CHAPTER Practical Approach to a Patient with ECG Changes

17 Shirish MS Hiremath

The ECG is the oldest cardiologic test, but even 100 years Acute or evolving changes in the ST– T waveforms and after its inception, it continues as the most commonly Q waves, when present, potentially allow the clinician used cardiologic test. to time the event, to identify the infarct-related artery, to estimate the amount of myocardium at risk as well as Historical milestones in ECG1 prognosis, and to determine therapeutic strategy. Various 1887: Augustus Desire Waller, recorded electric current algorithms predict the IRA in case of STEMI, though this preceding cardiac contraction. correlation is not valid in NSTEMI. 1903: Einthoven, developed string galvanometer. Coronary artery size and distribution of arterial segments, collateral vessels, location, extent and severity 1911: Sir Thomas Lewis published his pioneering work of coronary stenosis, and prior myocardial necrosis can on ECG all impact ECG manifestations of myocardial ischaemia. 1929: Dock, use of cathode ray oscilloscope for ECG Electrocardiographic evidence of myocardial ischaemia 1932: Wolferth CC and Wood CC, introduced chest leads in the distribution of a left circumflex artery is often overlooked and is best captured using posterior leads at 1942: Goldberger E, Introduced unipolar limb leads. the fifth intercostal space (V7 at the left posterior axillary ECG in emergency room: Despite the advent of expensive line, V8 at the left mid-scapular line, and V9 at the left and sophisticated alternatives, ECG dictates the timely paraspinal border). A cut-point of 0.05 mV ST elevation is diagnosis and management in recommended in leads V7–V9; specificity is increased at a (ACS) and . cut-point ≥0.1 mV ST elevation and this cutpoint should be used in men, 40 years old. ST depression in leads V1–V3 In a suspected case of ACS, ECG should be acquired and may be suggestive of infero-basal myocardial ischaemia interpreted promptly (i.e. target within 10 min) after (posterior infarction), especially when the terminal T clinical presentation, and initial ECG is non-diagnostic wave is positive (ST elevation equivalent), however this is then serial ECG should be acquired (15-20 minute interval) non-specific. In patients with inferior and suspected right 3 to catch the dynamic changes. ventricular infarction, right pre-cordial leads V3R and V4R should be recorded, since ST elevation ≥0.05 mV (≥0.1 R mV in men , 30 years old) provides supportive criteria for the diagnosis (ref Fig---). Other ECG signs associated with acute myocardial ischaemia include cardiac arrhythmias, intraventricular and atrioventricular conduction delays, Isoelectric line: horizontal PR ST segment level between cardiac cycles and loss of precordial R wave amplitude. Coronary artery size and distribution of arterial segments, collateral J vessels, location, extent and severity of coronary stenosis, P P QRS V= Vulnerable Table 1: ECG manifestations of acute myocardial ischaemia (in 1 period 2 absence of LVH and LBBB)4 ST elevation ST depression and T Phase 0 3 wave changes Phase 4 New ST elevation at the J New horizontal or down- QT point in two contiguous sloping ST depression leads with the cut-points: ≥0.05 mV in two Cell cytoplasm ≥0.1 mV in all leads other contiguous leads and/orT K+ K+ K+ Na+ K+ K+K+ Na+ than leads V2–V3 where inversion ≥0.1 mV in two – – – + + + + – – – – – the following cutpoints contiguous leads with + + + – – – – + + + + Cell membrane Na+ K+ apply: ≥0.2mVinmen≥4 prominent R wave or R/S Na+ Na+ K+ Na+ influx Efflux 0years;≥0.25mVinmen ratio >1. <40 years,or ≥0.15 mV in Fig. 1: The action potential, and the electrocardiogram2 women. CHAPTER 17 85

11 ≤1 mm) OCCLUSION CX or DISTAL OCCLUSION RCA DISTAL PROXIMAL OCCLUSION RCA Specificity 73% Sensitivity 66% descending artery Distal left anterior Positive predictive value 78% value predictive Positive Negative predictive value 62% value predictive Negative ST-segment depression ( ST-segment 5 ST-segment elevation in II, III, and aVF in II, III, ST-segment elevation 3 and V and 2 , V 1 Fig. 4: Value of ST-T changes in acute infero-posterior MI of ST-T Value 4: Fig. ST ä ≥ 1 mm POS T – WAVE NO ST ä : POS T – WAVE NEG T – WAVE poorly because of a low sensitivity of 10%, although the was high at 82%. specificity limit of normal value Using a criterion of twice the upper confirmation for standard’ ‘gold the as troponin serum for in the Wong et al. of myocardial injury, the investigators study demonstrate a high specificity for the criteria. study demonstrate a high specificity closely resembles acute coronary Acute very the ECG changes. and symptoms of in terms syndrome The two classical ECG are ST elevation findings(most sensitive and ofconsistent) and PR acutedepression (most specific). pericarditis Characteristic ST-elevation of and it is present in upwards is concave the majority of the standard ECG leads, except in leads depressed. always segment is V1 where the ST and AVR is often transient and are sometimes This ST-elevation followed (after a inversions. variable time) by diffuseforemost of palpitation is ECG at the time of Event T-wave importance in diagnosis and management of . of arrhythmia, traditional step-wise For evaluation i.e. rate, should be followed of event-ECG assessment cycle-length, QRS morphology, rhythm, axis, relationship. ECG during morphology, p-QRS p-wave in diagnosis has equal importance period asymptomatic i.e. p/QRS-morphology, QRS duration (QRSd), QT- 6 Specificity 98% Sensitivity 34% When descending artery in II, III, and aVF 8,9 Proximal left anterior Positive predictive value 93% value predictive Positive Negative predictive value 68% value predictive Negative ST-segment depression (>1 mm) ST-segment depression No ST-segment elevation in V elevation ST-segment LCX or Distal RCA Mid RCA, Fig. 2: Algorithm for identifying IRA in anterior wall MI wall identifying IRA in anterior 2: Algorithm for Fig. No No RV involvement No RV But this criteria performed this But 10 (>2.5 mm) LCx vs RCA 1 Inferior Wall AMI Inferior Wall No ST elevation V4R ST elevation (ST elevation II, III, aVF) II, (ST elevation Yes ST segment elevation III > II ST segment elevation or Yes ST segment elevation VI elevation RV involvement RV Proximal RCA with Sensitivity 12% Q wave or both or Q wave Specificity 100% descending artery Proximal left anterior RV Infarction RV Yes Proximal RCA and Positive predictive value 100% value predictive Positive Negative predictive value 61% value predictive Negative Fig. 3: Algorithm for identifying IRA in inferior wall MI wall identifying IRA in inferior 3: Algorithm for Fig. right bundle-branch block with right bundle-branch ST-segment elevation in V elevation ST-segment the patient has LBBB on arrival and no preexisting ECG the patient has LBBB on arrival is available for comparison, then there are specific ECG patients with distinguish between criteria which could new injury or infarction and those without. Sgarbossa et al. proposed specific electrocardiographic criteria for the diagnosis of AMI in the presence trial. patients in GUTO-I to of LBBB applied and prior myocardial necrosis can all impact ECG manifestations of myocardial ischaemia. and recent on admission When the patient has LBBB previous ECGs do not show LBBB, the patient is presumed which many investigators new-onset LBBB, to have of the equivalent as accept current guidelines and AMI. of supportive findings electrocardiographic 86 Table 2: Differential diagnosis of ST-elevation7 1. / Noninfarction, transmural ischemia (Prinzmetal’s , and probably Tako-Tsubo syndrome, which may also exactly simulate classical acute infarction) Acute myocardial infarction Postmyocardial infarction (ventricular aneurysm pattern) 2. Acute pericarditis 3. Normal variants (including “early repolarization” patterns) 4. Left /left bundle branch

CARDIOLOGY block 5. Other (rarer) Acute pulmonary embolism Fig. 5: An electrocardiogram in acute pericarditis. Brugada patterns (right –like Narrow QRS tachycardia pattern with ST elevations in right precordial (QRS duration less than 120 ms) leads)

Class 1C antiarrhythmic drugs Regular tachycardia? DC cardioversion Yes No Hypercalcemia Visible P waves? Atrial fibrillation Hyperkalemia /flutter with No Yes variable AV conduction Hypothermia [J (Osborn) waves MAT 6. Nonischemic myocardial injury Atrial rate greater than ventricular rate? Tumor invading left Yes No Atrial flutter or Analyze RP Trauma to ventricles atrial interval tachycardia Table 3: Sgarbossa criteria for diagnosis of AMI in LBBB (score 10 ≥3 have high specificity) Short Long (RP shorter than PR) (RP longer than PR) ECG criteria Score 1. ST-segment elevation ≥1 mm and 5 concordant RP shorter than 70 ms RP longer than 70 ms Atrial tachycardia PJRT with QRS complex Atypical AVNRT 2. ST-segment depression ≥1 mm in lead V 1 3 AVNRT AVRT AVNRT V 2 V 3 Atrial Tachycardia

3. ST-segment elevation ≥5 mm and 2 12 discordant with QRS complex Fig. 6: Algorithm for diagnosis of a narrow QRS tachycardia can be done with intravenous beta-blocker, calcium interval, presence of pre-excitation, presence of channel blocker or adenosine. Long-term management pathological q-wave. largely depends on number of recurrences and underlying First step in assessment of tachycardia is QRSd, less structural heart disease. For tachycardia involving AV- than 120msec is defined as narrow-complex tachycardia junction (AVRT/AVNRT) electrophysiological study with (NCT) and ≥120msec is defined as broad complex radiofrequency ablation is highly effective, with more tachycardia (BCT). With few exceptions NCT is almost than 95% curing rate in long-term and very low risk of always supraventricular in origin therefore less likely to recurrence. be life-threatening. With few exceptions BCT is almost For atrial (Afib, Aflutter and ATach), rate always ventricular in origin therefore more likely to be control versus rhythm control strategy depends on age of life-threatening. the patient and underlying structural heart disease. Initial step in assessment of NCT is regularity of R-R (VT) arises distal to the bifurcation interval, as AV-junctional tachycardias are always regular. of the His bundle in the specialized conduction system, In management of NCT, rate control in emergency room CHAPTER 17 87 VT 1 6 longer than 30 ms 1 R to nadir of S in V Irregular 12 LBBB pattern R in V • • greater than 60 ms qR or qS in V • VT 1 Atrial fibrillation Atrial variable with flutter/AT Atrial conduction and a) BBB or AP via b) antegrade conduction in V 1 After acute management of sustained VT, the goal of After acute management of sustained VT, sudden cardiac death and long-term therapy is to prevent with structural Patients recurrence of symptomatic VT. systolic dysfunction (ejection heart disease especially LV fraction ≤35%) are at highest risk of recurrence of VT and subsequent SCD. Idiopathic VT is defined as monomorphic VT in patients or coronary disease. without any structural heart disease are three distinct entities with characteristic There ECG pattern, based on the location of the VT—outflow tract tachycardia, annular tachycardia, and fascicular favourable very have tachycardia. These type of VTs † than V rate A rate faster Frontal plane axis Atrial flutter Atrial • range from +90 degrees to –90 degrees RBBB pattern qR, Rs or Rr • Atrial tachycardia Atrial Regular or irregular? Regular or VT No heart disease? Wide QRS-complex tachycardia QRS-complex Wide If yes, VT is likely If yes, (QRS duration greater than 120 ms) than 120 greater duration (QRS Previous myocardial infarction or structural Is QRS identical to Is QRS identical to that during SR? consider: If yes, SVT and BBB • • Antidromic AVRT VT Fig. 7: Algorithm for diagnosis of a wide QRS tachycardia 7: Algorithm for Fig. than A rate V rate faster Regular 1 to 1 AV 1 to 1 Precordial leads • Concordant* No R/S pattern • Onset of R to nadir • longer than 100 ms relationship? 13 SVT Vagal maneuvers or adenosine Yes or Yes unknown QRS morphology in precordial leads Typical RBBB or LBBB ventricular muscle, or combinations of both tissue types. ventricular Mechanisms include disorders (enhanced of impulse automaticity formation conduction or (reentry). triggered In of VT is good, but prognosis structural heart disease, patient activity) without and high risk of sudden there is with underlying heart disease underlying aberrant with SVT from VT Differentiating death. cardiac conduction is very important, though may be difficult at times. VT of early diagnosis for algorithms are available Various algorithm is the in emergency room. Of these, Brugada’s most commonly used. 88 Table 4: Brugada Algorithm: Steps13 SUDDEN CARDIAC DEATH - INCIDENCE AND TOTAL EVENTS Incidence Population segment Events ECG criteria Cumulative Cumulative Sensitivity for Specificity for General population VT VT High-risk subgroup 1. Absence of an 21% 100% RS complex in Prior coronary event all precordial EF < 30%; heart failure MADIT II SCD-HeFT

leads survivor AVID, CIDS, CASH Arrhythmia risk markers, 2. Precordial RS 66% 98% MADIT I, MUSTT interval >100 post-myocardial infarction ms 0 10 20 30 0 150,000 300,000 3. VA dissociation 82% 98% PERCENT ABSOLUTE NUMBER 4. Morphological 99% 97% Fig. 9: Impact of population subgroups and time from events on criteria for VT the clinical epidemiology of Sudden cardiac death (SCD)14 CARDIOLOGY

RBBB configuration LBBB configuration Advanced heart disease QRS width > 140 ms, left axis QRS width > 160 ms, right axis [1 per 4-10]

QR, R, RSr’ complex in V1 (A) Initial R in V1 > 30 ms 10-25%/year (B) Slurring or notching of B the downstroke of the S– Usual causes: A • Myocarditis wave in V1–2 • Hypertrophic CM (C) Begin QRS-nadir S– • Long-QT syndromes [Multiple risk factors] qR in V1 R in V1 Rabbit ear in V1 wave > 70 ms in V1–2 C • Right ventricular dysplasia General population[1 per > 35500-1,000] years of age

0.1%/year • Anomalous coronary artery RS < 1 in V6 QS in V6 Any Q V6 • brugada syndrome Individual high-riskIndividual subgroup low-risk subgroup

INCREASING RISK • Idiopathic VF [0-1 risk factor]

Usual causes: Any Q in V6 • Coronary atherosclerosis Adolescents/young adults • Dilated • Infiltrative heart diseases 13 [1 per 100,00] • Fig. 8: Brugada’s morphological criteria 0.001%/year prognosis and RF catheter ablation effectively eliminates AGE (years) 20 30 40 50 60 tachycardia in symptomatic patients. Fig. 10: Age-related and disease-specific risk for SCD Right ventricular outflow tract (RVOT) VTs have a on the basis of the level of disturbance in the hierarchy characteristic electrocardiographic appearance of a left of the normal impulse generation and conduction system bundle branch block contour in V1 and an inferior axis (from sinus node to AV node to His-Purkinje system). in the frontal plane. It responds best to vagal maneuvers, beta-blocker. Most probable mechanism is cyclic Sinus is defined as sinus rhythm at a rate adenosine monophosphate–triggered activity resulting slower than 60 beats/min. P waves have a normal contour from early or delayed afterdepolarizations. ECG of LV and occur before each QRS complex, usually with a outflow tract VT mimics RVOT-VT with presence of an S constant PR interval longer than 120 milliseconds. Sinus wave in lead I and an early precordial R wave transition arrhythmia often coexists. (V1-V2). Sick sinus syndrome is a term applied to a syndrome For mitral annular VT, the ECG pattern is typically right encompassing a number of sinus nodal abnormalities, like bundle branch block pattern (transition in1 V or V2), S persistent spontaneous inappropriate wave in V6, and monophasic R or Rs in leads V2 through for the physiologic circumstance; sinus arrest or V6. For tricuspid annular VT, the foci generally originate exit block; combinations of SA and AV conduction in the septal region, and thus the typical ECG pattern is disturbances; alternation of paroxysms of rapid regular left bundle branches block pattern (Qs in lead V1), an or irregular atrial tachyarrhythmias and periods of slow early transition in precordial leads (V3), and narrower atrial and ventricular rates (bradycardia-tachycardia QRS complexes. syndrome). Sick sinus syndrome can occur in the absence of other cardiac abnormalities. The course of the disease Left fasicular VT is characterized by a right bundle branch is frequently intermittent and unpredictable because it is block contour, those originating from posterior fascicle influenced by the severity of the underlying heart disease. have right-ward axis and those originating from anterior fascicle have left-ward axis. Re-entry is the probable An AV block exists when the atrial impulse is conducted mechanism, so they very well respond to calcium channel with delay or is not conducted at all to the ventricle blockers (verapamil/diltiazem) and highly amenable to when the AV junction is not physiologically refractory. radiofrequency ablation. The conduction disturbance is classified by severity into three categories. Most common cause is age-related Bradyarrhythmias are arbitrarily defined as a heart rate degenerative AVB followed by congenital, post-operative. below 60 beats/min. Bradyarrhythmias can be categorized CHAPTER 17 89 Camel-hump sign Roller-coaster sign sign-wave appearance sign-wave Low T wave, high U wave, low ST segment Ventricular fibrillation Ventricular standstill, Auricular block intraventricular PR interval, Prolonged depressed ST segment, high T wave High T wave Normal Low T wave Low T wave, high U wave This has been accepted by 6 U T P QRS Fig. 13: ECG changes in hyperkalemia 13: ECG Fig. 9 8 7 10 3 3.5 2.5 8 4D5 Serum

(mEq/L)

Purkinje system. Type II AV block, particularly in block, AV Purkinje system. Type II localized is block, branch bundle a with association to the His-Purkinje system. Third degree (complete atrial activity when no block occurs AV AVB): complete Third-degree or and therefore the is conducted to the ventricles are controlled by independent atria and ventricles dissociation. AV complete there is thus pacemakers, complete heart rate in acquired The ventricular congenital in faster be can but beats/min 40 < is block block can result AV block. Complete AV complete node (usually AV of the from block at the level congenital), within the bundle of His, or distal to it in the Purkinje system (usually acquired). potassium

Hyperkalemia Normal Hypokalemia Electrolyte disturbances in ICU: Potassium and calcium 3. ECG in intensive care medical or surgical ICU continuous ECG monitoring unit: For patients admitted essential for early recognition of myocardial is very in ischaemia, electrolyte disturbances, and dysarrhythmias. Myocardial ischaemia: applied standard criteria suggested by Ellestad commonly For and ischaemia colleague includes monitoring, depression of horizontal more than 1 or mm at 60 down point (‘J’ msec point is from where QRS complex the sloping changes its ‘J’ slope) lasting for at least 60 seconds. American college of cardiology. On ECG monitor, single best lead, for detection of ischaemia is V5. V4, II, V3 and V6 are in myocardial decreasing order of sensitivity. Chances of ischaemia detection among combined leads is; V5 & II in 80%, V4 & V5 in 90%, V4 , V5 & II in 96% and II & V2 -V5 in 100% of cases. ST Point J Point Electrolyte imbalance ST Segment inward outward 3 + K 2 2+ Ca + Automated ST segment monitoring: reference points ST segment Automated K + 1 First degree: During first-degreeAV block, every and a ventricles to the atrial impulse conducts but the PR rate is produced, regular ventricular exceeds interval 0.20 second in adults, mostly with PR interval no QRS aberration. Clinically important delay prolongation can result from a conduction in node the AV (A-H interval), in the His-Purkinje sites. or at both system (H-V interval), Second-degree: Blocking of some atrial impulses physiologic at a time when to the ventricle conducted constitutes second- interference is not involved typical block. Electrocardiographically, AV degree type I second-degree AV block PR prolongation culminating in a by progressive is characterized second- type II in whereas , wave P nonconducted constant remains block, the PR interval AV degree AV the In both cases, before the blocked P wave. block is intermittent and generally Type repetitive. of often antedates the development block AV II block, AV syncope and complete Adams-Stokes QRS normal block with a AV type I whereas not does benign and generally more is complex conduction AV forms of progress to more advanced block with a normal QRS AV disturbance. Type I of at the level place takes almost always complex AV I bundle. Type to the His proximal node, AV the block in a patient with a bundle branch block can or in the His- node AV by a block in the be caused Na 0 PR Point Isoelectric point 4 + Fig. 11: Automated ST-segment monitoring; reference points reference monitoring; ST-segment 11: Automated Fig. Fig. 12: A ventricular action of the 12: A ventricular with a schematic potential Fig. K ionic currents flowing during the phases of the action during ionic currents flowing potential 2. Depending on severity and level of block, there 3 types and level Depending on severity of AVB. 1. 90 are essential for maintenance of transmembrane potential 6. Gorgels AP, Engelen DJ, Wellens HJ. The electro cardiogram and propagation of action potential, so changes in these in acute myocardial infarction. In: Hurst’s the Heart. 11th electrolytes are reflected in resting ECG. But ECG changes edition, Fuster V, Alexander RW, O’Rourke RA (Eds.), don’t always correlate with serum level. McGraw-Hill: New York 2004:p.1351-60. 7. Braunwald E, Bonowro, Mann DL, Zipes DP Et Al, Editors. ECG changes in hypokalemia are due to delayed Braunwald’s Heart Disease: A Textbook of Cardiovascular repolarisation so the changes are seen in ST-segment, Medicine. 9th Ed. Saunders, An Imprint Of Elsevier 2012 T-wave and U-wave. These are most marked when serum 8. Edhouse JA, Sakr M, Angus J, et al. Suspected + K is < 2.7 mmol/L. myocardial infarction and left bundle branch block: Hyperkalemia is a medical emergency because it electrocardiographic indication of acute ischemia. J Accid leads to cardiac arrhythmias, increase in plasma K+ Emerg Med 1999; 16:331–5. concentration depresses intracardiac conduction, with 9. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA progressive prolongation of the PR and QRS intervals. guidelines for the management of patients with ST- Severe hyperkalemia results in loss of the P wave and a elevation myocardial infarction—executive summary: a report of the ACC/AHA Task Force on Practice Guidelines progressive widening of the QRS complex. (Writing Committee to Revise the 1999 Guidelines for the

CARDIOLOGY Extracellular calcium is important for transmembrane Management of Patients with Acute Myocardial Infarction). action potential so changes in serum ionised calcium level Circulation 2004; 110:588–636. affects conduction time leading to changes in QT interval 10. Sgarbossa EB, Pinski SL, Barbagelata A, et al., for the (no changes in QRS-T duration). Hypercalcemia causes GUSTO-1 Investigators. Electrocardiographic diagnosis of shortening and in severe cases absence of ST-segment, evolving acute myocardial infarction in the presence of left conversely in hypocalcemia there is prolong ST-segment. bundle-branch block. N Engl J Med 1996; 334:481–7. 11. Wong C-K, French JK, Aylward PEG, et al. Patients with Marked QT prolongation, sometimes with deep, prolonged ischemic chest pain and presumed-new left wide T-wave inversions, may occur with intracranial bundle branch block have heterogeneous outcomes bleeds, particularly subarachnoid haemorrhage (“CVA depending on the presence of ST-segment changes. J Am T-wave” pattern). Systemic hypothermia also prolongs Coll Cardiol 2005; 46:29–38. repolarization, usually with a distinctive convex 12. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al: elevation of the J point (Osborn wave). Similar J-point ACC/AHA/ESC guidelines for the management of patients elevation is also seen in severe Hypercalcemia, called as with supraventricular arrhythmias—executive summary: nonhypothermic Osborn wave. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and REFERENCES the European Society of Cardiology Committee for Practice 1. R S Atkinson, G B Rushman, J Alfred Lee. Notes on Guidelines [Writing Committee to Develop Guidelines Physiology. A Synopsis of Anaesthesia. Bombay: K M for the Management of Patients With Supraventricular Varghese Company, 1987; 51–52. Arrhythmias]. Circulation 2003; 108:1871. 2. Khan, M. Gabriel: On Call Cardiology, 3rd ed., Philadelphia, 13. P Brugada, J Brugada, L Mont, J Smeets and E W Andries, 2006, WB Saunders, Elsevier Science A new approach to the differential diagnosis of a regular 3. Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/ tachycardia with a wide QRS complex. Circulation 1991; AHA/WHF Task Force for the Redefinition of Myocardial 83:1649-1659. Infarction. Universal definition of myocardial infarction. 14. Myerburg RJ, Kessler KM, Castellanos A: Sudden cardiac Eur Heart J 2007; 28:2525–2538. death: Structure, function, and time-dependence of risk. 4. ThygesenK, AlpertJS, JaffeAS. Third universal definition Circulation 1992; 85[Suppl I]:I2. of myocardial infarction. European Heart Journal 2012; 15. Ellestad M H, Crooke DM Jr, Greenberg P S. Stress testing: 33:2551–2567. principles and practice. Philadelphia: F A Davis, 1980; 85. 5. Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis 16. London MJ, Hollenberg M, Wong MG et al. Intraoperative AJ, Dassen WR, et al. Value of the electrocardiogram in myocardial ischaemia: localization by continuous 12 lead localizing the occlusion site in the left anterior descending electrocardiography. Anesthesiology 1998; 9:232-241. coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999; 34:389-95.