ECG INTERPRETATION MANUAL

Transcription

1 Lancashire & South Cumbria Cardiac Network ECG INTERPRETATION MANUAL THE ABNORMAL ECG Lancashire And South Cumbria Cardiac Physiologist Training Manual

2 AV NODAL BLOCKS (HEART BLOCKS) Disturbances of intra cardiac conduction occur principally in the AV node. Causes: - Increased vagal tone in digitalis therapy IHD Rheumatic endocarditis Degeneration of the conducting tissue Sclerotic disease of the surrounding structures Cardiac surgery trauma When the AV node is damaged there is a delay or total block of impulses at the AV Node and conduction through it is affected.

3 FIRST DEGREE HEART BLOCK (1º) The impulse originates, as normal in the SA node but conduction through the AV node is slower than normal. This gives a prolonged PR interval. The rest of the complex is normal. ECG criteria Rate Normal Rhythm Regular P Wave Normal QRST Normal But: PR interval more than 0.2 seconds PR interval is constant Clinical significance If the rate is normal there is no affect on the patient. Treatment None indicated unless the rate is very slow then treat as bradycardia. If associated with organic heart disease it may progress to 2º or 3º heart block.

4 SECOND DEGREE HEART BLOCK (2º) Mobitz Type I (Wenkebach) Conduction through AV node becomes progressively delayed until it fails completely. The beat is dropped. The cycle repeats. ECG criteria Rate Normal or slow Rhythm Regular P waves Irregular QRS complexes P Wave Normal QRST Normal But: - PR interval increases with each cycle (not constant) - Dropped beat. Clinical significance If the rate is normal no affect. If the rate is slow symptoms. Symptoms Treatment Low cardiac output state Drop in BP Peripheral vasoconstriction Poor tissue perfusion Confusion LOC If CO is normal no treatment. Oxygen administration will relieve hypoxia. Drug therapy can increase SA node rate and therefore increase ventricular rate. NB: - can deteriorate to complete heart block.

5 Mobitz Type II (2º) Conduction times through the AV node are constant but there is a variability of the number of impulses which are conducted through the ventricles. ECG criteria Rate Normal or slow Rhythm Regular P waves Regular QRS complexes P Wave Normal PR interval Normal and constant But may be 2/3 P waves preceding QRS complexes NB Clinical significance and treatment is higher than Mobitz Type I. Permanent pacing is recommended 2 : 1 AV Block There may be 2/3 P waves preceding QRS complexes as a constant pattern Ratio 2 : 1 3 : 1 NB Clinical significance and treatment is the same as for Mobitz I

6 THIRD DEGREE / COMPLETE HEART BLOCK (3º) The AV node fails completely and none of the sinus impulses are conducted to the ventricles. There is no ventricular response to normal sinus P waves. Now pacemaker cells with the next fastest intrinsic discharge rate (or ventricular ectopic focus must take over to stimulate the ventricles. This is known as an idioventricular rhythm, but the intrinsic ventricular rate is very slow (30-40 bpm). The ECG shows complete atrio-ventricular dissociation, the P wave rate being normal whereas the ventricular rate is slow. If the idioventricular pacemaker fails it will lead to ventricular standstill which manifests clinically as Stokes-Adams syncopal attacks. Cardiac Syncope Stokes-Adams attacks Caused by 1. Complete heart block with slow ventricular rates and/or failure of pacing focus 2. Sudden onset rapid tachyarrhythmia usually paroxysmal VT or VF. The attack may last a few seconds to minutes. The patient may become unconscious, cyanosed and may convulse. The patients report dizzy do s or faints. Ambulatory monitoring can be used to confirm diagnosis. Treatment requires insertion of a permanent pacemaker. Transient complete heart block usually due to MI involves the insertion of a temporary pacing wire until normal AV Nodal conduction returns. KAP/LJR.. AVB001.

7 BUNDLE BRANCH BLOCK A delay of conduction in either of the bundle branches. Right Bundle Branch Block In RBBB the right ventricle is stimulated by the impulse from the left ventricle. Phase of activation:- BLOCK (1) (2) (2) (3) (( The septum depolarises from left to right as normal. (1) The left ventricle is depolarised as normal. (2) Finally the right ventricle is depolarised late (wide) in an anterior movement. (3) Resulting QRS is wide due to slow conduction through myocardial cells.

8 (1) (2) V1 (3) V6 Resulting complex in leads orientated towards the right ventricle have RSR1 complex in V1. The proximal limb of the complex (R1) is due to the stimulus spreading through the right ventricle and since it is late it is unopposed by LV depolarisation and it is therefore of high magnitude. In leads orientated towards left ventricle (V5, V6) and AVL a broad and slurred S wave is seen. This is due to the late depolarisation of the free wall of the RV away from electrode V6.

9 RBBB & MI If abnormal Q waves are present they will not be masked by the BBB pattern. This is because there is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can still be seen. Significance of RBBB RBBB is seen in :- (1) occasional normal subjects (2) pulmonary embolus (3) coronary artery disease (4) ASD (5) active carditis (6) RV diastolic overload ECG criteria for RBBB (1) QRS duration exceeds 0.12 seconds (2) RSR complex in V1 (3) Delayed S wave in Ι, V5, V6 (4) ST/T must be opposite in direction to the terminal QRS (is secondary to the block and does not predispose primary ST/T changes) Partial / Incomplete RBBB is diagnosed when the pattern of RBBB is present but the duration of the QRS does not exceed 0.1 seconds.

10 Left Bundle Branch Block In LBBB the left ventricle is activated from the right bundle. Phase of activation :- BLOCK (1a) (3) (2) (1b) Impulse passes to the left of the septum below the block (1a) at the same time as the paraseptal region. (1b) Activation of the RV follows (small magnitude). (2) Finally delayed activation of the LV which is slow due to conduction through normal myocardium. (3)

11 (1a) (3) (2) (1b) V1 V2 V6 (1) (1b) (2) (2) (1) (1a) (3) ECG criteria for LBBB (1) Prolonged QRS complexes, greater than 0.12 seconds (2) Wide, notched QRS (M shaped) Ι, AVL, V5, V6 (3) Wide, notched QS complexes are seen in V1 (due to spread of activation away from the electrode through septum + LV) (4) In V2, V3 small r wave is seen due to activation of paraseptal region

12 LBBB & MI MI should not be diagnosed in the presence of LBBB Q waves are masked by LBBB pattern. Significance of LBBB LBBB is seen in :- (1) Always indicative of organic heart disease (2) Found in ischaemic heart disease (3) Found in hypertension. Partial / Incomplete LBBB is diagnosed when the pattern of LBBB is present but the duration of the QRS does not exceed 0.1 seconds. LJR/KAP..BBB001.

13 ATRIAL AND VENTRICULAR ARRHYTHMIAS Remember normal sinus rhythm. Consider four components of the above : P wave PR interval QRS complex T wave Providing the process of depolarisation throughout the heart is initiated in the SA node and the conduction system is normal, then the above mentioned events will occur sequentially. - Atrial depolarisation - Atrial contraction - AV nodal delay - Ventricular depolarisation - Ventricular contraction - Ventricular relaxation If for any reason this sequence of events is disturbed then the effects will consequently be recorded on the ECG. The sequence can be disturbed for many reasons, one of these is the presence of an irritable focus or foci in some part of the atrial or ventricular myocardium, which initiates depolarisation of the atrium or ventricles before the next expected sinus discharge.

14 ATRIAL ECTOPIC BEATS E.C.G Criteria :- Premature P wave Bizzare shaped P wave Compensatory pause (resets SA NODE) Following the atrial ectopic beat, conduction through the AV node can be one of the following :- Normal Short Prolonged Blocked NB. The AV node acts as a safety mechanism protecting the ventricles from any atrial rhythm disturbances. SVE

15 ATRIAL FIBRILLATION E.C.G Criteria :- Small, rapid, irregular fibrillation waves ( bpm) QRS morphology is normal Ventricular rate is irregular ( bpm) Common causes: - Mitral Valve Disease Thyrotoxicosis Cardiomyopathies Treatment: - Digoxin (lowers ventricular rate) Sotalol DC Cardioversion

16 ATRIAL FLUTTER E.C.G Criteria: - Rapid regular atrial contraction ( bpm) Broad, Bizarre Flutter waves No Iso-electric shelf Usually regular ventricular rate (with ratio P waves: QRS) Common Causes: - Rheumatic Heart Disease Ischaemic Heart Disease Treatment: - DC Cardioversion RF Ablation Sotalol

17 VENTICULAR ECTOPICS E.C.G Criteria: - Premature Bizzare shaped QRS Wide Complex compensatory pause A run of 3 or more can be classified as VT. VE

18 VENTRICULAR UNIFOCAL ECTOPICS The ventricular ectopics arise from the same focus and therefore are the same morphology in any given lead. VENTRICULAR MULTIFOCAL ECTOPICS The ventricular ectopics arise from more than one focus and therefore have different morphologies in any given lead.

19 VENTRICULAR BIGEMINY An ECG which shows alternating sinus beats and ventricular premature beats is described as ventricular bigeminy. There is usually a constant interval between the sinus beat and the ventricular ectopic beat suggesting the sinus beat controls the discharge of the ventricular ectopic. VENTRICULAR TRIGEMINY A ventricular ectopic followed by two sinus beats. RV ECTOPICS The ventricular ectopic which arises in the right ventricle will give a Left Bundle Branch Block pattern. The main spread of the impulse is away from the electrode at V1 resulting in a downward V1 deflection. The spread of the impulse is towards the electrode at V6 resulting in an upward V6 deflection. V6 V1

20 LV ECTOPICS The ventricular ectopic which arises in the left ventricle will give a Right Bundle Branch Block pattern. V6 V1

21 VENTRICULAR FIBRILLATION Chaotic, uncontrolled, multiple depolarisation s resulting in non- uniformed ventricular contractions. No clearly identified QRS No cardiac output Loss of Consciousness Treatment: - DC Defibrillation VF LJR/KAP..AVA.001.

22 ATRIAL ENLARGEMENT / HYPERTROPHY The P wave reflects atrial depolarisation and is recorded as soon as the impulse leaves the SA node. The SA node is situated in the right atrium hence RA activation occurs before LA activation. The two processes overlap as LA activation actually begins before RA activation ends. AVNODE SA NODE

23 Hypertrophy is enlargement / thickening of the muscle in response to an increase in workload. When atrial enlargement occurs the P wave is altered with an increase in amplitude or width of the corresponding atrial component. Normal P wave Lead II pyramid shaped smooth apex amplitude not exceeding 2.5 mm duration not exceeding 0.12 secs RA COMPONENT LA COMPONENT RA COMPONENT LA COMPONENT Both RA and LA components are directed towards lead II positive waveforms.

24 Normal P wave Lead V1 The RA is situated anteriorly and to the right of the ventricles. The LA is situated more posteriorly, behind the ventricles. The RA force is directed towards lead V1 hence the 1 st (RA) component is upright in V1. The LA force is directed a little away from V1 and hence the 2 nd (LA) component is slightly negative. LA (2) (1) RA (1) (2) V1 As the two forces overlap the result is a P wave that is mainly upright with a slight negative terminal (Diphasic).

25 RIGHT ATRIAL HYPERTROPHY In RAH the RA component of the P wave is increased in voltage and duration. Since the RA component of the P wave is normally seen as a positive deflection in both II and V1 the P wave height is increased in both of these leads. NB: Since right atrial depolarisation is normally complete well before LA depolarisation the delay that occurs in conduction with RAH to the RA component is not enough to affect overall duration time of the P wave. Hence only amplitude of the P wave is affected in RAH, not duration.

26 II V1

27 ECG CRITERIA FOR RAH P wave amplitude is more than 2.5mm (some say 3mm) in leads II, III or AVF. [Occasionally the P wave vector is towards III and AVF (75º +) ] Associated Findings 1. positive part V1 greater than 1.5mm 2. usually RVH Clinical Significance 1. usually due to pulmonary disease leading to RVH and hence RAH, hence the term p pulmonale 2. any other disease that leads to RVH e.g. pulmonary stenosis 3. rarely RA infarction/ischaemia *p pulmonale peaked p waves *

28 LEFT ATRIAL HYPERTROPHY In LAH the la component of the p wave is increased in voltage and duration. Since the terminal part of the p wave is produced by left atrial depolarisation it follows that the total duration of the p wave is increased. Also since the La component increases in amplitude the p wave in lead II becomes bifid (notched) and in V1 the negative component becomes dominant.

29 II V1

30 ECG CRITERIA FOR LAH 1. m shaped p wave greater than 0.12 seconds in duration in leads II, III and avf 2. p wave in V1 shows a dominant negative component Associated findings 1. frequently LVH 2. with mitral stenosis only LAH can be found with RVH Clinical significance 1. any condition that gives rise to LVH, e.g. AS, AI, HOCM, hypertension 2. mitral stenosis 3. LA infarction/ischaemia, likely if ischaemic heart disease is present * p mitrale m shaped p waves *

31 BI-ATRIAL HYPERTROPHY To diagnose bi-atrial hypertrophy is not as difficult as with bi-ventricular hypertrophy. Each individual atria affects a different part of the p wave whereas hypertrophy of each ventricle affects the same part of the QRS. ECG CRITERIA Diagnosis can be made whenever the criteria for both right and left atrial hypertrophy are fulfilled. 1. p wave greater than 2.5 mm in height 2. p wave greater than 0.12 seconds in duration Limb leads 1. positive component greater than 2mm in height 2. negative component greater than 1 mm deep V1 Clinical significance Found in conditions which give rise to bi-ventricular hypertrophy. e.g. congenital heart disease HOCM pulmonary hypertension together with aortic valve disease or mitral incompetence. LJR..AE001.

32 VENTRICULAR HYPERTROPHY LEFT VENTRICULAR HYPERTROPHY The left ventricular myocardium will thicken as a reaction to hypertension, aortic stenosis and mitral regurgitation. These are conditions ventricle has to perform more work than usual. Results in an increase in muscle mass. ECG criteria Increased forces result in a longer intrinsic deflection time (or ventricular activation time). (1) V1 & V2 deep S waves greater than 30mm (2) V4, V5, V6, I & AVL tall R waves greater than 27mm (3) * Or sum of S wave V1 + R wave V6 should be greater then 37mm * (4) Left Axis Deviation (5) Ventricular activation time greater than 0.12secs Strain Pattern Leads facing the LV (V5 & V6) may show a strain pattern. This is a reflection of the abnormal state of the myocardium. ECG for strain (1) In leads facing the LV, usually in V5, V6, I & AVL (2) depressed, convex ST segment depression (3) inverted T waves

33 RIGHT VENTRICULAR HYPERTROPHY This usually occurs in cor pulmonale, and in some congenital heart defects when the RV becomes dominant. In RVH, the potential force of the RV is greatly increased. ECG criteria (1) R wave in leads over right ventricles V1, V2, V3. V4 (2) The S wave in V6 becomes more conspicuous (3) Right Axis Deviation moderate RVH R wave dominance V1, V2 severe RVH R wave dominance V1-V4 Strain Pattern (1) Seen in leads facing the right ventricle (V1, V2,V3) (2) Depressed convex ST segment (3) Inverted T wave

34 LEFT VENTRICULAR HYPERTROPHY RIGHT VENTRICULAR HYPERTROPHY

35 BI-VENTRICULAR HYPERTROPHY This is difficult to diagnose from the ECG since the phases of ventricular activation, occur together then the forces of activation may cancel each other out giving rise to a normal QRS amplitude. However, the duration may still be above 0.12 seconds. If either ventricle is more dominant then that ventricular hypertrophy will more evident on the ECG. ECG Criteria (1) It may exist without ECG changes (2) QRS duration may be to above 0.12 seconds. (3) T wave may be present in the precordial leads (4) ECG criteria met for LVH with an axis of +90 (RAD) is suggestive (not diagnostic) of biventricular hypertrophy (5) Occasionally RVH with LAD is seen Clinical Significance (1) Aortic valve disease + pulmonary hypertension (2) Cardiomyopathy (3) Occasionally congenital heart disease LJR/KAP..VH001.

36 CORONARY VASCULAR DISEASE The heart is a muscle whose function is to pump blood and Oxygen around the body, this muscle receives its own blood supply and Oxygen from vessels known as the CORONARY ARTERIES. Atheroma:- Is the build up of Plaque/Fat which cause narrowing in the CORONARY ARTERIES. Risk Factors:- Include Smoking, Hypercholesterolemia, Hypertension, Obesity, Diabetes and Family History. There are three main Stages of FIBRINOLYSIS NORMAL STAGE 1 STAGE 2 STAGE 3 STAGE 1 Moderate Atherosclerosis ANGINA STAGE 2 Severe Atherosclerosis CHRONIC ISCHAEMIA STAGE 3 Complete Occlusion MYOCARDIAL INFARCT

37 MYOCARDIAL INFARCTION Cross sectional analysis of an area of infarcted myocardium reveals the three electrically differentiated zones. E E = Electrode Infarcted Myocardium Injured Myocardium Ischaemic Myocardium

38 INFARCTED MYOCARDIUM - myocardium electrically dead. The electrode lying over the area of infarction has the effect of looking through the infarcted area as a window. This therefore will detect and record potentials from the myocardium directly opposite. INJURED MYOCARDIUM - myocardium is never completely polarized The electrode lying over the area of injury will record ST Segment elevation on the ECG because of the myocardium retaining its polarity. ISCHAEMIC MYOCARDIUM - myocardium exhibits impaired repolarisation The electrode lying over the area of ischaemia will record T wave changes on the ECG.

39 There are FOUR stages of myocardial infarction (MI) these are described as follows. STAGE 1 ACUTE STAGE HOURS OLD Acute stage of injury The myocardium is not yet dead and unless rapid intervention is possible then death of the affected area of muscle will certainly follow. In the case of rapid intervention then the area of death may be reduced although even with treatment some necrosis will take place. The typical shape of the ECG leads which are positioned directly over the injured area of myocardium will show significant ST segment elevation of greater than 2 mm, there may also be a reduction in the size of the R wave. There will be ST segment depression in the areas of myocardium opposite the injured area these are known as RECIPROCAL CHANGES.

40 STAGE 2 LATER PATTERN DAYS OLD In stage 2 the injured myocardium is now starting to necrose and this results in Q waves beginning to appear on the ECG which are representations of depolarization on the opposite wall of the heart, this is due to the window effect over the area of dead myocardium. Q - wave

41 Depolarisation of the ventricles demonstrates a Q wave appearance due to the activation of 1 and 2 travelling away from the electrode. The electrode is looking through the electrical window were no electrical activity occurs. The ST segment elevation will lessen as the area of injury either becomes Ischaemic or dies. T waves now begin to appear representing the area of ischaemia which is surrounding the infarcted muscle. STAGE 3 LATE PATTERN WEEKS OLD In stage three, the zone of injury has now evolved into infarcted myocardium. There is a pathological Q wave seen on the ECG due to the electrical window being present The ST segment has now returned to normal/iso-electric line because the injured area has now necrosed or become ischaemic. There is now a symmetrically inverted T wave present on the ECG which represents persistent ischaemia surrounding the area of infarct. Q wave

42 STAGE 4 OLD INFARCT MONTHS TO YEARS In stage 4 the zone of ischaemia has recovered and the ECG returns to almost normal. However there are changes which allow us to identify a previous infarct on the ECG. The pathological Q wave is considered the finger print for life of a previous myocardial infarction. The R wave height is reduced in the leads positioned directly over the area of infarct. Q wave NB in patients who have persistent ST elevation following an infarct this can be an ECG indication of a ventricular ANEURYSM.

43 SYMPTOMS OF MYOCARDIAL INFARCTION Chest pain usually occurs in 90% of patients, this is not relived by GTN. There may also be obvious signs of NAUSEA, SOB, and PERSPIRATION. Clinical Signs PALLOR, SWEATING, IRREGULAR PULSE, HYPOTENSION, RAISED JVP. ECG Changes Although the ECG changes occur relatively quickly in many patients there is a small percentage these changes may take anything up to 24hrs to occur. A small percentage of patients may have no E.C.G changes. Blood Tests Death to the myocardium causes a release of enzymes into the blood Stream, the main enzymes which are checked are CK, AST, LDH and Cardiac Troponin. The level of enzymes may give some indication as to the size of the Infarct. Prognosis 30% die within 3 hours of onset of pain. 18% mortality in Coronary Care Units. 80% of all cardiogenic shock patients die. 45% of deaths are due to primary arrhythmia s. (these are mostly out of hospital deaths)

44 CORONARY ARTERY ANATOMY LEFT CORONARY ARTERY Left Main Stem Left Anterior Descending Diagonal Intermediate Left Circumflex Marginals Septals

45 RIGHT CORONARY ARTERY Sino Atrial Branch Right lateral Marginal Intraventricular branch Posterior Descending Artery * In 90% of patients the PDA arises from the RCA indicating a right dominant system In the other 10% the PDA arises from the LCX.

46 CORONARY ARTERY BLOOD SUPPLY RIGHT The right coronary originates from just above the right coronary cusp of the aortic valve and supplies the following INFERIOR wall region of the left ventricle SA Node in 55% of patients AV Node in 90% of patients Bundle of His in 90% of patients The superior third of the Right Bundle Branch The postero inferior division of the Left Bundle Branch Vagus nerve fibres. Possible Complications Heart Blocks 1 st, 2 nd,3 rd Degree heart block Bradycardias Hypotension Other complications from MI are reduced LV function which may lead to cardiac failure and can increase the risk of tachyarrhythmias.

47 LEFT The left coronary artery originates from just above the left coronary cusp of the aortic valve and supplies the following. Anterior wall of the left ventricle (LAD) Posterior wall of the left ventricle (LCX) SA Node in 45% of patients (LCX) AV Node in 10% of patients (LCX) The inferior two thirds of the Right Bundle Branch The anterior superior division of the Left Bundle Branch A portion of the postero inferior division of the Left Bundle Branch Possible Complications Heart Failure Conduction defects RBBB Left Anterior Hemi-Block Left Posterior Hemi-Block 1 st, 2 nd, 3 rd Degree heart blocks Tachyarrhythmias

48 LOCATION OF INFARCTION Anterior - Posterior + - I, AVL, V LEADS + Inferior II, III, AVF Leads I, AVL and the V1 chest lead are orientated so they look at the anterior surface of the heart. Leads II, II and AVF are orientated so they look at the inferior surface of the heart. NB no leads are orientated towards the posterior surface of the heart.

49 INFERIOR INFARCT The inferior region of the heart is basically the inferior wall of the Left Ventricle. An inferior infarct is due to occlusion of the RCA, this will also causes damage to the Right Ventricle. ANTERIOR INFARCT An Anterior Infarct may cause damage to a larger area of myocardium dependent on were the occlusion takes place so an Extensive Anterior Infarct will be cause by Proximal occlusion of the LCA. ANTEROSEPTAL This is caused by an occlusion of the SEPTAL ARTERY of the LAD (proximal to the septal artery) ANTERO-LATERAL This is caused by an occlusion of the DIAGONAL BRANCHES of the LAD APICAL This is caused by an occlusion of the distal portion of the LAD An apical infarct may also occur due to occlusion of the RCA being an extension of an Inferior Infarct

50 ECG CHANGES INDICATING REGION OF INFARCT INFERIOR II, III and AVF RCA ANTERIOR I, and AVL LCA ANTERO-SEPTAL I, AVL, V1, V2, V3 ANTERO-LATERAL I, AVL, V4, V5, V6 EXTENSIVE ANTERIOR I, AVL, V1, V2, V3, V4, V5, V6 APICAL I, AVL, V3, V4

51 POSTERIOR WALL MYOCARDIAL INFARCTION The POSTERIOR wall of the heart involves the Poster-Basal aspect of the left ventricle. It is situated between the lateral (superior) and Inferior surfaces. The posterior region is fed its oxygen/blood supply via the Left Circumflex Artery. ANTERIOR POSTERIOR None of the conventional ECG leads are orientated towards the posterior surface of the heart therefore the diagnosis can only be made from the inverse or mirror image changes which occur in leads which are orientated to the UNINJURED anterior surface of the heart.

52 LEAD V1 Normal appearance Acute stage of Posterior Infarct ECG FEATURES 1) Tall and slightly widened R waves in right precordial leads (V1 V2) The Anterior forces are more dominant due to the lack of opposing posterior forces 2) Tall upright symmetrical T waves 3) Depression of the ST Segment which may look concave in leads (V1 V2) NB This could be ischaemia if points are not present

53 DIFFERENTIAL DIAGNOSIS OF TALL R WAVES V1 + V2 Right ventricular hypertrophy (check for Rightward axis and check T waves) Right Bundle Branch Block (check the T waves in RBBB they are usually Inverted) Type A WPW (check if there is a Delta wave)

54 ISCHAEMIA E J J+60 E POINT baseline between P and QRS J POINT compared to E point level of ST depression J equates to 60 ms, however other values can be chosen. measures the gradient /slope of the ST segment, from the J point.

55 NORMAL BORDERLINE (probably normal) Baseline Upsloping ABNORMAL ABNORMAL Flat Downsloping

56 THE MECHANISM OF ISCHAEMIC CHANGES Ischaemia is caused by transient subendocardial injury to the ventricular muscle mass. AVR V6 V5 In leads orientated towards the injured surface (i.e. AVR) the usual injury pattern of ST elevation is seen. In leads orientated away from the injured surface (i.e. V5,V6), ST depression is seen. In leads where ST depression is seen, the T wave will be inverted. An ischaemic T wave is symmetrical, taller and pointed. U WAVE

57 If after exercise an inverted U wave is seen, it is indicative of myocardial ischaemia. SUBENDOCARDIAL INFARCTION RV LV ECG evidence ; Primary ST segment depression T wave inversion Reciprocal ST segment elevation in the cavity lead Early Late CAVITY LEAD LEFT PRE CORDIAL LEAD The pattern simulates myocardial ischaemia. However the ischaemia will be transitory whereas the infarct will persist. If the PRIMARY change is ST segment depression it will be seen in all leads except AVR.

58 PRINZMETAL ANGINA Sub-epicardial injury, characterized by transient ST elevation in leads orientated towards the injury. Thought to be due to coronary artery spasm +/- coronary artery disease. ECG findings ST elevation in leads orientated towards the area of injury R wave amplitude is increased U wave inversion Frequently left anterior hemiblock Complications Ventricular Ectopics, Ventricular Tachycardia, Transient AV block. LJB