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Week 3 – ECG analysis and application

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IntroductionPreviously you have examined cardiac assessment and the analysis and treatment ofarrhythmias. Analysis of the 12 lead ECG is a vitalcomponent of cardiovascular assessment needed for many cardiac conditions. A systematic approach to the assessment of the ECG isvital and ensures success. This is a large module and will continue to be work in progress throughout the year. Most of this is assumedknowledge, so use it for revision and choose what is important in regard to your personal learning.Learning outcomes for this sectionUpon successful completion of this section, you should be able to:describe how the 6 limb leads of an ECG are obtainedidentify the sites of attachment of the six precordial leads and indicate over which region of the heart each electrode lieslist the leads which view the major surfaces of the heartdemonstrate a systematic approach to analysis of the 12 lead ECGdemonstrate a basic understanding of the physiology and characteristics of bundle branch blocksdemonstrate a basic understanding of the ECG characteristics of ischemia and infarctiondescribe the ECG changes associated with pericarditis and myocardial traumaidentify the changes associated with hyper and hypokalemia on an ECGidentify the major characteristics of chamber enlargement.3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 4/22Suggested readingsText readingThompson, P 2011, chapter 26 ‘Electrocardiographic monitoring’, in Coronary care manual, 2nd edn, ElsevierAustralia. – Click Here.Optional readingWoods, S, Froelicher, E, Motzer, S & Bridges, E 2010, Cardiac nursing, 6th edn, Lippincott Williams and Wilkins.Available online Flinders University Library www.flinders.edu.au/library through Ovid.3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 5/22The 12 Lead ECGA 12 Lead electrocardiogram consist of the following:

Six limb or extremity leadsThree standard (bipolar) leads, I, II &IIIThree augmented (unipolar) limb leads aVR, aVL & aVF.Six precordial (unipolar) leads V1-V6.So far this Study plan has concentrated on the bipolar and unipolar limb leads. The six precordial unipolar leads are a vital part of ECGanalysis as they give a view of the heart on its horizontal plane.The electrical activity of the heart consists of multiple individual currents with the ECG representing the sum result of these electricalimpulses from a point on the body surface. If the sum result of the electrical impulse or mean vector is towards the positive ECG pole apositive deflection is recorded. A current flowing towards the negative pole records a negative deflection.The following diagram illustrates the normal sequence of depolarisation through the heart as recorded by the limb and the precordialleads. These give a view of the heart on its frontal and horizontal plane.Figure 4.1: (A) Normal sequence of depolarisation through the heart as recorded by the frontal plane leads. This diagram also includesthe hexaxial reference system or axis wheel. (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010,Cardiac nursing, Lippincott.)Figure 4.2: (B) Cross section of the thorax illustrating how the six precordial leads record normal electrical activity in the ventricles. In bothexamples the small arrow (1) shows the initial depolarisation through the septum, followed by the mean direction ofventricular free wall depolarisation, larger arrow (2). (Adapted from Woods, S Froelicher, E, Motzer, S & Bridges, E (eds)2010, Cardiac nursing, Lippincott.)3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 6/22Activity—Review the followingThe correct sequence of R wave progression through the precordial leads. Relate this to the normalsequence of depolarisation of the heart.The sequence of ventricular depolarisation through the right and left bundle branches and relate this to theECG characteristics in the precordial leads.The configuration of lead AVR? Why does this lead normally record a negative deflection?12 Lead Interpretation Part 1: Introduct…3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 7/22Examining the ECG: the processExamination of the ECG should follow a defined process. You may find that this process differs from many different processes in your text.Find one which suits you and use it with all of you ECG analysis exercises and in clinical practice. Your process should includeexamination of the each of the following:Patient identification and calibration (as in week 2)Rate and rhythm (as in week 2)Intervals: Is the PR and QT intervals normal? Use your ECG text to determine the normal characteristics.Waveforms: Are the P QRS and T waves within normal range?Cardiac axis. Determine if the axis is normal, left axis deviation, right axis deviation or indeterminate.ST segments: Is there any indication of myocardial injury or infarction.Other abnormalities: Signs of electrolyte abnormalities hypertrophy.12 Lead Interpretation Part 2: The 6 St…3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 8/22Determining the electrical axisThe axis represents a measurement of the sum of the electrical vectors during depolarisation of the heart. Determination of the electricalaxis shows the mean vector generated by depolarisation of the ventricles as determined by examining the ECG leads of the frontal plane.Deviations in the electrical axis from normal or a change in axis may reflect anatomical alterations or significant pathology associated withmyocardial damage.Axis is most commonly represented using the hexaxial reference system on the frontal plane leads represented in diagram (A) above. Thislabels each of the 6 frontal plane leads within a 360° circle beginning with lead I at 0°. The mean QRS vector or normal axis lies between 0and +90°.There are several methods of determining the mean frontal plane QRS axis each of which require examination of leads I and AVF. Theexact axis as a percentage value can be plotted on the hexaxial wheel, or a simpler method classifies the axis as normal, left axisdeviation, right axis deviation or indeterminate as demonstrated in the following diagram.Figure 4.3: The four quadrants of the axis wheel. (A) If the QRS in lead I is positive and the QRS in aVF is negative, the axis is in the leftquadrant. (B) If the QRS is positive in both leads I and aVF, the axis is normal. (C) If the QRS in lead I is negative and the QRS in aVF ispositive, the axis is in the right quadrant. (D) If the QRS is negative in both leads I and aVF, the axis is indeterminate. (Adapted fromWoods, S Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)It is important that you can determine the axis within the four categories described above. Consult your ECG text to practice a method axisdetermination to achieve this. Consult your mentor or clinical facilitator if you have difficulty with this process.ActivityWhat is meant by electrical axis? Use your diagram of Einthoven’s triangle from the previous section todetermine the direction of the electrical axis in the limb leads.Read the section in your texts regarding determining the electrical axis. What are the characteristics andclinical significance of a left or right axis deviation? Relate this to the patients that you are caring for in theclinical area.12 Lead Interpretation Part 3: R-wave P…3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 9/22The normal ECGExamine this ECG and follow the examining process.Normal sinus rhythm is present at a rate of 110 beats per minute.PR and QRS intervals are normalThe QRS complexes and R wave progression is normalThe T waves are normalThere are no abnormal Q wavesThe Cardiac Axis is normalThe ST segment is at baseline in all leads.There are no other abnormalities.This ECG can be used for comparison as abnormalities are discussed throughout this module.Figure 4.4: The normal ECG(Adapted from Hampton, J 2014, The ECG made easy, Churchill Livingstone.)3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 10/22Q wave and ST segment abnormalitiesECG analysis involves careful analysis of the Q wave and ST segment for indicators of myocardial pathology.The Q wave represents depolarisation of the interventricular septum. The Q wave is always a negative deflection, and may be present insome leads of the 12 lead ECG. In all leads accept leads III and AVR a Q wave is considered abnormal or pathological if it is greater than0.04 second in duration and more than one third the height of the following R wave.Pathological Q waves are highly suggestive of myocardial damage. Dead tissue is electrically inactive, therefore an electrode placed oversuch an area will see through it (like a window) to detect the electrical force generated by the opposite wall, i.e. current flow moving awayfrom it as the cells are depolarised from the endocardium to epicardium. It is important to be aware of the characteristics of and be able todistinguish between normal and pathological Q waves.Figure 4.5: (A) Lead III in a healthy patient. (B) The same lead in the same patient 2 weeks after undergoing an inferior myocardialinfarction. Note the deep Q wave.(Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)The ST segment of the ECG is the line following the QRS complex connecting the QRS to the T wave. This represents the repolarisationsegment of the ECG and is highly indicative of myocardial injury ischemia and infarction which can delay the repolarisation process.Analysis of the ST segment necessitates identification of the J point, or the connection between the end of the QRS and the beginning ofthe ST segment. A normal ST segment is flat with a variation of a minimum of 0.5-1.0 mm from the isoelectric line.Figure 4.6: ST segment elevation associated with myocardial infarction(Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)Figure 4.7: Different types of ST segment depression highly indicative of myocardial ischemia. This example shows (A) down-sloping (B)up-sloping (C) horizontal ST depression(Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)ActivityRead your ECG text to become familiar with the characteristics of normal and abnormal Q waves and STsegments.Distinguish between the characteristics of normal and pathological Q wave.Describe the characteristics for ST elevation and depression in the both the precoridial and limb leads.3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 11/22The indicative leads in altered state ECGsFigure 4.8: Localising myocardial ischemia, injury, or infarction using the 12-lead ECG. The different areas of the heart are pattern-coded.Standard 12-lead ECG format is illustrated at upper right with leads pattern-coded to correspond to the area of the heart that each leadfaces.(Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)Now you have examined the characteristics of all the leads in the ECG you can begin to determine their relationship to the relevant partsof the heart. This is particularly useful when identifying an area of the myocardium which is affected by an alteration in blood supply. Thefollowing diagram identifies the anatomical lead groupings of the heart.ECG activity 1Check your answers when you reach the end of this section.Take a look at the ECG below.Can you identify the leads which show ST segment elevation?Which surface of the heart are these leads viewing?What coronary artery supplies the area of the ECG that is altered?Use your ECG text to determine what coronary arteries supply each of the patterned areas in Figure 4.8.3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 12/22ECG—ischemia patternsMyocardial ischemia results from an imbalance between oxygen supply and demand. The ECG changes associated with myocardialischemia are associated with changes in the depolarisation process, and therefore are often reflected by an inverted T or depressed STsegment. However T wave inversion may also associated with other conditions such as bundle branch block, and it can be normal in somepeople. A diagnosis of myocardial ischaemia is often made based on the presence of chest pain and ECG changes. These changes maybe transient, and may occur during chest pain or exercise testing.Figure 4.10: ECG patterns and myocardial ischaemia. Refer to the grey area for the identified change.(Adapted from Huszar 2002, Basic dysrhythmias: interpretation & management, 3rd edn.)Figure 4.11: ECG patterns associated with myocardial ischemia.(Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)ECG activity 23/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 13/22ECG—injury and infarctionMyocardial injury is the next stage beyond ischaemia. Injured myocardial cells are still alive, but are vulnerable to progress to infarction(cell death). Diagnosis is made in by analysis of the ECG as well as specific and sensitive cardiac biochemical markers, such as troponinwhich detect myocardial damage.The underlying pathophysiology of myocardial infarction is associated with that of a ruptured plaque and subsequent thrombus formationwhich may partially or completely occlude a coronary vessel. The injury pattern that is recorded on the ECG as a result are classified asST elevation myocardial infarction, (STEMI) non ST elevation myocardial infarction NSTEMI depending on the ECG pattern andmeasurement of cardiac enzymes.The term myocardial infarction (MI) is used loosely to encompass both myocardial injury and necrosis. Not all patients who have a MIactually develop tissue necrosis. Early reperfusion intervention can reverse the injury and prevent muscle death.The ST segment changes are caused by changes produced by injured myocardial cells. Hence the leads which are facing the injured areawill reflect a raised or depressed ST segment. The degree of ST segment elevation or depression is variable, an increased or decreasedof more than one millimetre above the isoelectric line in two or more leads is considered as abnormal. ST changes usually occurs withinminutes of the onset of infarction.Certain characteristics of the Q, ST segment and T wave can provide some clues to the age of the infarction:Prominent Q wave (normal ST segment)—old MIQ wave + ST elevation (with or without T wave inversion)—acute MIQ wave + inverted T wave—indeterminate ageReciprocal changesThis is reflected as ST depression in the reciprocal leads, or those opposite the zone of injury. This is a common phenomenon seen inECG leads facing the opposite side of the area of injury, e.g. ST depression will be seen in the anterior lateral leads in the presence of anacute inferior MI.This is illustrated in the following diagram.Figure 4.12: ECG reciprocal changes(Adapted from Huszar 2002, Basic dysrhythmias interpretation and management, 3rd edn.)Diagnosis of right ventricular and posterior changesThe right coronary artery (RCA) supplied the inferior and posterior wall of the left ventricle, as well as the right ventricle. Hence occlusionof the RCA often results in damage to the inferior posterior wall of the left ventricle with extension into the right ventricle (RV) free wall. Thebest lead to detect RV infarction is Lead V R.The key indicator of RV infarction is ST segment elevation of greater than 1 mm in this lead. In the clinical setting a recording of V R, V Rand V R is made to facilitate interpretation. Q wave is normally seen in these leads because of the electrical axis of the heart duringnormal ventricular depolarisation.ECG diagnosis of damage to the posterior wall of the heart also requires careful consideration. As we do not routinely place electrodes onthe back of the chest to view this surface of the heart directly, diagnosis is reliant upon the presence of reciprocal changes.44 563/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 14/22Figure 4.13: The placement of the right ventricular leads(Adapted from Huszar 2002, Basic dysrhythmias: interpretation & management, 3rd edn.)eReadingThe following reading gives a good overview of the ECG changes with myocardial ischemia and infarction. Youmay wish to consult your ECG text to supplement this reading.Jacobsen, C 2010, chapter 22 ‘Acute coronary syndromes’, in Woods, S, Froelicher, E, Motzer, S & Bridges, E(eds), Cardiac nursing, Lippincott Williams and Wilkins, pp. 511-534.(Available Flinders University Library, www.flinders.edu.au/library, books at Ovid.)ActivityConsult your text to create a list of the ECG changes commonly associated with myocardial ischemia andinjury. What other diagnostic tests are necessary to distinguish between these?Consult your text to create a list of the diagnostic ECG criteria for STEMI in each major zone of the heart.Include the associated reciprocals changes. Relate each of these to the coronary arteries affected.Classify the ECG changes associated with myocardial infarction into early and late changes.Take particular note in the above reading of the section on posterior MI. As we do not routinely placeelectrodes on the back of the chest to view this surface of the heart directly, diagnosis is reliant upon thepresence of reciprocal changes. Describe the changes associated with posterior MI and list the other zonesof injury and infarction with which it is normally associated.3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 15/22Evolution of MITake note of the ECGs in the reading by Wood. In particular note the ST segment T wave changes and evolution of Q waves which occurduring an acute infarct.Serial ECGs are often recorded of a patient following a STEMI to monitor for these changes. Take a look at the ECGs A, B, C & D.ECG AECG BECG CECG DThe raised ST segment in leads V , V and V on ECG D is typical of a fully evolved phase of MI. There are times when ST segments mayremain elevated (pattern of phase 2) for more than 72 hours. Abnormal conditions such as pericarditis, a common post-MI complication, ora left ventricle aneurysm may be the cause of persistent ST segment elevation. The T wave is usually inverted towards the end of theacute phase. Look at V in ECG D and may return to an upright position within weeks to years’ post MI.2 3 433/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 16/22ECG activity 3Can you identify the leads which are showing reciprocal changes on the ECG A?ECG activity 4Can you identify the leads with pathological Q wave on the following ECG?Which surface of the heart are these leads viewing?Which coronary vessel supplies this area of the heart?3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 17/22Intraventricular conduction delaysDelays in intraventricular conduction of cardiac impulses may result from abnormalities in the His-Purkinje system or in ventricular muscle,and may be caused by structural changes or by the functional properties of the cardiac conduction system.Fascicular blockUnder normal conditions, activation of the left ventricle begins almost simultaneously at the insertion points of the fascicles of the leftbundle branch. Absolute or relative delays in conduction in a fascicle, fascicular block, results in an abnormal sequence of earlyleft ventricular activation that, in turn, leads to characteristic electrocardiographic patterns. Even modest delays in conduction through theaffected structure may be enough to alter ventricular activation patterns sufficiently to produce characteristic electrocardiographic patterns;a complete block of conduction is not required. Refer to figure 14.14.Left anterior fascicular blocks have a frontal plane mean QRS axis = −45 to −90 degrees, a qR pattern in lead aVL, a QRS duration < 120 msec and time to peak R wave in aVL ≥ 45 msec. Right posterior fasicular blocks have a frontal plane mean QRS axis = +90 to +180 degrees, a rS pattern in leads I and aVL with qR patterns in leads III and aVF and QRS duration < 120 msec at exclusion of other factors causing right axis deviation (e.g., right ventricular overload patterns, lateral infarction) Figure 4.14: Diagrammatic representation of fascicular blocks in the left ventricle. Left, Interruption of the left anterior fascicle or division (LAD) results in an initial inferior (1) followed by a dominant superior (2) direction of activation. Right, Interruption of the left posterior fascicle or division (LPD) results in an initial superior (1) followed by a dominant inferior (2) direction of activation. AVN = atrioventricular node; HB = His bundle; LB = left bundle; RB = right bundle. (From Goldberger, AL 2011, Clinical electrocardiography: a simplified pproach, 8th edn, St Louis, CV Mosby.) 3/24/2020 Study plan: Week 3 – ECG analysis and application https://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 18/22 Bundle branch blocks Left Bundle Branch Block results from conduction delay or block in any of several sites in the intraventricular conduction system, including the main left bundle branch, each of the two fascicles, the distal conduction system of the left ventricle or, less commonly, the fibers of the bundle of His that become the main left bundle branch. The result is extensive reorganization of the activation and recovery patterns of the left ventricle that produces extensive changes in the QRS complex and ST-T wave. The prevalence and severity of left ventricular dysfunction increase progressively as QRS duration increases. LBBB is associated with a higher than normal risk of cardiovascular mortality from infarction and heart failure. Complete Left Bundle Branch Block has a QRS duration ≥ 120 msec, broad, notched, or slurred R waves in leads I, aVL, V5 and V6, small or absent initial r waves in right precordial leads (V1 and V2) followed by deep S waves. Also there are absent septal q waves in leads I, V5, and V6 and a prolonged time to peak R wave (>60 msec) in V5 and V6.Right Bundle Branch Block is a result of conduction delay in any portion of the rightsided intraventricular conduction system. The delaycan occur in the main right bundle branch itself, in the bundle of His, or in the distal right ventricular conduction system. The new onset ofRBBB predicts a higher rate of coronary artery disease, congestive heart failure, and cardiovascular mortality. When cardiac disease ispresent, the coexistence of RBBB suggests advanced disease with, for example, more extensive multivessel disease and reduced longtermsurvival in patients with ischemic heart disease. Complete Right Bundle Branch Block has a QRS duration ≥ 120 msec, rsr′, rsR′, orrSR′, patterns in leads V1 and V2, S waves in leads I and V6 ≥ 40 msec, a wide a normal time to peak R wave in leads V5 and V6 but >50msec in V1.The term multifascicular block refers to conduction delay or blocks in more than one of the structural components of the specializedconduction system—that is, the left bundle branch, the left anterior and posterior fascicles of the left bundle branch, and the right bundlebranch. Conduction delay in any two fascicles is termed bifascicular block, and delay in all three fascicles is termed trifascicular block. Theterm bilateral bundle branch block has been used to refer to concomitant conduction abnormalities in both the left and right bundle branchsystems.Figure 4.15: Comparison of typical QRS-T patterns in RBBB and LBBB with the normal pattern in leads V1 and V6. Note the secondary Twave inversions (arrows) in leads with an rSR′ complex with RBBB and in leads with a wide R wave with LBBB. (From Goldberger AL:Clinical Electrocardiography: A Simplified Approach. 8th ed., St. Louis, CV Mosby, 2011.)eReadingJacobsen, C 2010, chapter 16 ‘Conduction abnormalities’, in Woods, S, Froelicher, E, Motzer, S & Bridges, E(eds), Cardiac nursing, Lippincott Williams and Wilkins, pp. 360-364.(Available Flinders University Library, www.flinders.edu.au/library, books at Ovid.)ActivityUse the above reading and your ECG text to complete the following.Research the identifying features of both right and left bundle branch blocks.Describe the blood supply to the bundle branches. Damage to what areas of the heart are likely to result in bundle branch blocksWhat is the clinical significance of bundle branch blocks? In what way may their presence affect your analysis of other features o3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 19/22Other ECG abnormalitiesThere are other abnormalities that can be detected by the ECG including changes in chamber size, electrolyte and drug effect andmyocardial damage associated with pericarditis and trauma. Review your learning outcomes to achieve the necessary understanding inthis area. Those working in a cardiac speciality may wish to go into more detail.Chamber enlargementEnlargement of each of the four chambers of the heart are detected by the ECG as changes in the size and morphology of the P and QRSwave as well as some changes in the cardiac axis. It is important to note that these often reflect chronic or long term changes to thecardiac structure.Electrolyte imbalancesElectrolyte imbalances which can affect the ECG include potassium magnesium and calcium imbalances. The effect of elevated serumpotassium on the ECG is demonstrated in the following diagram.Figure 4.14: Changes in Lead II caused by varying levels of serum potassium (Adapted from Huszar 2002, Basic dysrhythmias:interpretation & management, 3rd edn.)ActivityResearch the effect of atrial and ventricular enlargement on the ECG and with what physiological conditionsis this associated.Make a list of the ECG changes associated with hypokalemia, hyperkalemia and calcium and magnesiumimbalances.Describe the ECG changes associated with pericarditis and myocardial trauma.Can you diagnose the next series of ECGs?Where appropriate, try and identify the coronary vessel which may be involved with each type of MI.ECG activity 53/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 20/22http://www.facebook.com/media/set/?set=t.656473137ECG activity 6ECG activity 73/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 21/22Lifespan IssuesPaediatric ConsiderationsSuggested eReading onlineGalli, M., & Danzi, Gian Battista. (2013).Chapter 2, Normal Parameters of Pediatric ECGs in A Guide to Neonatal and Pediatric ECGs. Dordrecht: Springer. pp 57-71.As well as the cardiovascular differences discussed in week 2, paediatric ECG’s will also exhibit a number of differences compared to adult ECG’s. ECG lead placementdiffers slightly in children less than 5 years of age. In younger children the right ventricle extends further to the right side of the sternum than in adults. This necessitatesthe inclusion of a lead (V4R on the right side of the chest, at a point comparable to the left sided V4;ECG placement in children less than 5 years of ageV4R – 5th intercostal space, right midclavicular lineV1 – 4th intercostal space, right sternal borderV2 – 4th intercostal space, left sternal borderV3 – use this lead for V4RV4 – 5th intercostal space, right midclavicularV5 – anterior axillary line, same horizontal plane as V4V6 – midaxillary line, same horizontal plane as V4Use your structured method of ECG analysis as you would in adults.Some differences to note when analysing paediatric ECG’s are;Heart rate will exceed 100bpmDominant R wave in V1‘RSR’ pattern in V1Rightward QRS axis > +90°Sinus arrhythmia is common in children, along with J point elevation and T wave inversion in right precordial leads.Have a look at the ECG below to see if you can spot any of the above features. It is taken from a healthy 2 year old boy. Note the heart rate is 110bpm (normal for age)and TWI in leads V1-V3Figure 1: ECG courtesy of Life in the Fast Lane (accessed 9/1/2016).Paediatric ReferencesDriscoll, D. (2006). Fundamentals of Pediatric Cardiology. Philadelphia, PA, USA: Wolters Kluwer. – Available online through Flinders University Library – Click HereLife in the Fast Lane Pediatric ECGs web site – Click HereECG Tutorial: Interpretation of the 15 L…3/24/2020 Study plan: Week 3 – ECG analysis and applicationhttps://flo.flinders.edu.au/mod/book/tool/print/index.php?id=2585801 22/22The Older AdultAlways keep the patient’s age in mind when interpreting ECGs. ECG changes in the older adult include increased PR, QRS, and QTinterval, , decreased amplitude of the QRS complex and a shift of the QRS axis to the left.These ECG changes are in reference to the following:• arterial stiffening• endothelial dysfunction promoting vasoconstriction• elevated systolic blood pressure and increased pulse pressure• increased left ventricular wall thickness• reduced early diastolic filling• impaired cardiac reserve• alterations in heart rate rhythm• prolonged cardiac action potential• a decline in renal function that contributes to improper maintenance of extracellular fluid volume and composition.These age-associated changes in cardiovascular function precede clinical disease (hypertension, stroke, atherosclerosis, etc.).The post Week 3 – ECG analysis and application appeared first on My Assignment Online.

  

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