Clinical skills: the physiological basis and interpretation of the ECG

Ehsan Khan
itii the uiiprovenieiu ot" computerized automation and decrtasf in prices of electronic technology, electrocardiograph (EGG) is Tiow more accessible to nursing staff". Better understanding of disease is also now prompting healthcare professionals to use ECG interpretation skills in illnesses that are not directly associated with the cardiac patient (Booker et al, 2003). ECG monitoring is increasingly being implicated in mental health because of the Q-T interval-prolonging etTect of many antipsychotic medications (Hennessy et J1. 2(H)2: O'Brien and Oyebode, 20(13). Therefore, it is now beeoniing necessary that all nurses have a basic understanding of ECG. Many articles have been published on ECG interpretation; however, few clearly discuss the pliysiological basis of the ECG waveforms. The ECG IS a pictorial representation of electrical conduction and myocardial excitation in the heart (Despopoulos and Silbernagl,, 201)3). To understand this picture, one needs to understand the relationship between the waveforms seen in the ECG and the conduction events that cause them. This article will try to address these physiological events and apply them to ECG interpretation, in an attempt to make the ECC; more comprehensible.

Abstract
Electrocardiograph (ECG) interpretation is a complex subject that requires considerable experience. However, an understanding of the principles underlying generation of the ECG can make this learning process easier. This knowledge is necessary if interpretation is to be founded on understanding rather then being a pattern recognition-based process. The aim of this article is to introduce the practitioner to the basic processes and mechanisms that govern formation of the normal ECG. These principles will largely be applied to the normal ECG and include cardiac anatomy applied to the ECG, how the ECG leads look at the heart and how the normal ECG waveform is formed. Examples of how the ECG changes when the underlying mechanisms are disturbed will also be given. Together, this knowledge should help the practitioner to have a clearer understanding of interpreting the abnormahties seen on an ECG. Key words: Anatomy and physiology Cardiovascular system and disorders Electrocardiography Patient assessment

Hlstofy of the ECG

Current generated by the heart was first recorded in humans by Augustus D Waller (1S56-1922) in St Mary's Hospital, London. Unfortunately, Waller fiiiled to recognize the clinical potential of his discovery (Sykes and Waller, 1HK7). It fell to Willem Einthoven of Leiden (1860-1927) to refine Waller's techniques and generate a clinically relevant ECG (Hurst, 1998). It is for this reason that Einthoven is generally recognized as the father of ECG. It was Einthoven who labelled the ECG waveform as PQRST (Snellen. 1995). It is suggested
Ehsiin Klian is LcitiirLT in ("ntiijl t'.ari'. King's l.aiidoii
Accepted for pulilicntion: March 2004

I'igure 1. Diagramtnatie representation of the ctinduction system of tbe heart.

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iliac he may have used the Ictrcn iu rhe middle ot tlic alphabet because he was tuit sure it lie had determined all the waves present in the ECCi and wanted to make sure there were enough letters available to accommodate any newly discovered waves (Hurst. l'J98), Einthoven subsequently discovered the U wave a few years later (Snellen, 1993), Impulse conduction In the heart I he elet trieal unpulses that cause contraction in che heart are conducted via specialized modified muscle tissues that make up the conduction "^ysteni in the heart (Levick. 21100). Although the myocardium coudticts electrical impulses, the specialized coudtiction fibres conduct the electrical impulse 2-3 times faster than the myocardium (Levick, 2(KI0). The conduction system, therefore, produces an organized rapid progression of the electrical impulse throughout the heart. The main .structures involved in this system are shown in Fii^urc /.They inchide the sinoatrial (SA) node, atrial conduction pathways, the atnoventricular (AV) node and the ventricular conduction pathways. The atria and ventricles are separated by a thick layer of fibrous tissue the atrioventricular ring or annulus fibrosus (Marriot and Conover, 1998; Meek and Morris, 2(tO2).This fibrous ring electrically insulates the atria from the ventricles, so that under normal conditions the only path of conduction from the atria to the ventricles is via the AV node (Marriott and C~onover, I 998). Sinoatrtal node (SA node) The SA node, which is found in the right atrium near the inlet of the superior vena cava. is composed ot a group ot specialized cells that have the property of autoniaticity (Opie, 1998; Huszar. 2001). Automaticity is the abihty of the tissue to generate automatically an action potential (current) (Marriot and Conover, 1998). Automaticity occurs because of a small but contmuous leak of positive ions into the cell (Waldo and Wit, 2(101). The rate of automaticity in the SA node can be modulated by a number of mechanisms, including the autonomic nervous system and some hormones (Opie, 1998). As the SA node normally possesses the fastest rate of autoniaticity in the heart at 60100 impulses/minute, it is the physiological pacemaker of the heart (Berne and Levy, 1992).

Direction of heart impulse current

Impulse current travelling away from a lead gives a negative deflection on the ECG

Heart impulse travelling towards a lead, therefore a positive deflection is recorded by the ECG

Impulse current travelling at right angles to a lead gives a positive and negative deflection (biphasic deflection) on the ECG

are known as the internodal pathways and they carry the electrical impulse trom tbe SA to tbe AV node, causing the atrial myocardium to contract as it travels down the atrium. Tbe fourth atria! conduction pathway runs from tbe SA node to tbe left atrium and is known as tbe Bacbuiann's bundle (Berne and Levy, 1992). Atrioventricular node (AV node) Tbe AV node is an important part of the conduction system. It has a number of specific functions. As mentioned, it acts as a bridge to allow current to cross the atrioventricular ring, Tbe AV node bas a .slow conduction speed of approximateiy 0.2m/second (Waldo and Wit, 2001); tbis slows down electrical impulses from the atria, delaying their entry into tbe ventricles, allowing time for adequate ventricular filling. Tbe AV node does not possess the property of automaticity itself; however, tbe portion of conduction tissue joining the AV node to tbe bundle of His (the AV junction) does. Its intrinsic rate is less than tbat of the SA node with an approximate automaticity firing rate of 40-60 impulses/second (Berne and Levy, 1992). This enables tbe AV junction to become a secondary pacemaker in tbe event of an abnormal reduction in SA node tiring rate. Finally, the AV node acts as a frequency filter, by reducing the number of atrial beats entering the ventricles when tbe atrial firing rate is very rapid. This characteristic of the AV node is only evident when tbe atrial tiring rate is above 1 KO200 impulses/minute (Berne and Levy, 1992), Fast atria! tiring rates are bardly ever

Figure 2. Principles of impulse recording; hy {be electrocardiograph (Oocheriy, 200J).

owing to SA node activity as the SA node firing rate does not normally exceed 170-190 impulses/minute as the maximum sinus tacbycardia is normally calculated as 220-age (University of California San Francisco. 2003). Tbey are likey to be owing to an area ot abnormal automaticity tbat may be present in tbe conduction fibres or myocardium ot the atria (Huszar, 2001), The degree to which impulses are inhibited by the AV node depends on the impulse rate, such that the atrialventricular conduction ratio (atrial waves: ventricular beats) may be 2:1, 3:1, etc. as the atrial firing rate increases (Marriot and Conover, 1998).Therefore, the AV node acts as a frequency filter (Opie, 1998), It is tbis frequency tittering tunction of the AV node that allows only a proportion of tbe fast atrial waves to enter the ventricles resulting in a lower ventricular rate, thus resulting in the appearance of atrial t!utter (Puech, 1956). Ventricular conduction fibres Ventricular conduction tlbres consist of the bundle of His and its branches (see Figure /), The bundle of His is divided into two main branches, tbe rigbt and left bundle brancbes. The left bundle branch is then tlirtber divided into two and sometimes tbree otber brancbes; tbe sub-branches of the left bundle branch are named according to the path they take in the lett ventricular wall. They are tbe anterior

Internodal pathways
The impulse generated by the SA node is conducted throughout the atria via conduction pathways. There are four main atrial pathways: three in the right atriuin and one in the left (see I'lfjnn- 1). The three right atrial pathways

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i,s actually seen on an ECG recording is more cotnplex. A stirface ECG tracing records the net electricity generated by tbe heart during the cardiac cycle (Huszar, 2(HlI). Before tbe origin of tbe ECG waveforms is looked at in terms ot cardiac contraction, ,1 brief description of tbe position and perspectives of tbe various leads would be beneficial, c) Lead III ECG leads

a) Lead I

b) Lead II

Limb leads
There are six litnb leads that can be recorded using a combmation ot tbree leads or electrodes, Tbe three leads used in recording tbe limb lead waveforms are placed as follows: Right arm: (normally red lead) Left arm: (normally yellow lead) Left foot: (normally green lead) (Kigbt foot is normally black lead, wbich is neutral). These leads are further divided into bipolar and unipolar or augmented leads.

d) Lead aVR

e) Lead aVL

f) Lead aVF

Figure J. Bipolar and augmented lead recording; modified from Despopoulos and Sifbernagl (2003).

superior fascicle: this is a tinn branch that radiates anteriorly and superiorly across tbe left ventricular wall. Tbe other main sub-branch of tbe left bundle branch is tbe posterior inferior fascicle, which, as its name suggests, radiates posteriorly and interiorly across the lett ventricular wall. This fascicle is quite thick compared with the anterior fascicle. The final sub-branch of the left bundle branch is the mid-septal fascicle (Demoulin and Kulbertus, 1972). This branch is present in approximately a third of the population (Kulbertus and Demoulin, The Purkinje fibres These are tbe final part of tbe conduction system and result trom subdivisions ot tbe bundle brancbes. The Purkinje fibres send tbrtb brancbes t)r extensions into the myocardiiun and run through the subendothelial connective tissue layer. Thus contraction ot tbe myocardium occurs from deep witbiu the heart and tollows an endocardialepicardial or insideoutward direction (Schamroth, 1990). The ECG and what It records The EC^G records electrical activity genenited by the heart, by recording ctirrent from terminals or leads placed on specitlc areas ot tbe body. DitTerent leads look at tbe beart trom difterent directions. Depending on which direction tbe current is travelling in respect to tbe observing lead (i.e, tbe ECG lead in question, e,g. lead I, aVF, VI, etc.), the lead will record a positive wave when the current is

moving towards it, a negative wave when tbe current is moving away from it and a biphasic Bipolar limb leads deflection (positive and negative) wave wben These leads arc called bipolar because tbey tbe electrical impulse is at rigbt angles (90'') to have two definite poles: a positive and a tbe observing lead (Docherty, 2003) {Fij^ure 2). This is tbe principle by which the ECG Figure 4. Intercoslai spaees/12-leiid electrocardiograph records the electrical activity of tbe heart. What ptacemeni (from Docberiy, 2003).

4th intercostal space

Mid-clavicular line

Anterior axillary i line

i Mid-axillary line

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Unipolar chest leads negative electrode. Tbe iead that picks up the Also called precordial leads, tbe chest leads current is known as tbe exploring, observing are made up of a combination of leads. In or facing lead. Conventionally,, tbe exploring or this case, although all three limb leads eomfacing lead is always positive (Scbamroth, bine to make up a single neutral lead, tbe 1990),The limb leads include; exploring lead is the chest lead tbat is norLead I: This lead is made of the terminal on mally placed on one of six positions on the the right arm and the terminal on tiie left arm. chest wall {Fi^^tirc 4). Tbe riiibt arm is the negative terminal and tbe left arm the positive {Fij^iirc .Jij).This lead looks The cbest leads are placed in a horizontal at t!ie heart on the frontal plane and picks up plane along tbe chest wall. The placement for activity from the lateral side of the beart, i.e. these leads is as follows (Huszar, 2001): tbe left lateral ventricle wall. Lead II: Lead !1 runs from tbe right arm (negative) to tbe left foot (positive) {Fij^ure 3b). It again is a frontal lead and looks at tbe inferior aspect of tbe beart. It is normally positive and usually sbows tbe greatest deflection of all tbe limb leads in a normal beart (Schamroth, 19911), Lead III: Tbis lead runs from tbe lett arm (negative) to the left foot (positive) {Flj;<urc 3c). This frontal lead also looks at the inferior surface of the heart, but at a more rigbthanded aspect than lead II (Huszar, 2001), Unipolar leads
Tbe unipolar leads include tbe augmented leads ,ind tbe chest leads. These are called unipolar because tbey only have tine definite pole. For ease of understanding, tbe lead receiving the electric current will be referred to as tbe positive or exploring lead.Tbere is no real negative terminal as tbe combination of all tbree limb leads forms a 'neutral' terminal; this 'terminar is as if there were a terminal in the centre of tbe cbest, .1 null reference point (Docherty. 2003), In all tbe unipolar leads tbe current generated by the heart is measured from tbe centre of tbe chest to the exploring lead. because the cardiac axis is normally directed towards tbis lead (Scbamroth, 1990).The electrical events that lead to contraction in myocardial cells are known as depolarization and tbe relaxation of myocardium results in electrical activity known as repolarization (Scbamrotb, 1990). Thus, depolarization pertains to contraction of myocardium and repolarization to its relaxation. Cardiac contraction starts in the right atrium from tbe SA node. First tbe rigbt atritim contracts

PQ
interval

U wave see text) Q wave S wave

QRS complex

VI Right side of sternum on sternal margin, fourth intercostal space V2 Left side of sternum on sternal margin, fourth intercostal space V3 Before putting on leadV3,V4 sbould be located tben V3 is placed in a direct hne Augmented leads betweenV2 andV4 aVR: In tbe aVR unipolar lead, the positive (exploring) terminal is the right arm {Figure 3d). V4 Fiftb intercostal space in tbe mid-clavicular hne. It has been suggested that adipose tisThis lead looks at the beart from the rigbt sue causes minimal aberration to ECCJ upper surface of the heart. Tbis lead is nearly recording (Rautabarju et al. 1998), always negative, as it looks down onto the cavit\' Tberefbre, the electrode should be placed of the heart, thus tbe P wave, QRS and T waves on top of tbe breast in women so as to are normally negative.This lead is positive wben attain the appropriate placement tbe patient is dextrocardiac (heart ou the right side) or when tbe left and rigbt arm leads bave V5 Placed on the fiftb intercostal space on the been swapped over (Ho and Ho, 2001). anterior axillary line aVL: In tbis lead tbe positive (exploring) terV6 Same plane asV4 andV5 but placed o!i the minal is on tbe left arm {Figure 3c). This lead mid-axillary line. looks at the left lateral aspect of the heart; however, it looks at the lateral wall from an angle of The ECG and Its origins from cardiac approximately 30", whereas lead I looks at tbe contraction lateral wall on a horizontal plane (Huszar, 2001). Expanding a little more on wliat has already aVF: III this lead tbe positive (exploring) termibeen discussed, the production of the ECG nal is tbe left leg lead (fi^'HR- .J/).This lead looks waveform will now be explored, Wben observat the inferior aspect of the heart (Huszar, 2001), ing the ECG limb lead II is usually used

Figure S. Origin of the waveforms seen on the electrocardiograph (ECG). Events during ihe cardiac cycle are colour coded to the wapeforms seen on the ECG.

via the internodil pathways, then the Bacbmann's bundle carries tbe impulse into tbe left atrium and tbis contracts (red brackets, Fi^'urc 5), This activity forms the P wave (Scbamrotb, 1990), Tbe impulse now enters tbe AV node where it is delayed; this generates a flat segment on the ECG, called the PQ interval (i-ViiNrc 5, orange arrow), Tbe segment is flat because the small amount of tissue involved in conduction only generates a small amount of electrical activity that cannot be perceived by surface ECG recordings (Waldo and Wit, 201)1). Following tbe AV node delay, the impulse enters the bundle of His and travels down botb bundle brancbes. As the impulse travels through tbe bundle of His, the septum contracts. Tbe septal muscle mass is small, thus its contraction results in a comparatively small-sized wave. As the mean direction of electrical activity generated during septal contraction is from tbe bottom left of the septum upward, the waveform recorded in lead II is negative, as the current is moving aw-ay from

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speed (25 mm per second) Deflection magnitude

(mV)

lmV

-1-

Time (seconds) 1 small square = 0.04 seconds 0.5 mV \ 0.04 s 0,2 1 large square = 0.2 seconds 1 large square - 0.5 mV 1 small square = 0.1 mV

x5 = 1 second

7),These definitions are given below see Huszar (20(H) for a detailed discussion. P wave: Normally the first positive deflection of the ECG cycle, usually symmetricaliy rounded. Q wave: First negative detlection that precedes tbe first positive detlection (normally the P wave). R wave: First positive detlection of the QRS complex, ECX"!s may bave more than one positive deflection in tbe QRS. The first detlection is labelled R or r depending on tbe size of tbe deflection. If the detlection is hirge tben tbe wave will be called R, if it is small it will be r. The next positive deflection in a QRS complex is denoted R' or r' (R prune). Subsequent positive deflections are described as R" or r" and so on.

Figure 6. Electrocardiograph graph paper

measurements.

ECG paper Now the way cardiac couductiou tbrnis the difl-erent ECXi waveforms has been examined, normal dimensions cau be assigned to these waves. To understand ECG waveform dimensions, one needs to understand the graph paper on which die ECG is recorded. Time is plotted along the horizontal axis (X-axis) of the ECG grapb paper and along the vertical axis (Yaxis), the paper shows deflection magnitude in mV {Figure 6). The graph paper is divided into small squares of 1 mm each and five small squares make up a large square. As the normal running speed of ECG paper is 25nim/second, one siuall square on the X-axis equals (.).()4 seconds and one large square (five small squares) equals 0.2 seconds (5x0,04^0.2), Therefore, five large squares is equal to 1 secFinally, the muscle around the major valves contracts {Fii>im' 5, purple arrows). As tbis elec- ond (5 X 0.2=1) (Huszar, 2001). trical activity is directed upwards towards tbe The vertical plane of the ECG paper base of tbe heart and away trom lead II, the describes tbe detlection magnitude of the cardetlection formed on the ECG is negative and diac conduction.Tbe ECG recorder is calibrated snKiil in size because of the .small amount of such that 10 small squares or two big squares muscle iu tbis area. This negative detlection is give a detlection of 1 mV (Huszar, 2001).Tbis is known a.s the S wave (Schamroth, 1990), Tbe important as changing this calibration may lead ventricles relax and repolarize, which is seen to misinterpretation of the ECG, on the ECG as a positive waveform after tbe S wave the T wave (Fij^iire .5. blue arrows) Deflections on the ECG (Schamrotb, 1990), Although the physiologiciil basis of tbe In some cases, an additional wave may be ECG waveforms bas been described, tbese seen after theT wave tbe U wave {Figure 5). waveforms sonietime.s bave a slightly different Tbe origin of this wave is unclear; however, it meaning from an interpretational point of view

it (Figure 5. pink arrows). This first negative detleetion on the ECG after the P wave is known as the septa] q wave and is most clearly seen m V5-V6 dud hmb lead II (Huszar,2(H)1). Following septa! contraction, the impnise enters both ventricles almost simultaneously and cruises contraction of the ventricles trom the apex ot the heart upwards (Fi^^urc 5, green arrows). Contraction of the myocardium occurs from the endocardium outwards (Scbamroth, 1990). The net direction of the electrical activity generated durmg ventricular contraction is. tlierefore, downward towards the apex of the heart and a little towards the left. Tbis is because tbe left side ot tbe benrt (left ventricle) consists of more muscle than the right side and, therefore, when it contracts it generates more electrical activity. As tbe lead that faces this orientation is lead II, ventricular contnictioii is most clearly seen in tbis lead; bence bealtbcare protessionals norniallv monitor m lead II and lead II is also tbe average normal conduction. The contraction of the main part ot the ventricles results ill the formation of the R wave on the ECG (Schamroth, 1990).

has been suggested that it is prodticed after depolarizations in tbe ventricles, by repolarizatiou of tbe His-Purkmje system, or by prolonged repolarization of a specific cell layer (M-cells) in tbe mid-myocardium (Ritsema van Eck et al, 2003). This wave is seen best in tbe rigbtward chest leads, especially in V3 (Ritsema van Eck et al, 2003).

Figure 7. Electrocardiograph waveform

nomenclature.

S wave: The first negative deflection after the R wave. Similar to the R wave, tbe S wave may be written as S or s depending on its size. Again, as in tbe R wave, tbe second negative deflection following au R wave is called S' (S prime) and tbe third S", etc. T wave: Generally, tbe T wave is the next detlection to follow the QRS complex and is normally in the same direction as the preceding QRS complex. It tends to be less symmetrical than a P wave and is normally sloped on one side, U wave: Small, normally positive deflection tollowing tbeT wave. Its presence or absence is not patliological but it is important to recognize it because it may be mistaken as a P wave. Time durations associated with the above waveforms are given in liibic i. It should be noted tbat tbe QT interval and tbe ST segment durations are rate-dependent. Out of tbese two measurements the QT iuterval (or QTc, as it is known once its duradon has been corrected for beart rate) is the most important (Huszar, 2001). Q T interval: Prolongation of tbis interval leads to a specific form of ventricular tacbycardia known as torsades de pointes.This form of VT has an oscillacing pattern iu thar tbe

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g d e of tbe ventricular waveforms oscillate from a small amplitude to a large amplitude waveform (Huszar, 2001). Prolongation of tbe Q T interval may be caused by genetic congenital abnormalities in the he^irt or by drug induction (Kban. 2002), General QRS wave shape: Little cau be said for certain from a rhythm strip about tbe QRS waveform, apart from tbe gross cbanges of ventricular rbythnis, hypertrophy and inf'arction. For an indeptb analysis of the QRS. the precordial leads from a 12-lead ECG should be used. However, tbe rhythm strip can yield important information about tbe QRS duradon, e.g, qRS widening asstjciated with bundle brnncb blocks may be seen here (Huszar. 2001), Rate; Bradycardic, iu)jm,il, tachycardic. Rhythm: Regular or irregular remember .ill regular rhythnis are not normal. Sinus tachycardia, vcutricul.ir tachycardia and first degree AV block are all examples of rt;j;ular rbythms (Scbamroth. 1990), begins witb tbe precordial wave forms. Prt'cordial waveforms are used because they are the closest leads to the heart and are, therefore. more sensitive leads. The following interpretation toot is an adaptation of tbe 12-lead ECG interpretation tool described by Huszar (2001), witb detail from Schamrotb (1990). Tbaler (2003) and others as indicated,

ECG interpretation
Before starting to interpret an ECG, a few rules need to be observed. These include proper labelling of tbe ECG with tbe patients name, tbe time and date of the recording aud, if the ECG is one of a series, tbe series number of tbe EC'G information. The presence and type of chest pain is important in assessing ischaemic beart disease, as tbis may allow a differential diagnosis between cardiac and nonc.irdiac cbest pain. Care sbould be taken to ensure a good-quality recording devoid ot artefacts tracings on tbe F.CG froui sources other than cardiac in nature, e.g. skeletal muscle inovemeut or tremors ^ind e.\terual electrical .ictivity (Htiszar, 2001). Interpretation of an ECCi may be iu one of two forms: rhythm strip interpretation or 12-lead interpretation. A single rbytbm strip only contains information recorded from one perspective of the beart, whereas a 12-lead ECG contains information recorded from many difTerent perspectives. When doing any kind of ECG interpretation, it is important to be systematic, otberwise

12-iead ECG analysis

Analyse inajor shape of QRS complexes Rate (ventricular .uid .itrial if necessary) Precordial lead analysis Limb lead analysis (including axis determination) P wave analysis PR interval analysis.

P wave duration and height: Prolonged

and humped P w;tves may indicate left atrial bypertropby, wbereas tall P waves (>2.5 mui) may signify rigbt .itrial hypertrophy (Scbamroth, lWO), PR interval: Short PR intervals (<(>. 12 second) signify a bypass of the AV node, a phenomenon known as pre-excitation, which can be associated with some supraveutricular tacbycardias (.Schamroth, 1990). Prolonged PR intervals (>0,2 second) may be caused by AV uode iscbaeinia and increased parasympathetic stimulation (Huszar. 2001). PR ratio (number of P waves to R waves): There should always be a oue-to-oiie relationship

Major shape of the complexes

Look for obvious signs ot ventricular abnormality, such as ventricular tachycardia and signs of infarction; ST segment elevation. Rate: Similar to rhythm strip analysis. Rhythm: Similar to rhythm strip analysis. Check for appropriate R wave progression: Tbe first precordial lead (Vl) sln>u]d be predominantly negative and leads V5-V6 should be predominantly positive (Huszar, 2001). This gives an indiciition of the average direction of the contractile force in the ventricles, R wave progression changes in tbe presence of hypertrophy and iiitr.iventricu!ar conduction blocks (Schamrotb, 1990).

Table I. Durations of some waves and intervals of the ECG

PR interval 0.1 sec

QRS duration 0.07-0.1 sec Rate dependent Adult female (msec) <450 450-470 >470

Precordial leads
Tbe duration should not be more than It, I seconds. Anything over tbis, especially durations over 0.12 seconds suggest significant intraventricular conduction delay (Schamroth, 1990), Such delayed conduction is conmionly seen with ventricular conduction blocks and witb ventricular ectopic beats (Schamrotb, 1990). The height of tbe R wave should not exceed 26mni and the depth of the S waves should not be more than 30mm. Abnormally t.ill R waves or deep S waves indic;ite hypertrophy of the ventricles (Huszar, 2001), The Q wave depth should not be more than one quarter the ensuing R \v;tve height. Abnormally deep Q waves in any lead normally sigmfy an infarction in the part of tbe heart facing those leads (Schmaroth, 1990).

0,18-0,2 sec Adult male (msec) <430 430-450 >450

Rating Normal Borderline Prolonged

Source: Huszar (2001); Strnad (2002); ECG = electrocardiograph subtle cbaiiges may be uussed tbat lead to uiisiliterpretation of the ECG (Schamroth, 1990; Marriott and Conover, 1998).Ventricular activity is normally tbe most important feature ot an ECG (Marriot and Conover, 199H) because a rhythm strip has limited use in detailed analysis of ventricular beats. Therefore, in tbe absence of obvious ventricular arrhythmias an anatomical approach is normally sufficient for rliytbm strip analysis. between the P wave and the qKS couiplex. Arrhythmias in which there are uiore P waves per QRS complex include second and third degree AV block, Atrial flutter aud atrial fibrillation are also associated with a disparately high atrial activity when compared with the QRS waveform. However, in this case tbese v/aves are not called P waves, tbey are known as flutter and fibrillation waves, respectively (Huszar, 2001).

12-lead ECG interpretation Rhythm strip interpretation

The following need to be analysed: general QRS shape; rate; rhythm; P wave; PR interval; P-R ratio. All the initial recording considerations given in rhythm strip interpretation remain the same for 12-lead interpretation, but as mentioned, wben performing a l2-!ead ECXi. analysis

T wave
The T wave is the most unstable part of the ECG recording and is, therefore, found changed witb a number of EC'G abnormalities (Schamroth, 1990),TheT wave in Vl may be

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endocardium to epicardium (outwards), the axis IS normaUy directed dowiiward.s and as the lefthand side of the heart is more muscular than the right, the axis is shifted slightly towards the left (Schamrotli, 1 990). Therefore, the cardiac axis is ntirmally directed towards the left foot (towards lead II). The normal axis is found between limb le,id aVL aiid aVF on the hexa.xia! reference system (I-i^^urc 8) (Huszar, 200|).The hexaxial reference system IS made up by superimposing the directions of the six limb leads on top of each other using the heart as a central point (see b'ii;itrc H).
f 8. Htxjxial refrrencc system. ECGs thai have an axis between the arrows have a normal axis.

Hui-scJW (I'J'W) Naming iii'the wavLs in the ECCi. with ,1 brLet",uaHiiit of thL-ir genesis. Cimilutn'ii 98: 1437-42 H u s z a r J R (2(inl) Bjfi, Dyfrhythmias: UiUrprctation and \hiun^cmviii. 3rd edn, Mostn*. St Louis Jones I (2(10,1) AiiUf L-iironary iVTidromes: identification and patient cau.-. [>r,'!'\iinc 18: 28')-')2 Khan lA (2O(l2) Lonj^ Q T syndmme: diagnosis and ni.inagenieiit. .HJJI Hi:irlJ 143: 7 - H Knlliertiis HiE. Dcniouiin J C {]'>7(<) !'ath(ii(^i.;i] BASLS of concept k-ft hcmililock. In: WVIIL-TLS HJJ. Lie KI,J,iiise MJ. c-ds. Ilic (^>>inliuvoii .S'pfnTi ofilic Hon. Lea and Fcbigcr. I'liiladelphia
LL-vick J k {2(K)(l) All liitrodik-rioii lo (^ardwitisciikr Physiohi^.

Upright or may be hiphasic or inverted, unless originally upright in the same patient. Normally V2 is similar to VI and V3-Vf) arc normally upright. Inverted T waves may he a sign ot .\n inhnrtion (Morris and Brady, 2I.HI2).

Precordial ST segment
The ST segment should he on the baseline in most cases. The ST segment should be measured 2 mm fnim the J point (Huszar. 211(11). The J point is the point where the S wave comes up to the baseline and begins the ST segment (Schamroth. 1990).This may sometimes be difficult to see. as tbere may be no clear demarcation between the beginning ot the ST segment and :he end of the S w;!ve. An ST segment 0.5 mm below die baseline coiiunonly signifies ischaemia (Jones. 2003). A downward slurred ST segment may be seen with ventricular muscle strain found in hypertrophy (Schamroth. 1990). An elevated ST .segment in two consecutive leads indicates an acute infarction: > 1 mm in limb leads and >2mni in chest leads (Morris and Brady, 2002; Jones. 2003). Persistent ST elevation may occur for a number of reasons, including formation of a ventricular aneurysni (Thaler, 2003). Pericarditis may also cause persistent ST segment elevation; however, this tends to be found tbrougbout the chest leads commoiily associated with a notch on the end of the QRS (Smith et A, 2002).

The direction of the normal cardiac axis depends on normal muscle contraction, which in turn depends on an intact conduction system and myocardium. Therefore, axis shifts (movement away from lead II but still within normal limits) or deviations (axis outside the normal limits) may be seen in condiicrion blocks such as bundle branch, hemiblocks or in hypertrophies, where one side ot the heart becomes abnormallv dominant in terms of contractihty than the other (Schamroth. 1990). For a simple method to determine axis see Docherty (2003).

P wave analysis and PR interval analysis

This is similar to the analysis found in rliythni strip analysis. As a result of the effects of preexcitation on precordia] waveforms, it may be appropriate to preclude the presence of preexcitation betbre analysing the precordial leads.

Conclusion
C'ontident ECG interpretation takes experience and practice. When setting out to learn ECG interpretation, it might help to enlist the help of a knowledgeable senior. However, a basic understanding of the physiology underlying the waveforms is helpful. Coupled with this, an understanding of the "view' ECG leads have on the heart will help the practitioner to make a logical interpretation of the ECXJ.This article has tried to give a foundation for both these principles. QQ
Bcrnu RL, Levy MN (19')2) Cirdioiwaihir Pliysioiony. dtli edn. Mostly. Sc Loins Bookor K[. Holm K. I >R-n U| ct ,il (2liO3) Frei.|iifiii.y .md oultomt-s ot" tnnsient niyi.ic.irc1id] ist-hcmia ill iTiticilly ill .idults jJinitteJ tor iioiicjrdiac coiiditioTis. AiiiJ C.rii Cue 12: 51IH-K1 Dciiiouliii JC. Kiilbertiis HE (1972) HistopathulogiLjl L'x.iniiiiiition of Ii'ti: licrniblDL-k Hr HcnrrJ J 4 : 81W I )espopQiilos A, Sil!ieni.i^I S (20(13) Color AiLif of Phy.'.iohvy. 5th i-du. Stiittg-.ii-t. New York Dothcrty B (2Oll3) ll-le.icl ECC. lntcrprutjiion aiiJ thoM pain nianat;eiiient. Br I \'im 12: 124S-55 Hennessy S.UitkcrWB.kd.iuwJS er ;il (2lK)2) C^irdiac Arrest .iiiJ vetirnL-iilir jrrh\thnii.i in p^itifTHs t^ikinir antipwchotif dniip: cohort sCiidy using ailrniliLstrativi- daa. B.\fji25: ln7l>-2 Ho KK, Ho SK (2(1(11) Usi- of"the sinus P w-avc in Jiagiiosing electrocardiograph it limb lead niispltcenieiit nut mvnlvinii tliL- right leg (gRHiiid) lead, f nitvriM.irili,'! 34: Ui I -71

3rd edn. Arnold. London MarriDt HJL. CoDiiver MJ (IWH) Admiccd CoiicepH in .\nhyihmhif.?'K\ edn.Mostly.St Louis Meek S. Morns F (21102) ABC: of clinical etectrocardiograpliy: introduction, i Leads, rate, rhythm, and cardiac a>;is.BA//324: 415-18 Miirns F; Brady WJ (2O(i2) ABC: ofdinica; eiecCKK-ardiography.Acute iiiyocardial infarction p.in I . K \ / / 3 2 4 : 831-4 t)"Brien i^ Oyt-bode F (20(13) Psychotropic nicdlairioii and the lieart. .4Jniiiff.i in PsyiliumicTn-atmail 9: 41423 Opic LH (1998) 'liw Hem: Physiology from Cell lo ChaiUiioii. 3rd edn. Lippincotc Williams & Wilkins, Philadelphia Puech P (I'156) L'liaivitc niccirupic Aiiriiiil.iire .\'oriihi!i' vl I'.iilh'ioiiiqiu: Massou ik Cie. Paris kautah.!rju PM. Park t_. ti.autali.irju S, Crow R (199K) A staridialized pnxediirc for locaring and doaimcnting ECG chest electmdc positions: cnrisidL-ratKin afthe etfeit of ba-ast rissue on EtX; amplitudes in wonicjij Hlranmrdioi iU 17-2'^ Kitsema van Eck HJ, Kors JA, van Herpen C: (2003) The elusive U wave; .i simple (explanation ot its genesis / HInrroamlio! Z6{Supp\): 133-7 Schamroth L (1990) An Itinodiiaio'i !< Hh\!>oniriiioi;riipliy. Ulackwell Science, Oxford Smith SW, Zvosec I_)L, Sharkey SW. Henry T O (2(:i<:)2) 'Ihc hCG ill Acute .Ml: .-ill Eiidcnce-hased Aiaimal of Rcpctfiision Vifnipy Lippincott Williams and Wilkins, Phil.idelpliia Snellcn HA (1995) [IV//t'fir Eimlmtv (lH6(f-l927l: rather of FAcarociirdio^^riipliY. Kluwer Academic Publishers, Dordrecht, Netherlands Strn.id t;F (imi) Vie Clinical Evaliiatio)} of QT/QTr Inrcrva! Prohii^<iiiti,<n and Proarrhythinic Potential for \oihantiartjiythiiiic Dnii^f. Therapeutic Prodiucs Directorate (www.hcsc, gc, c a / hptb-d gp sa/ tp d - dpt / qr__c o n c ep tjiaper_e, h nut) (tast accessed 7 April 21104) Sykes AH. Waller AD (1887) The electrocardiogram, RMJ (Clin Re^ nd) 294: 139(1-8 Tluter MS (2003) Vw Only HK(; Book'You'll Erer Seed. 4tU edn, Lippincott Williams and Wilkins, Philadelphia University of tlalifornia Siin Francisco (2003) Apimyatli lo Regular Nanmi'-Complcx Tachycardias. University of C^tbriiia San Francisco (http.V/medicine.ucsf.edu/housestafr/ Chieli_covcr_sheets/na,pdf) (last accessed 7 April 2(104) Waldo L, Wit AL (21101) Mechaiii,sn5i of cardiac arrhydimi.LS .iiid conduction disturbance. In: Fuster V, Alexander RW, tVKoiirke R, Roberts R. King SB 111, Wellens H[|, eds, Huysi\ ihr Hijrf, McGraw Hill, New York: 7,S I

KY POINTS
I Electrocardiograph (ECG) recording and interpretation is becoming more prevalent in many healthcare environments. I Intelligent ECG interpretation necessitates an understanding of the basic physioiogy behind the waveftarms. I Proper ECG analysis requires an understanding of the different views a 12-iead ECG has on the heart. I To ensure a comprehensive analysis of the ECG, a systematic approach to ECG interpretation needs to be adopted. I To gain confidence and expertise in ECG interpretation, nurses shouid practice under the supervision of a proficient practitioner.

Analyse limb leads

Analysis of limb leads is similar in most cases to precordial leads, although the magnitude of the waveforms is slightly less as they are further away from the heart. Cardiac axis The cardiac axis is determined from the limb leads. The cardiac axis shows the mean direction of the flow of electrical activity generated in the heart. As the myocardium contracts from

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