRS deflections, with the sum of the Sin V1 and the R in V5 or V6 over 35mm indicating hypertrophy. (In the abovepicture, also note the predominantly negative deflection of the P wave in V1,suggesting left atrial enlargement). A host of other criteria have beenproposed. 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 .

LV diastolic overload

Features of LVH may be present (as above). Enormous R waves may be seenin left-sided leads, especially with aortic or mitral regurgitation. In contrastto systolic overload, where septal q waves in the lateral leads are oftendiminished or absent, in diastolic overload, prominent lateral Qs are noted.Unlike systolic overload (where the T waves are often inverted), T waves areusually upright, very symmetrical, and somewhat pointed.

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


13/18

RV hypertrophy

A number of ECG abnormalities have been associated with right ventricularhypertrophy. These include:

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

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

posterior myocardial infarction RV hypertrophy Right bundle branch block Wolff-Parkinson-White syndrome (with an appropriately placedaccessory pathway) Other rare causes such as dextrocardia, Duchenne musculardystrophy, and so on and, of course, incorrect lead placement!

Bundle branch blocks

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

RBBB

Diagnostic criteria for right bundle branch block are somewhat empiric, but

useful. Here they are:

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

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

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

LBBB

Diagnose this as follows:

1. No RBBB can be present;2. QRS duration is 0.12s or more;


14/18

3. There must be evidence of abnormal septal depolarization. The tinyq waves normally seen in the left-sided leads are absent. (And likewisefor the normal tiny r in V1).

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

Fascicular blocks

Left anterior hemiblock (LAHB) is interruption of the thinanterosuperior division of the left bundle. Suspect it if there isleft axis deviation (past -45o) without another cause (such asinferior myocardial infarction, or some types of congenital heart disease oraccessory pathways).

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

LAHB may indicate underlying heart disease, but is much more worryingwhen associated with other abnormalities (such as PR interval prolongationor 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 commonfinding is a prominent J wave.

Ischaemic heart disease - ST changes

In addition, there may be delayed VAT , QRS prolongation, and nonspecific Twave abnormalities, with QT prolongation. Eventually, blocks, ventricularextrasystoles, and finally ventricular fibrillation occurs, below 30oC.

One should always remember that more than a quarter of people presentingwith an acute myocardial infarction will have no ECG evidence of ischaemiaor infarction! The ECG on its own is a blunt-edged tool in the detection ofcoronary 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):

1. increased VAT


15/18

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

Note that Q waves are not seen early on.

Established acute myocardial infarction

We now lay great emphasis on ST segment elevation indiagnosing acute MI (In the past, Q waves wereremarked on, but as noted above, these are oftenabsent, early on). The features of `full blown' MI may be:

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

Remember our previous warning, that a significantproportion of people having an acute MI will have a normalECG, so do not rely on any of these features to exclude MI.

Posterior MI

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

Right ventricular infarction

This occurs in about 1/3 of patients with inferior MI, but is often missed. It

would be distinctly unusual in the absence of inferior MI. Sensitivity can beimproved by looking at V4R --- V4, but put the lead on the rightside of thechest! Look for ST elevation which is higher than that in V1 -- V3. Anothersuggestive feature is lackof ST depression in V1 with evidence of MI in theinferior leads (look for ST depression in V2 under 50% of the ST elevation inAVF).

Non-ST elevation MI

There are no reliable correlates of "subendocardial" or non-ST elevation MI,and the diagnosis is based on the combination of clinical and laboratorycriteria (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 presenceof coronary artery disease is where exercise reproduces the patient's chestdiscomfort or pain. Other findings may be:

ST segment depression (It is customary to apply the Sheffieldcriteria, that is, 1mm (0.1mV) ST depression 0.08s after the J point; failure of suppression of ventricular ectopy, or (especially)development of ectopy in the recovery period;


16/18

Failure of the blood pressure to rise with exercise (an ominousfinding); ST segment elevation T-wave changes (which may be rather nonspecific) Development of inverted U waves, which, although subtle, is said tobe 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 STsegment elevation with this variant form of angina is that the predominantarea of ischaemia is epicardial. This disorder is thought to be related tovascular spasm, and angiography shows coronaries without a significantburden of atheroma. Many other morphological abnormalities have beendescribed with this disorder.

Other morphological abnormalities

'Early repolarisation'

This is common --- ST segment elevation is conspicuous, often with aprominent J wave. It has been remarked upon in athletes, particularly. It'simportant to relate the ECG to the clinical context, as always, as otherwiseone might inappropriately suspect serious underlying heart disease.

T waves

T wave abnormalities are common and often rather nonspecific. T-wavechanges that suggest ischaemia are a very sudden junction between the STsegment and the T wave, and very symmetrical T waves. A variety of

changes may be seen with cardiomyopathies, intracranial haemorrhage andso on. Symmetrical deep T-wave changes most prominent in V3 and V4suggest ischaemia in the territory of the left anterior descending artery (LADT0-waves). We should all know the features of hypo- and hyper-kalaemia.

Hyperkalaemia

Initial features are tall "tented" T waves. Later, despite the continuation ofsinus rhythm, the P waves disappear, and finally, the QRS complexesbroaden and become bizarre, the ST segment almost vanishes, and thepatient dies from ventricular arrhythmia or cardiac standstill.


17/18

For features of hypokalaemia, see below .

Measures - QT

This is the time from onset of QRS to end of T wave. Because QT varies withrate, it is common to apply 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 are acceptable in women). Be particularly concerned ifthe value is over 0.5, as may be seen in poisoning with tricyclicantidepressants, congenital QT syndromes, hypocalcaemia, and toxicityfrom a variety of other drugs (quinidine, procainamide, amiodarone, sotalol,erythromycin, etc). Other cause have been reported, including hypothermia,head injury, acute myocardial infarction (!), and hypertrophiccardiomyopathy.

U waves

Hypokalaemia

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

Several syndromes

Myocarditis

Common findings are tachycardia, heart blocks (first degree, LAHB), andincreased VAT . A variety of ST changes may be seen, including those ofmyopericarditis. Atrial and ventricular extrasystoles are common.

Myopericarditis

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

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

Pericardial effusion

The most common finding here is simply diminished amplitude of the ECGdeflections. There may also be T wave inversion, and sometimes one seeselectrical alternans .

Pulmonary thromboembolism


18/18

Apart from sinus tachycardia, ECG abnormalities are not common. The`classical' S1Q3T3 syndrome occurs in under 10%. Other features may bethose of right atrial enlargement, RV hypertrophy or ischaemia, RBBB andatrial tachyarrhythmias.

Digoxin effect

ST segment changes are pretty characteristic, with their "reverse tick"conformation. These changes are not indicative of toxicity, but merely the

presence of digitalis. With toxicity, practically any arrhythmia can be seen,although certain arrhythmias are highly suggestive, for example, thepresence of both increased irritability and AV nodal block (such asparoxysmal atrial tachycardia with a 2:1 AV nodal block).

Electrical alternans

Here, there is no rhythm disturbance, but the QRS amplitude alternates ---tall one beat, shorter the next (and so on...). At fast rates, this is said to beof little significance, but at slower rates usually signifies severe heartdisease, or pericardial effusion.

how the ecg works

Documents