The. ECG. Made Easy. EIGHTH EDITION. John R. Hampton. DM MA DPhil FRCP FFPM FESC. Emeritus Professor of Cardiology. University of Nottingham, UK. John R. Hampton-The ECG Made Easy-Churchill Livingstone ().pdf. Ashraf Alqudwa. Figure The structure of [M(N2S2)]. The ECG Made Easy For. 𝗣𝗗𝗙 | A true medical classic should be novel, stimulate thought and discussion, transcend both The ECG Made Easy I also enjoyed Hampton's perhaps.

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The ECG Made Easy. 8th Edition. Authors: John Hampton. eBook ISBN: eBook ISBN: Paperback ISBN. The ECG Made Easy. 9th Edition. Authors: John Hampton Joanna Hampton. eBook ISBN: eBook ISBN: Paperback ISBN. ECG Made Easy - John R Hampton - Free ebook download as PDF File .pdf), Text File .txt) or read book online for free. ECG Made Easy.

Atrial activation causcs tlrc P wave. Any'upward deflection is an I wave. A downward deflection after an. Wlren the depolarization wave sprcads towards alead, the deflection is predominantly upward. When the wave sprcads away from a lead, tlre dcflection is prcdt-rnr i rra rr tly downwa rd. Lead V, is'positioned vcr thc right venl,riclc, and lead V,, over the left vt. We can ttiir',t of conduction problems in tlre orcler in whiclr the, depolariz.

I enrernbcr in all tlrat follows that we are assuming clcpxrlarizatiotr bcgilrs in l,hc ntlrnral way in the SA node, The rhythm of the heart is best interpreted from whichever ECG lead shows the P wave most clearly. This is usually, but not always, lead II or lead Vr. You can ilrinurnr. TIre tin're taketr for the spreacl of depolariz. Q4d is not rrormally Sfeater than 0,2s one large squarclEcG events are usually timed in irrilliscctln. Interference with the conduction Process '", causcs tlrc ECC phcrr.

AV node or ttrc bundle of I'lls. Wlrcn tlrisl. There may be progressive lengthening of thc, Pli irrtc'rvnl and thcn fallu rc of concluctlon of arr atrial Lreat,.

Tlris is called '2: F'ff Qt ll. Wlren this occtrrs the 33 i. Abnorrnally-slraporJ QRS comploiog bocauso ol abnorm al apread ol dopolarlzation from a vontricutar focus.

Broad ORS complexes ms Blght bundlo hranch block pallorn Ths cause ol the block could not tlo determlned, though ln most pationts it rcsulla lrom llbrosls of lhe bundlo ol Hls.

If llrc dcpolariz. Thc extra time taken for depolarization of the whole of the ' vcrrtricular rrrusclc causes widcning of tlre QRS complcx, lrr tl're rrorrrral heart, tlre tirrre taken for the depolarizr,tion. Illock of both bundle branchcs has the same effect as block of the His bundle, and causes complete third degree ': Remembep see Ch. The eeptum ie nornrally clepolirriz. Excitation spreading towards a leacl caLlses an uprward. Excitation tlren spreacls to tlre left ventricle, causinll arl in lead V1 and an R wave in tcacl V6, Fig.

It takes longer than in a nornral Ircart for excitation to reaclr tlre righ"t ventricte bccausc of tlrc faiturc oI ltrc normal conducting pathway. The right ventriclc, thert,forc' ctepolarir,esafter ttrc lcft. Tlris causr,lr il! It is seldom of significance, ancl can be congidered to be a normal variant. S wave. Tlre right ventrlcle is clepolar. Subrequent depolarization of llrc tcft vcrltrictc causes nn lead V1 and another R wave irr leacl V6, trig.

The cardi. Upr,vards Fig. Always remelnber that it is the patient who should be treatt: I elief of symptoms always comes first. I lowcvcr; sotllc gcrrcral ptlintr can bc made about the action that rnight bc takur if tlrc liCC shows conduclion arbnornra litics. First degree block. Often sccn in nornral pcople, Think about acute myocardial infarction.

No specific action needed. Third degree block Atwnyn inclicntcn conductirrg timue diseasc - lrlor often fibrosiE tlrarr isclracnric. Consider a temporary or Pcrmanent pacemaker. Risht buncllebronch block t? B t3E. Think about an atrial septal defcct. No spccific treatnrent. P0irr, I-ll lil i may indicate. Left oxis d"r,iotion olia ,rnt',t bundle bronch btock o lndlcafclr severe conductllrg tisstrc cliscttsc. No specific treatment needed. Pacemaker rgquired if the paticnt ltas synrptoms suggcstive of intermittent complctc heart block.

A conduction abnormality citn dcvclop at arty of tltesc. Conduction problems. IJlock of the anterior division or fascicle of the left bundle. Depolarization can, lrowever, bcgirr in otlter pllccs. Abnormalltlcs of carcliac rtrythnl ilrc casy: The two things to look at are the P waves and tl're widtl-r of tlre QRS conrplexes.

Atrial contractiorr is associated wil. Tl'rerefrlre the rate of t rrrrlr',rt'liorr of llrrt vt,rrtrir: Conslant PR interval. Progresslve beal-lo-beat change in R-R interval. Supraventricular rhythms. Ventricular rhythms have wide QRS complexes. Abnormal;ftythms arising in the atrial nrttscle', thc iuncfionrdl resion or the ventricular rDrtscle can t're slt-lw arrd 'sustgy'ne.

Whclr activation of the atria or ventriclcs is Iotrrlly tlisor'1ialr. Tl'ris is erchit: If the SA node fails to depolarize, control will bc i. These slow and protective rhythrns are called escape rhyl. Escape rhythms are trot primary disordcrs, but are the rcsporlsc to problcrlts Irighcr in thc'conducting pathway. A ,atriol escope t-- tf the rate of depolarization of the SA node slows down and a focus in the atrium takes over control of tlre hear't, tlte rhyl.

Atrial t'scaire beats can occrrr singly. After one sinus beat,the SA node fails to depolarize. After a delay, an". Thd remaining beats show a return to sinus. U ';'. Ventricular escape rhythms can occur withotrt conlpletc heart block. Ventricrrlar e'scapc beats carr be single i.

The rlrl,tlinr is called'accelerated idioventricular rhyth rn' Fig. Althougl'r the appearance of the ECC is sinrilar to ttrat of ventricular tachycardia descriLred la ter , accelcra [c.

Vc'ntricular tachycarclia shoulcl not trc-rliagnosecl rrnlcss tlrc heart rate exceeds lnrin' e. L-vL'r'rtric,rar nrtrsctC, iS trrc sa,lle as rtrat.

ECG Made Easy - John R Hampton

I Ir t QIis c rrpl" rrig. I atri;rr arrtr jtlrrctiort. Supraventricular beats look thc sanre, velrtricular beats look different. Is tlrc T wave the sanre way up as in the normal beat? In sa' l. Docs thc rrcxt P wave aftcr thc cxtrasystole appear at an cxpcctcrl tirnc? SA noclc clischarge and P wrrve collles late.

QRS complex and an abnormal T wave: A ventricular extrasystolc, orr the othe. Three sinus beats are followed by a junctlonal extrasystole. Three sinus beats are followed by a ventricular extrasystole. No P wave is seen after this beat, but the next P wave arrives on time.

Jr Foci in the atria, the junctional AV nodal region, and ventricler. The criteria already descritrt'd carr ['re trsctl to decicle the origin of the arrhythrnia, ancl trs before tht nrost important thing is to try to identify a P wave.

P waves can be seen superimposed on the T waves of the prececling beats. The QRS complexes have the same shape as those of the sinus. If the irtrial rate is faster than this, 'atrioverrtricular block' occurs, with some P waves not followcd by QRS complexes.

When atrial tachycardia or atrial flutter is associatecl with 2: Any arrhytlrfiia should be identified from the lead in which P wlfus can most easily be seen. Full lcacl ECCs are thgre-fore better than 'rhythm strips'. In the record in Figure 3.

The lirst ol the two P waves associated with each ORS complex can be mistaken lor the T wave ol the preceding beat, but P waves can be identilied by their regularity. Narrow QBS complexes of normal shape. NormalT waves best seen in the V leacls; ln the limb leads it is dilficult to distinguish. Caroticl sirrus pressLlrc ntay havr: Cnroticl sirrtrs prcssurc rrctivates a icflex thai lcar. It is the latter which is important in the cliagnosis ancl treatment of arrhythmias.

Carotid sirrtrs pressnre slows thc ventricular ratc in sonle s!! Junctionol nodol tachycordio arci'l art t,u1cl thc AV rrorlc dcpolrrrizcs. The lower lraco is lrorn lho same patienl, in sinus rhythm. The ORS complexes have esscnlially llrc same slrape as tltose ol the junctional tacltycardia. Ventriculqr tochycordins If a focus in thc ventricular muscle dcpolarizes with high f re-elue ncyrGu si rU, in e ffec t, ra pidly repea ted ven tri.

The QBS complexes become broad, and lhe T waves are ditlicult to identify. The final beat shows a return to -sinus rhythm. The QRS cornplexes are wide and the T waves are inverted. I-t'l'I axis tlcvi. Il'tltrrirrl; thc t. No P wavcs - irreuul;rr ltir: Narrow QnS complexcs of normal shapo. Doprossorj Sl' soglrtcrrts in lontls Vs-V,. Sonre peol'rlc,, horvever, lrarrc ntr cxtt'a 'rr'ilcccss r'y' concltrcting lrtrirr'!

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While such an 'enhanced atrtonrat'icity' ccrtainly accounts for somc tarchycardias, others are due to re-errtry circuits withirr the heart muscle. It is not possible to distirrguish enhanced automaticiLy from re-entry tachycardia on standard ECCs, but fortunately this c-liffcrcntiation has no practical. Althotr13,h this book is not interrclecl to discuss thcrapy irr any dctail, it seenrs appr'opriatc [o outlinc sot'ltc sinrp-rlc a-lpproaches to paticnt nlanagernent tl'rat logictrlly follow interpretation of an IICC;.

For fast or slow sinus rhythnr, trc;rt tlte r,rnderlying callsc.

The ECG Made Easy

Ilxtrasystc'llcs rarcly neccl treatlnent. Irr patients with acute heart failure or. Patier-rts with arry bradycarrdia tlrat is affectirrg the circulatioll catl be trcatec-l with atropine, but if this is incffc,ctivc thcy will ncccl tcnrpt or lrcrntanent p". Occasi6nat P waves are visible, but are not related to the QRS complexes. Tlre OnS conrplexes are precedcd by a brief sJliltt', representing lhe pacemakcr stimulus.

The ORS comptexe-ar': Abrrormal rhythms can arise irr tl're atrial muscle, the region arourrd the AV node the f unctional region and in tlre ventricular muscle. L ccusional carly clcpolariz;rtion of any part of the heart ca uscs arr cxtrasystolc. Asytrclrrotrous cr. Apal'[ fronr the rate, the ECC pfltte'rn of an escape rhytlun, an extrasystole arrcl a tachycar.

All sLlpravcntricular. Iiccogrrizirrg ECC abrrorn'ralitics is to a large extent like ilrr clcPlrun[ - ncc scen, llcvcr forgottcn. Are tl'rc vcntricles contracting regularly or irregularly? Arc thcrc atry abtrornralitics of thu P wave? What is tlrc Jarcliac axis? The sr segment can only be rrormal, elevated or.

Left atria. Lclt ventricular leads rnfritslrow Q waves dtte to septal. Tlrt'rc will [ru n clct,P s wnvc irr lt,ntl v,,. In pulmonary embolism the ECC may show features of rigirt vutt l rir,'trlrtr lrypcrtruphy,. I'cakccl P wtrvcs ,,.. A shil't ol' tr. A deep S wave will persist in lead V6.

Vc cli Vo nrrrl n tlc,ep S wnvc iri'ir. The origin of Q Snrall sr,ptal 'Q' w. However, Q waves greater than one sniall square in wirltlr r't-,Pt'uriulltlug,11l rus , rtnrl greitter tltrttr 2 tuttr irr tlepth have a quite different significance.

Thereforc, crir clcctrocle placed in the cavity of a ventricle would record only a Q wave, because all the -r. Lhe h-'ntls irr wlrich tlrc e wave afrpears givc. VL, itrrtl Vo-Vu ltiH. The right ventricle occupies the l'r'trnt ol' thu lrr: The resutt is a clontilant s wave in legrd V1 see ch. In a right ventricular lead V1 , the S wave this is nearly always abnormal Fig.

There is greater than the R wave. In a left ventricular lead V5 or V6 , the height of the R wave is less than 25 mm. Left ventricular leads may show Q waves due to septal depolarization, but these are less than 1 mm across and less than 2 mm deep. In each case, the increased width S indicates that depolarization has spread V6 through the ventricles by an abnormal and therefore slow pathway.

Peaked P waves. Right axis deviation S waves in lead I. In pulmonary embolism the ECG may show 3. Tall R waves in lead V1.

Right bundle branch block. Inverted T waves in lead V1 normal , abnormal other than sinus tachycardia. When a spreading across to lead V2 or V3. A shift of transition point to the left, of the following: If in doubt, V4 clockwise rotation.

A deep S wave will treat the patient with an anticoagulant. Left ventricular hypertrophy causes a tall R However, do not hesitate to treat the patient if wave greater than 25 mm in lead V5 or V6 the clinical picture suggests pulmonary embolism and a deep S wave in lead V1 or V2 Fig. It is difficult to diagnose minor degrees of left ventricular hypertrophy from the ECG. However, Q waves greater than one small square in width representing 40 ms and greater than 2 mm in depth have a quite different significance.

The ventricles are depolarized from inside 4. Therefore, an electrode If the infarction involves both the anterior placed in the cavity of a ventricle would record and lateral surfaces of the heart, a Q wave will only a Q wave, because all the depolarization be present in leads V3 and V4 and in the leads waves would be moving away from it. Q waves greater than one small square in The right ventricle occupies the front of the width and at least 2 mm deep therefore indicate heart anatomically, and normally depolarization a myocardial infarction, and the leads in which of the right ventricle moving towards the the Q wave appears give some indication of the recording electrode V1 is overshadowed by part of the heart that has been damaged.

Thus, depolarization of the left ventricle moving away infarction of the anterior wall of the left from V1. The result is a dominant S wave in lead ventricle causes a Q wave in the leads looking V1.

For more on myocardial becomes more obvious, and a dominant R wave The presence of a Q wave does not give any infarction, see develops in lead V1. The appearance of the ECG indication of the age of an infarction, because once pp. The leads between the T wave and the next P wave — but in which the elevation occurs indicate the part Fig.

Downward-sloping — as opposed to horizontally Horizontal depression of the ST segment, depressed — ST segments are usually due to associated with an upright T wave, is usually a treatment with digoxin see p. The older term for the in lead V3 in some black people. Ischaemia Left ventricular hypertrophy causes inverted T 3. Ventricular hypertrophy waves in leads looking at the left ventricle I, II, 4. Right ventricular 5. Digoxin treatment. Subsequently, Q waves appear, and branch block is usually associated with an the T waves become inverted.

The ST segment abnormal path of repolarization. Therefore, returns to the baseline, the whole process taking inverted T waves associated with QRS a variable time but usually within the range complexes which have a duration of ms or 24—48 h. T wave inversion is often permanent. A high depression of the ST segment Fig. It is potassium level causes peaked T waves with helpful to record an ECG before giving digoxin, the disappearance of the ST segment. The QRS to save later confusion about the significance of complex may be widened.

The effects of T wave changes.

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T wave and QT interval measured from the onset of the QRS complex to the end of the T wave are most commonly affected. T wave inversion is associated with ECG and in complexes originating in the bundle branch block, ischaemia, and IP ventricular muscle. It is also seen in ventricular hypertrophy.

For more on the Wolff—Parkinson—White syndrome. Right be due to electrolyte abnormalities, but see pp. For example, Figure 5. All the ECGs in this chapter came from health screening clinics, and we The T wave will assume that the individuals considered U waves themselves to be healthy. Automated ECG reporting often fails to do this. Supraventricular extrasystoles are of no clinical Occasional ventricular extrasystoles are significance, although atrial extrasystoles need experienced by many people with normal hearts.

In an individual patient, however, their medically when they are so frequent as to presence is not a good predictor of such risk. This does not cause symptoms and When depolarization is initiated from a focus is usually of no clinical significance. Tall P waves alone may indicate tricuspid The upper limit of the PR interval in a normal stenosis, but this is rare. However, the ECGs of healthy individuals, ECG Bifid P waves in the absence of signs of especially athletes, not uncommonly have PR IP associated left ventricular hypertrophy can intervals slightly longer than ms, and these For an example indicate mitral stenosis now fairly rare , but a can be ignored in the absence of any other mitral stenosis, bifid and not particularly prolonged P wave is indication of heart disease.

The ECG in Figure 5. Nevertheless, PR interval The P waves of atrial extrasystoles tend to be prolongation to this extent is probably evidence ECG abnormally shaped compared to the P waves of of disease of the conducting tissue. IP the sinus beats of the same patient Fig. Second degree heart block of the Mobitz 1 For more on P waves cannot always be seen in all leads, Wenckebach type may be seen in athletes, but hyperkalaemia, but if there is a total absence of P waves the otherwise second and third degree block are see p.

It is common in healthy subjects, the patient has had a myocardial infarction, particularly if they are tall, as with the ECG in raising the possibility of left posterior Figure 5. Right bundle branch block with Depolarization of the whole ventricular muscle a QRS complex duration greater than ms mass should occur within ms, so this is sometimes seen in healthy subjects, but represents the maximum width of the normal should be taken as a warning of things like an QRS complex.

Any widening indicates atrial septal defect. Partial incomplete right conduction delay or failure within the bundle bundle branch block RSR1 pattern in lead V1, branch system, pre-excitation see below , or a but with a QRS complex duration less than ventricular origin of depolarization — any of ms; Fig. The QRS complex 5 Fig. The deviation, or T wave inversion in leads V2—V3 , Sokolow—Lyon criteria define left ventricular this can be a normal variant Fig.

In fact these criteria are unreliable, and a QRS If the QRS complexes seem too small to be complex height greater than 25 mm is often consistent with the clinical findings, check the ECG seen in fit young men.

Left ventricular calibration of the ECG recorder. If this is correct, IP hypertrophy can only be diagnosed with possible explanations of small QRS complexes For more on left confidence when tall QRS complexes are are obesity, emphysema and pericardial effusion.

This is sometimes referred to developed changes of an ST segment elevation see pp. Narrow Q likely to be normal, even when associated with waves in the inferior and lateral leads Fig. These features and sometimes even quite deep ones, may also often disappear if the ECG is repeated with the be perfectly normal. Occasionally, a normal heart may be Tall and peaked T waves Fig.

Peaked T hypokalaemia. However, the best examples of waves are also associated with hyperkalaemia, prominent U waves come from normal people ECG but in fact some of the tallest and most peaked Fig. V6 septal Q waves. There are a few features of chest pain that The ECG in patients with intermittent make the diagnosis obvious. Chest pain that chest pain radiates to the teeth or jaw is probably cardiac The ECG in patients with breathlessness in origin; pain that is worse on inspiration is either pleuritic or due to pericarditis; and pain in the back may be due to either myocardial Chest pain is a very common complaint, and ischaemia or aortic dissection.

The ECG will when reviewing the ECG of a patient with help to differentiate these causes of pain but it chest pain it is essential to remember that there is not infallible — for example, if an aortic Box 6.

The first is infarction the rupture of atheromatous plaque within a associated with ST segment elevation, known as coronary artery. The diagnosis of lost. If a patient has chest pain and there is ECG Box 6. The diagnosis of anti-platelet agents and a beta-blocker.

STEMI can also be accepted if there is left During the first few hours after the onset of bundle branch block which is known to be new. Otherwise, after a repeatedly in a patient with chest pain that variable time, usually within a day or so, the ST could be due to cardiac ischaemia, but whose segments return to the baseline, the T waves in ECG is nondiagnostic.

If In unstable angina there is ST segment anterior ST segment elevation persists, a left depression while the patient has pain Fig. Once the pain has resolved the ECG returns to Figures 6. These that is damaged: This is with inferior infarction. A few days later pain and a few days later, and they show the Fig. Figure 6. In a routine ECG there will be dominant R wave that can be a normal variant.

Normal ECG. Raised ST segments. Appearance of Q waves. Normalization of ST segments. Inversion of T waves. However, there is Fig. With time the T waves may revert now treatment PCI or thrombolysis that can to normal, but inversion may persist.

Patients whose chest pain is due to oesophageal 1 2. If a diagnosis of angina is in doubt, ECG changes can be induced by exercise. The has great advantages over coronary angiography: The onset of any symptoms.

After confidently be made if there is horizontal ST For more on recording the ECG at rest, exercise is segment depression of at least 2 mm. If the ST exercise testing, progressively increased in stages of 3 min. The segments are depressed but upward-sloping, see pp. Figures 6. The two low-level stages the 6. The ECG in patients with intermittent chest pain 6 Fig.

ECG evidence of cardiac When the ECG of a breathless patient shows enlargement may point to the cause of an arrhythmia or a conduction abnormality, or breathlessness. For example, ECG evidence evidence of ischaemia or of atrial or ventricular of left ventricular hypertrophy may be due to hypertrophy, then the breathlessness may be hypertension or to mitral or aortic valve disease. V1 or V2 greater than 35 mm. Pulmonary embolism often presents as a In practice, it is not a very reliable indicator combination of chest pain and breathlessness.

Although the chest pain is characteristically one-sided and pleuritic, a major embolus affecting the main pulmonary arteries may cause pain resembling that of myocardial infarction. This is because the heart is rotated, diseases do not usually cause the ECG changes with the right ventricle occupying more of the associated with severe pulmonary hypertension, precordium than usual.

The only way of NORMAL ECGs being certain that a cardiac problem is the cause of either phenomenon is to record an Symptoms may not be due to heart disease — the ECG when the patient is having a typical patient may have epilepsy or some other attack, but this is seldom possible.

Nevertheless, condition. In a young associated with exercise think of anaemia or person, who is unlikely to have coronary disease, anxiety, and the palpitations build up and slow this pattern pattern suggests hypertrophic down, sinus tachycardia is likely to be the cause cardiomyopathy Fig.

In paroxysmal tachycardia, with arrhythmias, syncope and sudden death. In both cases an abnormal block, which may be due to aortic stenosis; or pathway bypasses the atrioventricular AV node, right ventricular hypertrophy, which may be causing the short PR interval.

This may be pathway connects the atrium and the ventricle, confused with right ventricular hypertrophy. In the WPW syndrome type A, the right-sided, connecting the right atrium and pathway is left-sided, connecting the left right ventricle, and this is called the WPW atrium and left ventricle, and causes a syndrome type B Fig.

Here, lead V1 has dominant R wave in lead V1 Fig. Figure 7. A few seconds before the cardiac arrest, he A QTc interval longer than ms is likely developed a transient broad complex tachycardia to be abnormal. QT interval prolongation can in which the QRS complexes were initially be congenital, but is most often due to drugs, upright but then changed, to become particularly to antiarrhythmic drugs Box 7. Box 7. It can also be associated with a variety of Fig. However, such It is important to consider the possible combinations may also be associated with higher underlying causes of heart block, and these are degrees of block, and ambulatory recording may summarized in Box 7.

The QRS complexes in paroxysmal change of axis compared to sinus rhythm; tachycardia can be narrow i. Narrow complex tachycardias may indicate: Figure bundle branch block is normally present. It is usually temporary, predominantly upwards or downwards and does not need pacing unless there is in the chest leads.

When complete block complicates an to be atrial fibrillation with bundle branch anterior STEMI, a large amount of myocardium block, or atrial fibrillation in the WPW has usually been damaged, and temporary syndrome a dangerous combination. When no spontaneous activity is sensed, the pacemaker Pacemakers produce a small electrical discharge stimulates the right ventricle; and when that either replaces the function of the sinoatrial spontaneous activity is sensed, the pacemaker is node or bypasses a blocked His bundle.

The inhibited. The ECG looks like that in Figure 7. If the pacemaker does not sense Pacemaker function can be assessed from the spontaneous atrial depolarization, it stimulates resting ECG.

If no atrial activity is sensed within a predetermined 1. The first letter describes the chamber s period, the atrial pacing lead will pace.

A paced A for right atrium, V for right maximum PR interval is also predetermined, ventricle or D for dual, i. The second letter describes the chambers will be paced. A pacemaker inhibition. The fourth letter R is used when the rate one or two pacing leads.

In either pulseless electrical activity PEA. The The shockable rhythms are ventricular treatment sequence after the first two steps is: Action in either case, following 1. Adrenaline 1 mg i. CPR Atropine 3 mg i.

Precordial thump. If unsuccessful, continue adrenaline 1 mg 2. One shock at J. Resume chest compressions at Particularly in cases of PEA, consider 4. If unsuccessful, defibrillate at J. If unsuccessful, give adrenaline 1 mg i. The description should always be given in the same sequence: Rhythm 2. Conduction intervals 3. Cardiac axis 4. A description of the QRS complexes 5. A description of the ST segments and T waves. However, you must think about all the findings every time you interpret an ECG.

The interpretation of an ECG indicates whether the record is normal or abnormal: Figures 1. Lead V1 is positioned over the right ventricle, and lead V6 over the left ventricle.

Recognizing the limits of normality is one of the main difficulties of ECG interpretation. If the first deflection is downward, it is a Q wave. Any upward deflection is an R wave.

A downward deflection after an R wave is an S wave. When the wave spreads away from a lead, the deflection is predominantly downward. The conduction of this wave front can be delayed or blocked at any point.

However, conduction problems are simple to analyse, provided you keep the wiring diagram of the heart constantly in mind Fig. We can think of conduction problems in the order in which the depolarization wave normally spreads: Remember in all that follows that we are assuming depolarization begins in the normal way in the SA node.

The rhythm of the heart is best interpreted from whichever ECG lead shows the P wave most clearly. This is usually, but not always, lead II or lead V1. First degree heart block is not in itself important, but it may be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbances. There may be alternate conducted and nonconducted atrial beats or one conducted atrial beat and then two or three nonconducted beats , giving twice or three or four times as many P waves as QRS complexes.

It is important to remember that, as with any other rhythm, a P wave may only show itself as a distortion of a T wave Fig.

There are three variations of this: There may be progressive lengthening of the PR interval and then failure of conduction of an atrial beat, followed by a conducted beat with a shorter PR interval and then a repetition of this cycle. Most beats are conducted with a constant PR interval, but occasionally there is atrial First degree heart block Fig. The Wenckebach phenomenon is usually benign, but Mobitz type 2 block and 2: You have to look at the PR interval in all the leads to see that there is no consistency.

Complete heart block may occur as an acute phenomenon in patients with myocardial infarction when it is usually transient or it may be chronic, usually due to fibrosis around the bundle of His. It may also be caused by the block of both bundle branches. The extra time taken for depolarization of the whole of the ventricular muscle causes widening of the QRS complex.

In the normal heart, the time taken for the depolarization wave to spread from the interventricular septum to the furthest part of the ventricles is less than ms, represented by three small squares of ECG paper.

If the QRS complex duration is greater than ms, then conduction within the ventricles must have occurred by an abnormal, and therefore slower, pathway. A wide QRS complex can therefore indicate bundle branch block, but widening also occurs if depolarization begins within the ventricular muscle itself see Ch.

However, remember that in sinus rhythm with bundle branch block, normal P waves are present with a constant PR interval. We shall see that this is not the case with rhythms beginning in the ventricles.

Block of both bundle branches has the same effect as block of the His bundle, and causes complete third degree heart block. Left bundle branch block LBBB is always an indication of heart disease, usually of the left ventricle. It is important to recognize when bundle branch block is present, because LBBB prevents any further interpretation of the cardiogram, and RBBB can make interpretation difficult. Remember see Ch. The right ventricle therefore depolarizes after the left.

It is seldom of significance, and can be considered to be a normal variant. Excitation then spreads to the left ventricle, causing an S wave in lead V1 and an R wave in lead V6 Fig. It takes longer than in a normal heart for excitation to reach the right ventricle because 44 Conduction and its problems Conduction in right bundle branch block: The right ventricle is depolarized before the left, so despite the smaller muscle mass there is an R wave in lead V1 and an S wave often appearing only as a notch in lead V6 Fig.

Remember that any upward deflection, however 2Problems in the right and left bundle branches 45 Conduction in right bundle branch block: Subsequent depolarization of the left ventricle causes an S wave in lead V1 and another R wave in lead V6 Fig. Conduction in left bundle branch block: The depolarization wave therefore spreads into the ventricles by three pathways Fig.

The cardiac axis see Ch. Because the left ventricle contains more muscle than the right, it has more influence on the cardiac axis Fig.

If the anterior fascicle of the left bundle branch fails to conduct, the left ventricle has to be depolarized through the posterior fascicle, and so the cardiac axis rotates upwards Fig. When the right bundle branch is blocked, the cardiac axis usually remains normal, because there is normal depolarization of the left ventricle with its large muscle mass Fig. If the right bundle branch and both fascicles of the left bundle branch are blocked, complete heart block occurs just as if the main His bundle had failed to conduct.

Relief of symptoms always comes first. However, some general points can be made about the action that might be taken if the ECG shows conduction abnormalities. When depolarization begins in the SA node the heart is said to be in sinus rhythm. Depolarization can, however, begin in other places. When attempting to analyse a cardiac rhythm remember: The keys to rhythm abnormalities are: Look for the lead in which they are most obvious.

The stars in the figures in this chapter indicate the part of the heart where the activation sequence began. The SA node normally has the highest frequency of discharge.

Therefore the rate of contraction of the ventricles will equal the rate of discharge of the SA node. The rate of discharge of the SA node is influenced by the vagus nerves, and also by reflexes originating in the lungs. Although Figure 3. In the supraventricular 58 The rhythm of the heart Division of abnormal rhythms into supraventricular and ventricular Fig.

In ventricular rhythms, on the other hand, the depolarization wave spreads through the ventricles by an abnormal and slower pathway, via the Purkinje fibres Fig. The QRS complex is therefore wide and is abnormally shaped. Repolarization is also abnormal, so the T wave is also of abnormal shape. Abnormal rhythms arising in the atrial muscle, the junctional region or the ventricular muscle can be categorized as: The QRS complex is therefore normal, and is the same whether depolarization was initiated by Spread of the depolarization wave in supraventricular rhythms Fig.

However, the protective mechanisms must normally be inactive if competition between normal and abnormal sites of spontaneous depolarization is to be avoided. This is achieved by the secondary sites having a lower intrinsic frequency of depolarization than the SA node. The heart is controlled by whichever site is spontaneously depolarizing most frequently: Escape rhythms are not primary disorders, but are the response to problems higher in the conducting pathway.

They are commonly seen in the acute phase of a heart attack, when they may be associated with sinus bradycardia.

It is important not to try to suppress an escape rhythm, because without it the heart might stop altogether. Atrial escape beats can occur singly. Ventricular escape rhythms can occur without complete heart block, and ventricular escape beats can be single Fig. The rhythm of the heart can occasionally be controlled by a ventricular focus with an intrinsic frequency of discharge faster than that seen in complete heart block.

Although the appearance of the ECG is similar to that of ventricular tachycardia described later , accelerated idioventricular rhythm is benign and should not be treated.

The ECG appearance of an extrasystole arising in the atrial muscle, the junctional or nodal region, or the ventricular muscle, is the same as that of the corresponding escape beat — the difference is that an extrasystole comes early and an escape beat comes late.

Atrial extrasystoles have abnormal P waves Fig. In a junctional extrasystole there is Accelerated idioventricular rhythm Fig. The QRS complexes of atrial and junctional extrasystoles are, of course, the same as those of sinus rhythm.

Ventricular extrasystoles, however, have abnormal QRS complexes, which are typically wide and can be of almost any shape Fig. Ventricular extrasystoles are common, and are usually of no importance. However, when they occur early in the T wave of a preceding beat they can induce ventricular fibrillation see p. It may, however, not be as easy as this, particularly if a beat of supraventricular origin is conducted abnormally to the ventricles 64 The rhythm of the heart R on T phenomenon: Ventricular extrasystole Fig.

It is advisable to get into the habit of asking five questions every time an ECG is being analysed: Does an early QRS complex follow an early P wave? If so, it must be an atrial extrasystole. Can a P wave be seen anywhere?

A junctional extrasystole may cause the appearance of a P wave very close to, and even after, the QRS complex because excitation is conducted both to the atria and to the ventricles.

Is the QRS complex the same shape throughout i. Supraventricular beats look the same as each other; ventricular beats may look different from each other. Is the T wave the same way up as in the normal beat? In supraventricular beats, it is the same way up; in ventricular beats, it is inverted. Does the next P wave after the extrasystole appear at an expected time? The effects of both supraventricular and ventricular extrasystoles on the following P wave are as follows: The criteria already described can be used to decide the origin of the arrhythmia, and as before the most important thing is to try to identify a P wave.

The difference between this sort of atrioventricular block and second degree heart block is that in atrioventricular block 66 The rhythm of the heart No P wave Expected P waveP Ventricular extrasystole Fig.

When atrial tachycardia or atrial flutter is associated with 2: Any arrhythmia should be identified from the lead in which P waves can most easily be seen.

In the record in Figure 3. Junctional tachycardia: Junctional nodal tachycardia Fig. The QRS complexes have essentially the same shape as those of the junctional tachycardia Junctional nodal tachycardia If the area around the AV node depolarizes frequently, the P waves may be seen very close to the QRS complexes, or may not be seen at all Fig.

The QRS complex is of normal shape because, as with the other supraventricular arrhythmias, the ventricles are activated via the His bundle in the normal way. The lead ECG in Figure 3. Carotid sinus pressure activates a reflex that leads to vagal stimulation of the SA and AV nodes. This causes a reduction in the frequency of discharge of the SA node, and an increase in the delay of conduction in the AV node.

It is the latter which is important in the diagnosis and treatment of arrhythmias. Carotid sinus pressure completely abolishes some supraventricular arrhythmias, and slows the ventricular rate in others, but it has no effect on ventricular arrhythmias. Excitation has to spread by an abnormal path through the ventricular muscle, and the QRS complex is therefore wide and abnormal. Wide and abnormal complexes are seen in all 12 leads of the standard ECG Fig. Remember that wide and abnormal complexes are also seen with bundle branch block Fig.

If a patient with an acute myocardial infarction has broad complex tachycardia it will almost always be ventricular tachycardia. However, a patient with episodes of broad complex tachycardia but without an infarction could have ventricular tachycardia, or supraventricular tachycardia with bundle branch block or the Wolff—Parkinson—White syndrome see p. Under such circumstances the following points may be helpful: Finding P waves and seeing how they relate to the QRS complexes is always the key to identifying arrhythmias.

Always look carefully at a full lead ECG. If possible, compare the QRS complex during the tachycardia with that during sinus rhythm.Clinical diagnosis depends mainly on a pratient's lristory, and to a lesser extent on the physical examinatiorr.

It is usually temporary, predominantly upwards or downwards and does not need pacing unless there is in the chest leads. Right vontriculqr hyporfrophy. In a junctional extrasystole there is Accelerated idioventricular rhythm Fig. Most of this gives the heart rate, so the distance between the time is taken up by delay in the AV node Fig.

It's an easy step-by-step readable guide to how to interpret ECGs.

DONETTE from Port St. Lucie
Also read my other articles. One of my extra-curricular activities is butts up. I fancy properly.