Interpretation of the Electrocardiogram

Accurate interpretation of an E .C .G. may provide valuable information on the assessment of a patient’s cardiovascular system. Students, both under-graduate and post-graduate, may have to interpret an E.C.G. in the course of their daily ward duties or during a clinical examination and in this article emphasis is placed on the main diagnostic features of some of the more common E.C.G. abnormalities. Numerous books are available for more advanced study. The E.C.G. is particularly useful in the diagnosis of cardiac rhythm and myocardial infarction. It may reveal evidence of conduction defect, hypertrophy of the myocardium or pericarditis and may also indicate therapeutic response in certain electrolyte disturbances. On the other hand, non-specific E.C.G. changes


E L E C T R O P H Y S IO L O G Y
L ik e every living cell a cardiac m u scle fibre at rest is polarised; th e cell m em brane has a positive charge on its outer surface and a negative charge w ithin.W h e n stim ulated th e p olarity reverses and th e in tra c ellu lar p oten tial b ecom es positive.T h is rapid change "(depolar isation) is follow ed by a slow er recovery phase (repolarisation) u n til th e cell is again in its resting or polarised state.
As this activity spreads along th e m u scle c ell an actio n p o te n tial is produced w hich m ay be d etected by co n n e ctin g suitably placed m icro-electrodes to a recording galvanom eter.
T h e E .C .G . is a m eth od o f recording these electrical forces w h ich occu r in h e a rt m uscle.T h e in stru m en t is designed to produce a posi tive or upward d eflection on th e tracing when an im pulse passes towards an electrod e and vice versa.A t rest, i.e. when no cu rren t is flowing, th e base lin e of th e tracing is h o rizo n tal or iso-electric.

G E N E S IS O F T H E E .C .G .
In a norm al h eart the sino-atrial node orig inates th e cardiac im pulse.T h is im pulse spreads over b o th atria to reach th e atrio v entricu lar node.I t then passes through the b u n d le of H is and down the m ain con d u ctin g bundles on the le ft and right of the interv en tricular septum .
T h e ventricular m uscle is stim ulated as the im pulse passes from endo cardial to epicardial surface through the specialised con d u ctio n tissue of P u rk in je.
T h e s e events are illustrated diagram atically in F ig .i .T h e v entricu lar septal activation Conduction pathway of the heart to show the gen esis of the ECG recorded from 2 electrodes one over the right ventricle (V I) the other over the left ven tricle (V6).
in the normal heart passes from the left to the right side.
Thereafter, both ventricles are activated sim ultaneously but the wave form produced by stimulation of the left ventricle predominates over that of the right ventricle since its muscle mass is always greater.
E .C .G .waves are designated by the letters:-P.Q .R .S. T .U . ( F i g .2); small letters may be used for relatively small waves, e.g.q, r, s.T h e P wave is produced by atrial depolarisation; the O R S com plex is produced by depolarisation of the ventricular septum and muscle of both ventricles while the S T segment represents com plete ventricular depolarisation.Subse quent recovery (or repolarisation) is denoted by the T wave and U wave.
T V i -fourth right interspace adjacent to sternum V 2 -fourth left interspace adjacent to sternum V 3 -mid-way between V 2 and V 4 V 4 -fifth le ft interspace in mid clavi cular line V 5 -in same horizontal plane as V 4 but in the anterior axillary line V 6 -as for V 5 in mid-axillary line U nipolar leads record electrical forces at the site of the exploring electrode on the indiv idual lim b or position on the chest.These routine leads provide a satisfactory survey of the electrical forces over different parts of the heart in the frontal (limb leads) and horizon tal (chest leads) planes for routine recording but if more extensive cover is necessary add itional leads may be recorded on the right (V 3 R , V 4 R ), round the back of the chest (V 7 to V 9) and in higher interspaces.

V5 V6
W h en these leads are related to the elec trical forces in the norm al heart it w ill be apparent that the significance of the different E .C .G .waves varies with the lead in which they are recorded ( F ig .3).A few examples will m ake this c le a r : 1.A V R faces the cavities of the heart.T h e electrical force from the S A node spreads over the atria away from the electrode and the P wave is therefore negative.D epolarisation of the septum and the ventricles also passes away from the electrode and produces a deep neg ative wave (Q).T h e T wave is also negative.2. V i usually faces the heart in the region of the right atrioventricular junction.
T h e electrical force from the S A node m ay pass towards the electrode producing an upright P wave or m ay be interm ediate and produce a diphasic P as illustrated; the electrical force through the ventricular septum is towards the electrode and the initial ventricular deflection is therefore a small r wave.As the ventricles are activated, the greater mass of the left ven tricle generates the dom inant electrical force away from the electrode and this is reflected in the deep S wave.T h e T wave is also neg ative.3. V 6 faces the epicardial surface of the left ventricle; the initial electrical force through the ventricular septum is away from the elec trode so that an initial small Q wave precedes the tall R wave produced by le ft ventricular activation.

ARTEFACTS
A n E .C .G .tracing m ay be distorted by electrical currents w hich are not produced by the heart, e.g.m uscle m ovem ents o f the body (shivering), faulty contact between skin and electrode, electrom agnetic disturbances in the environm ent.
T h e patient should therefore be relaxed, com fortable and warm ; electrodes should be clean and firm ly applied and the instrum ent m ust be adequately earthed.

MEASUREMENT AND TIM ING OF E.C.G. WAVES
E .C .G .tracing paper is squared in m illi metres with bold lines every 5 m m .(Fig. 2).
In order to ensure uniform ity, all records should be standardized so that an im pulse of 1 mv.produces a deflection of 10 m m . in height on the tracing.Records from the same patient at different times and those from other patients m ay then be com pared.Each mm.length represents a time interval of 0.04 second and a bold line occurs every 0.2 second.
T h e P R interval or atrioventricular conduction time represents the time interval between the onset of atrial and the onset of ventricular depolarisation.It is measured from the start of the P wave to the beginning of the Q wave of the ventricular com plex.
In adults the norm al range fo r the P R interval is between 0 .12and 0.20 second (3 and 5 small squares).T h e norm al Q R S com plex is less than 0 .10second and seldom m ore than 0.08 second (2 small squares).

HEART RATE
H eart rate is m ost readily calculated by counting the num ber of bold lines between com parable points on successive cardiac cycles (usually the peaks o f the R waves).
T his number, divided into 300 (300/ 5ths of a second per minute) gives the heart rate per m inute, i.e. 3 = 100 per m inute; 4 = 75 per m inute; 5 = 60 per m inute; 6 = 50 per minute.I f the points do not co-incide with a bold line, the num ber o f sm all squares m ay be counted and this num ber divided into 1500 (1500 times 0.04 second = 1 m inute).W h en the rhythm is irregular, the heart rate m ay be calculated b y m ultiplying the num ber of car diac cycles between 30 bold lines (6 seconds) by 10.

E.C.G. INTERPRETATION
T h e norm al E .C .G .pattern in the different leads varies to som e extent with the position of the heart in the chest, obesity, chest and spinal deform ities, the phase of respiration and the height of the diaphragm.T h ere is therefore a wide range o f norm ality which has to be taken into account before changes in the pattern can be attributed to heart disease.It m ust also be recognised that the normal E .C .G .per se does not exclude serious under lying heart disease.

DISORDERS OF RATE, RHYTHM AND CONDUCTION
Interpretation o f an E .C .G .should always be correlated with the patient's age, clinical features and current or previous digitalis ad m inistration.
O ne should always look over the whole record since the rate and rhythm need not necessarily remain constant.A t this initial survey one can also see if the rhythm is regular or irregular, whether the ventricular complexes are consistent in shape or whether bizarre form s are present.T h e next step is to look for P waves and check their relationship to the Q R S complexes.T h is is usually seen m ost clearly in leads I I and V i .N orm al sinus rhythm (F ig .4A) is present when P waves precede each Q R S complex; the P R interval remains constant (within the norm al range); the ventricular com plexes occur regularly and the cardiac rate is between 60 and 100 per m inute.Sinus rhythm with a rate less than 60 per m inute is a sinus brady cardia and when over 100 per m inute is con sidered to be a sinus tachycardia.Variation of the heart rate with respiration, becom ing faster with inspiration and slower with expir ation, is called sinus arrhythm ia (F ig.4B).It is a normal variant and should not be confused with sino-atrial block which is abnormal.Sino atrial block is caused by failure of the S A node to initiate a cardiac impulse resulting in absence of a com plete cardiac cycle (F ig .4C ).
Atrioventricular block which is also abnor m al m ay occur in various forms.First-degree atrioventricular block is present when the P R interval exceeds 0.2 second (F ig .4D ).Seconddegree A V block occurs in two forms.T h e first is characterized by a series o f cardiac cycles in which there is progressive lengthening of the P R interval until an im pulse is blocked and fails to initiate a Q R S com plex (F ig .4E ).

A. B c.
D.

E. F.
G. T h is sequence is known as a W enckebach period.

I. h
Follow in g each blocked beat the sequence is repeated.W enckebach periods m ay be short or long but are usually constant in any particular patient.In the other form of second-degree atrioventricular block the P waves are regular and the P R interval is con stant but the im pulse is blocked usually after every second atrial beat (2 : 1 atrioventricular block) (Fig. 4 F) or less frequently in a more com plex pattern (3:1, 3:2).Third-degree or co m p lete heart block is characterised by com plete independence of P waves and Q R S com plexes (F ig .4 G ). T h e atrial rate is usually norm al while the ventricular rate, although regular, is slow at about 40 per m inute o r less.T h e ventricular com plexes often have a bizarre shape since their focus of activation lies outwith the norm al conduction pathway.

ATRIAL ARRHYTHMIAS
Irregularities of the rhythm m ay arise from ectopic foci in the atria or A V node.T h ese supraventricular ectopics have norm al Q R S com plexes but the P wave m ay be distorted and the P R interval depends on the distance between the ectopic focus and the A V node (F ig.5A).W h en the ectopic focus is in the A V node itself the P waves are inverted in leads II, I I I and A V F and m ay precede (Fig .5B) or follow (F ig .5D ) the ventricular com plex.T h is depends on the delay in retrograde conduction into the atria.Som etim es the P wave cannot be seen (F ig .5C ), since it is in corporated into the ventricular com plex.A rapidly recurring series o f supraventricular ectopic beats constitute a supraventricular (atrial or nodal) tachycardia (Fig. 5E ).T h e rate m ay vary from 15 0 to 250 per m inute but is perfectly regular in any particular case.P waves which are often small and of abnormal shape, m ay be difficult to identify.T h e ven tricular com plexes have a norm al configur ation.If the tachycardia continues for m ore than a few hours secondary m yocardial ischaemia m any cause S T segment and T wave changes.
A trial flutter, like paroxysmal atrial tachy cardia, is due to a rapid series of impulses arising from an ectopic focus w ithin the atria.Atrial flutter distorts the base line o f the E .C .G .by so-called " saw-toothed" , regularly recurring flutter waves at a rate of 200 to 350 per m inute (Fig .5F).
T h e ventricles can seldom respond to such a rapid rate bu t are activated by every second or third flutter wave.T h e ventricular rate is usually regular (2:1, 3:1 or 4:1) and the Q R S complexes have a normal configuration although the S T seg ments are distorted by the flutter waves.Sometimes the ventricular response varies with resultant irregularity of the heart rate.
Atrial fibrillation is characterised by com pletely disordered atrial activity (F ig .5G).
T h e E .C .G .tracing shows an irregular base line which may vary from coarse irregular waves to almost a flat line.T he ventricular response is totally irregular.
Before leaving atrial arrhythmias, mention should be made of paroxysmal atrial tachy cardia (PAT) with block (Fig. 5H).This is un common and when present it is usually due to digitalis toxicity.T he atrial rate is about 180 per minute (120 to 250) but in contrast to atrial flutter there are iso-electric intervals be tween peaked P waves.
Ventricular ectopics are readily distinguish ed from those of supraventricular origin by their broad, bizarre shape and inverted T waves (F ig .5I).This is because their conduc tion pathway to the rest of the myocardium is through ventricular muscle rather than through normal conducting tissue.Ventric ular beats arising from the same focus have the same bizarre shape in any particular lead but when they arise from different foci the complexes vary in shape.Ventricular ectopics may occur singly or in runs of 2 or 3 in rapid succession.
W hen a ventricular ectopic follows each normal beat this is known as coupled rhythm.
A rapidly recurring series of ventricular ectopic beats constitute ventricular tachycardia (Fig. 5J).Th e rate usually varies between 150 and 200 per minute and is slightly irregular.P waves may sometimes be detected occurring at an independent slower rate.Ventricular tachycardia is a dangerous arrhythmia usually due to serious myocardial disease.It may herald the onset of ventricular fibrillation (F ig.5K) with cessation of ventricular contraction.

C A R O T ID S IN U S P R E S S U R E
T he electrocardiographic interpretation of tachycardia is not always easy but can often be clarified by the response to vagal stimul ation produced by carotid sinus massage.Carotid stimulation should be performed with the patient recumbent while an E .C .G .trace is being recorded.T h e carotid sinus is at the bifurcation of the common carotid artery.This point lies just below the angle of the jaw and once the vessel has been palpated, gentle massage is applied postero-medially in the line of the vessel with either the thumb or two or three fingers.T h e vessel lumen should not be obliterated.Each side should be massaged separately, since one side is fre quently more sensitive than the other.Sinus tachycardia responds with temporary slowing of the heart rate whereas a supraventricular tachycardia will cease abruptly or remain un affected.W ith atrial flutter the ventricular response is temporarily slowed to reveal the characteristic " saw-toothed" flutter waves which previously may have been obscured by the ventricular complexes (F ig .5F).Very occasionally, atrial flutter may revert to sinus rhythm.P A T with block responds to carotid sinus pressure in the same way as atrial flutter.T he ventricular rate in atrial fibrillation is sometimes slowed temporarily but ventricular tachycardia is unresponsive.
Atrial Hypertrophy.Atrial hypertrophy may be revealed by the size and shape of the P waves.Tall peaked P waves (over 2.5 mm. in height), seen best in leads II, III and A V F and in the right chest leads, suggest right atrial hypertrophy (F ig .6B).Broadened bifid P waves (longer than 0 .12second) usually seen best in leads I, II, a V R and a V L suggest left atrial hypertrophy.These P wave changes which are sometimes transient may result from temporary atrial hypertension, but are seldom sufficiently marked to constitute cer tain evidence of hypertrophy of the atrial walls.2. Ventricular Hypertrophy.T he amplitude of the Q R S complex is increased by ventric ular hypertrophy but it may be affected by many other factors such as body build and the closeness of the heart to the chest wall.In contrast, significant degrees of ventricular hypertrophy may be present before the ampli tude of the Q R S complex affords certain E .C .G .confirmation of its presence.
Left ventricular hypertrophy.In an adult of normal build, left ventricular hypertrophy is suggested by the following criteria: (a) a combined amplitude of the S wave in V i and the R wave in V 5 or V 6 ex ceeding 35 mm.(Fig. 6A).
(b) an R wave in a V L exceeding 1 3 m m.(c) an R wave in a V F exceeding 2 1 mm.N one of these figures is absolute and not all of them need be present in any one case.In children and thin adults sim ilar large voltage com plexes m ay be norm al variants.
R ig h t ventricular hypertrophy.T h e E .C .G .changes of right ventricular hypertrophy are less striking since right ventricular hyper trophy seldom exceeds the bulk of the norm al left ventricle.
N evertheless, leads over the right ventricle (V I, V 3 R , V 4 R ) m ay show a dom inant R wave instead o f the norm al S wave ( F ig .6B).T h ese additional leads should always be recorded when right ventricular hypertrophy is suspected b ut is not revealed in lead V I.
In m ore advanced cases of ventricular h yper trophy, repolarisation is abnorm al. T h e S T segm ent m ay be depressed and the T wave asym m etrically inverted in leads over the left ventricle in left ventricular hypertrophy ( F ig .6A) and in leads over the right side o f the heart in right ventricular hypertrophy ( F ig .6B).
Som e T wave inversion is a normal variant in leads V 4 R , V 3 R and V I so that these changes are only significant o f right ventricular hypertrophy when marked or ex tend to lead V 2 or V 3 .T h e S T segm ent and T wave changes are due to relative ischemia or replacem ent fibrosis and constitute a m ani festation o f " strain" on the relevant ventricle.Som etim es a " strain" pattern occurs w ithout electrocardiographic evidence o f ventricular hypertrophy.

BUNDLE BRANCH BLOCK
C o m p lete bundle branch block produces broad, notched or slurred Q R S com plexes (their duration measures 0 .12sec.or more) and abnorm alities o f the S T segments and T waves in all leads.T h ese changes are due to: 1) the excitation wave passing through atypical pathways in the m yocardium on the side of the blocked conduction bundle.2) asynchronous activation o f the two ven tricles.3) abnorm al repolarisation after delayed ventricular activation.T h e shape o f the com plex depends upon whether the le ft or right main bundle branch is blocked.In right bundle branch block delayed acti vation of the right ventricle causes a tall secondary R wave in the right ventricular leads and a slurred terminal S wave in the left ven tricular leads (Fig .7).
In left bundle branch block the initial small Q wave of septal activation is absent in the left ventricular leads and late activation of the left ventricle delays the peak of the R wave which is notched or slurred on the upstroke by earlier right ventricular activation.This also causes notching or slurring of the QS complex in the right ventricular leads.These changes are best seen in the chest leads The E.C .G .usually develops characteristic changes after a recent myocardial infarction.
In leads overlying an infarcted area these changes, in order of their appearance, are:-1 ) elevation of the ST segment, 2) the appear ance of a pathological Q wave, 3) symmetrical inversion of the T wave.
The recognition and interpretation of these changes becomes clearer if the mechanism of their origin is understood.

C H A N G ES IN T H E ST S E G M E N T S
As noted previously a resting normal muscle has a positive surface charge but when stim ulated or injured this surface charge becomes negative (the negative current of injury).An anoxic area on the epicardial surface of the heart will therefore have a constant negative charge while surrounding healthy muscle will carry a normal positive charge.This differ ence of potential between injured and normal myocardium is reflected in the E .C .G .as a depression of the normal base line in leads overlying the injured area and as an elevation in leads over normal m yocardium (F ig .8 A).
W h e n the healthy m uscle is activated it also becom es negative and current will cease flow ing.T h e depressed base line therefore re turns to the normal iso-electric level giving the impression of an elevated S T segm ent (F ig .8B).W h e n healthy m uscle is restored to its resting state the negative current of injury reappears and the base line again becomes depressed.
Pathological Q waves of myocardial infarc tion exceed 0.04 second in duration and may be deep.
T h e y only appear when the in farct involves the w hole thickness of the ventricular wall (transmural infarction) and do so because the infarcted m yocardium , being dead, is " electrically inactive" .Leads overlying an infarcted area of left ventricle there fore record electrical forces of exactly the same pattern as those w ithin the cavity of the ven tricle, i.e. the deep Q wave of a V R in the normal E .C .G .(vide supra).

SYMMETRICAL T W AVE INVERSION
T his does not appear until recovery of the infarcted m uscle has begun.
E .C .G .changes of m yocardial infarction follow a sequence, the tim e intervals of which vary within wide lim its.S T elevation usually disappears within the first few days w hile the pathological Q waves may decrease in size but usually persist for years and often remain as a perm anent abnorm ality.
Inverted T waves w hich develop as the S T elevation subsides usually becom e upright during the first few months bu t also m ay persist for years.T h is sequence of events is illustrated in F ig .6C. Leads facing the opposite side of the heart m ay show reciprocal S T depression during the acute stage and tall peaked T waves as re covery takes place (F ig .6D).
T h e position o f the infarcted area can be localised by the leads in w hich the infarct pattern develops.
Anterior myocardial infarction is shown in the chest leads and norm ally in leads I and a V L .
Inferior myocardial infarction is shown in leads II, III and a V F .
W h e n an infarct does not involve the whole thickness of the ventricular wall (intra-m ural infarction) the changes affect only the S T segments and T waves.Q waves do not develop.
A lthough the characteristic E .C .G .changes of m yocardial infarction develop w ithin the first few hours of its occurrence this is not invariable and diagnosis then depends on the clinical picture and elevation of certain scrum enzym e levels.It m ust be recognised that in som e patients E .C .G .confirm ation of a m yo cardial infarction m ay never occur while in others it m ay only develop after an interval of days.A dditional leads in higher interspaces or round the back of the chest m ay be re quired to detect and localise an infarct.

ANGINA PECTORIS AND MYOCARDIAL ISCHAEMIA
Angina pectoris is usually diagnosed from the patient's history of exertional chest pain.T h e E .C .G . is usually norm al but m ay show evidence of m yocardial ischaemia, especially if recorded while the patient has pain.W h en the history is equivocal and the resting record negative an exercise test m ay establish the diagnosis (vide infra).T h e E .C .G .feature of acute m yocardial ischaemia is plateau type S T depression (i m m. or more) in leads overlying the ischaem ic area.In ischaem ia, in contrast to infarction, m uscle injury is interm ittent and confined to the sub-endocardial region of the ventricles.
As a consequence, E .C .G .leads facing the surface of the heart record the changes o f uninjured m uscle and show S T depression during phases of ischaemia.A n terior ischaemia is best shown in the chest leads, inferior ischaem ia in leads II, I I I and a V F .Biphasic or sym m etrically inverted T waves m ay develop in the same leads during recovery from an ischaem ic episode and pro vide confirm atory evidence of the diagnosis.

EXERCISE TEST
A resting record is taken and then the patient is exercised by clim bing repeatedly over steps, b y clim bing stairs or by using a bicycle ergom eter or tread m ill.T h e am ount of exercise is determined for each patient, consideration being taken of age, sex, weight and general clinical state.A n exercise test should not be carried out in elderly people or those in poor physical condition.It is value less when patients are having digitalis or other sim ilar drugs which affect the E .C .G .and is unnecessary when S T segm ent and T wave changes are already present.Exercise should be stopped if anginal sym ptom s or other features of distress develop.T h e E .C .G . is repeated during or im m ediately after the exer cise, after five m inutes rest and subsequently at five m inute intervals if the record is not return ing to norm al. D evelopm ent o f S T depression of over 1 m m ., especially if follow ed b y inver sion or diphasia of the T wave, constitutes a positive test.T h e changes are usually transi tory but occasionally persist for over an hour.

PERICARDITIS
A cute pericarditis, like acute m yocardial in farction, produces S T elevation bu t in con trast to m yocardial infarction, the elevation is concave upwards, the changes are m ore w ide spread and occur in all the lim b leads reflect ing epicardial potentials as well as in the chest leads (F ig.6 E ).
Pathological Q waves are absent unless there has been associated m yo cardial infarction.D uring recovery the S T elevation disappears and is replaced by T wave inversion before returning to normal.

ELECTROLYTE ABNORMALITIES
Disturbances o f the electrolyte balance can produce m ost bizarre E .C .G .changes, partic ularly affecting the S T segm ent and T waves.T h e m ost frequently encountered electrolyte disturbance concerns potassium .
H yperkalaemia (F ig .9A) produces tall peaked T waves and reduces the height of the R wave.T h e Q R S com plex is broadened and P waves m ay disappear.T h e extent of these changes depends on the severity of the electrolyte upset.H ypokalaem ia (Fig .9B) is associated with prom inent U waves, flattening o f the T wave, S T depression and prolongation of the P R interval.

DIGITALIS
D igitalis often affects the E .C .G .; the changes m ay mask or sim ulate changes of underlying heart disease and before interpret ing the record it is essential to know whether a patient has taken this drug.
T h e m ost ., M.B., Ch.B., M.R.O.P.(Edin.)A ccu rate in terp retatio n o f an E .C .G .m ay provide valuable in fo rm atio n on the assess m e n t o f a p a tie n t's cardiovascular system .S tu d en ts, b o th under-graduate and post-gradu ate, m ay have to in terp ret an E .C .G . in the course o f their daily ward duties or during a clin ical exam in ation and in this article em phasis is placed on th e m ain d iagnostic features of som e o f th e m o re com m on E .C .G .abnor m alities.N um erous books are available for m ore advanced study.T h e E .C .G . is particularly useful in the diagnosis o f cardiac rh ythm and m yocardial in farctio n .I t m ay reveal evidence o f con d u c tion d efect, hypertroph y o f th e m yocardium or pericarditis and m ay also in d icate th erapeu tic response in certain electrolyte disturbances.O n th e o th e r h an d , non-specific E .C .G .changes are com m on.
h e routine E .C .G .consists of 12 lead s: (a) standard lim b leads Lead I -right arm to left arm Lead II -right arm to left leg Lead II I -le ft arm to left leg These leads are bipolar and record the differ ence of potential between two lim bs in such a way that relatively positive electrical forces in the left arm (Lead I) and left leg (Leads II and III) are represented as upward deflections on the E .C .G .(b) unipolar lim b leads a V R -right arm a V L -left arm a V F -left leg (c) unipolar chest leads

F ig . 6 , 4 .
Left ventricular hypertrophy SV I + RV 6 > 35mm.B. Right ventricular hypertrophy.Note that an R wave is the sole deflection in the ventric ular complexes over the right side of the heart.The P wave in V 1 is tall and peak ed (P pulmonale); T wave inversion ex tends to V 4. C. Serial electrocardiographic patterns from an electrode overlying a myocardial infarction (compare D below).(a) Normal complex.(b) ST elevation (concave downwards).(c) Pathological Q wave; ST elevation; T wave inversion.(d) ST segment isoelectric.(e) T wave low upright.(f) Persisting pathological 0 wave; T wave normal.D. Serial electrocardiographic patterns from an electrode facing the opposite side of the heart to an infarcted area (compare C above).(a) Normal complex.(b) Reciprocal ST depression.(c) ST depression less marked.(d) Peaked T wave.(e)(f) Normal complex.E. Acute pericarditis ST elevation (concave up wards) in all leads except a VR.L .B.B.B.

F i g . 7
Genesis of the E C G complex in right bundle branch block an d left bundle branch block a s recorded from 2 electrodes one over the right side of the heart (V 1) the other over the left (V 6).(see text) . Tall peaked T waves; dimin ished amplitude of R waves.B. Hypokalaemia.Prominent U waves; flattening of T waves; slight ST depression (V 4).C. Digitalis toxicity.Coupled ventricular ectopics of multifocal origin; prolongation of PR interval; sagging ST segment.comm on change is sagging of the S T segm ent which m ay m im ic m yocardial ischaemia.Bradycardia, prolongation of the P R interval and occasional ventricular ectopics are also com m on.M ore serious toxic effects of digit alis are infrequent in the absence of over dosage or hypokalaem ia secondary to in adequately controlled diuretic therapy.In these circumstances ventricular ectopics be com e m ore frequent, they m ay be coupled ( F i g .9 C ), m ultifocal in origin or progress to ventricular tachycardia.C om p lete heart block or paroxysmal atrial tachycardia w ith block may develop.S U M M A R YIn this paper the more com m on E .C .G .abnorm alities encountered in clinical practice have been outlined and explained in an attem pt to clarify their interpretation.A C K N O W L E D G E M E N TI am very grateful to D r. R .M .M arquis for helpful advice on th e preparation of this paper.