Electrocardiography in myocardial infarction

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Electrocardiography in myocardial infarction
12 Lead EKG ST Elevation tracing color coded.jpg
12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative of an anterior wall myocardial infarction.
PurposeDetecting ischemia or MI

Electrocardiography in suspected myocardial infarction has the main purpose of detecting ischemia in emergency department populations coming for symptoms of myocardial infarction (MI). Also, it can distinguish different types of myocardial infarction.

Main patterns

An acute STEMI involving the inferior and right ventricle. Reciprocal changes are seen in the anterior leads.

The 12 lead ECG is used to classify people into one of three groups:[1]

  1. those with ST segment elevation or STEMI equivalents (suspicious for acute injury and a possible candidate for acute reperfusion therapy,
  2. those with ST segment depression or T wave inversion (suspicious for ischemia),
  3. those with a non-diagnostic or normal ECG. However, a normal ECG does not rule out acute myocardial infarction.

Changes in the ST segment may be measured with respect to the TP segment or the start of the QRS.[2]

OMI

Occlusion myocardial infarction (OMI) includes STEMI and STEMI equivalents.[3]

The 2018 definition of ST segment elevation acute myocardial infarction require new ST elevation at the J point of at least 1 mm (0.1 mV) in two adjacent leads other than leads V2-V3.[2] For leads V2-V3: ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, or ≥1.5 mm in women regardless of age. This assumes usual calibration of 1mV/10mm.[4] Anatomically contiguous leads are I, aVL, V5, V6 correspond to the lateral wall; V3-V4 correspond to the anterior wall; V1-V2 correspond to the septal wall; II, III, aVF correspond to the inferior wall.[1]

STEMI equivalents include De Winter syndrome (ST depression in V1 to V6 with tall T waves); ST depression in V1 to V4 representing a posterior MI; Wellens syndrome which when pain free involves biphasic or inverted T waves in V2 and V3 with no Q waves; hyperacute T waves; Sgarbossa criteria, and a "shark fin" ECG pattern.[5][2]

A posterior OMI may present with ST depression in leads V1 to V3 of ≥0.5 mm.[6] If an ECG is done which has leads V7 to V9 ≥0.5 mm of ST elevation may be present.[6]

NOMI

Non-occlusion myocardial infarction (NOMI) presents with ECG patterns other than STEMI and STEMI equivalents.[3][7] This may include ST depression in V4 to V6 and II for example.[7] This ST depression should be ≥0.5 mm in adjacent leads.[2] New T inversion in adjacent leads with large R waves may be another pattern.[2]

Progression

The earliest presentation of acute myocardial infarction may be hyperacute T waves, which is treated the same as ST segment elevation.[2][8] In practice this is rarely seen, because it only exists for 2–30 minutes after the onset of infarction.[9] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.[10]

In the first few hours the ST segments usually begin to rise.[11] Pathological Q waves may appear within hours or may take greater than 24 hr.[11] The T wave will generally become inverted in the first 24 hours, as the ST elevation begins to resolve.[11]

Long term changes of ECG include persistent Q waves (in 90% of cases) and persistent inverted T waves.[11] Persistent ST elevation is rare except in the presence of a ventricular aneurysm.[11]

Differential diagnosis

However, acute myocardial infarction is not the most common cause of ST elevation.[12] Over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.[13]

Other causes of ST elevation include left ventricular hypertrophy, WPW, after cardioversion, high potassium, early repolarization, pericarditis, Brugada, hypothermia, ventricular aneurysm, Takotsubo cardiomyopathy, high calcium, pulmonary embolism, LBBB, paced rhythm, TCA toxicity, and intracranial injury.[13][14][15]

Pericarditis

A STEMI can be differentiated from pericarditis by STEMI having ST elevation together with ST depression in leads other than aVR and V1; a flat or concave down ST segment; ST elevation greater in III than II; or new Q waves.[16] PR depression can occur in either, but if all of the above are negative it supports pericarditis, as does downward slopping of the TP segment.

Other ECG changes that support STEMI include the R-T sign were the R wave goes immediately into a steep upward T.

Decision tools

There are decision tools such as the TIMI score which help prognose and diagnose MI.[17] Based on symptoms and electrocardiographic findings, practitioners can differentiate between unstable angina, NSTEMI and STEMI, normally in the emergency room setting.[18] Other calculators such as the GRACE[19] and HEART score, assess other major cardiac events using electrocardiogram findings, both predicting mortality rates for 6 months and 6 weeks, respectively.[20]

Technical issues

The standard 12 lead electrocardiogram (ECG) has several limitations. It represents a brief sample in time. Because unstable ischemic syndromes have changing supply versus demand characteristics, a single ECG does not represent the entire picture.[21] It may be desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, some use computers capable of continuous ST segment monitoring.[22] The standard 12 lead ECG also does not directly examine the right ventricle, and is relatively poor at examining the posterior basal and lateral walls of the left ventricle. Acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG.[21] The use of additional leads like right-sided leads V3R and V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of limitations, the 12 lead ECG stands at the center of risk stratification of people with suspected acute myocardial infarction. Mistakes in interpretation are common, and the failure to identify high risk features has a negative effect on the quality of care.[23]

References

  1. 1.0 1.1 Ecc Committee, Subcommittees Task Forces of the American Heart Association (2005). "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care — Part 8: Stabilization of the Patient With .......Acute Coronary Syndromes". Circulation. 112 (24_suppl): IV–89–IV–110. doi:10.1161/CIRCULATIONAHA.105.166561. PMID 16314375. Archived from the original on 2010-06-28. Retrieved 2023-11-20.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Kreider, Daniel L. (November 2022). "The Ischemic Electrocardiogram". Emergency Medicine Clinics of North America. 40 (4): 663–678. doi:10.1016/j.emc.2022.06.006. PMID 36396214.
  3. 3.0 3.1 Buttner, Robert; Cadogan, Mike; Cadogan, Robert Buttner and Mike (2 January 2021). "OMI: Replacing the STEMI misnomer". Life in the Fast Lane • LITFL. Archived from the original on 30 December 2023. Retrieved 21 January 2024.
  4. Thygesen, Kristian; Alpert, Joseph S.; Jaffe, Allan S.; Chaitman, Bernard R.; Bax, Jeroen J.; Morrow, David A.; White, Harvey D. (October 2018). "Fourth Universal Definition of Myocardial Infarction (2018)". Journal of the American College of Cardiology. 72 (18): 2252. doi:10.1016/j.jacc.2018.08.1038. PMID 30153967. Archived from the original on 2020-09-29. Retrieved 2023-11-20.
  5. Asatryan, B; Vaisnora, L; Manavifar, N (December 2019). "Electrocardiographic Diagnosis of Life-Threatening STEMI Equivalents: When Every Minute Counts". JACC. Case reports. 1 (4): 666–668. doi:10.1016/j.jaccas.2019.10.030. PMID 34316902.
  6. 6.0 6.1 Bracey, Alexander; Meyers, Harvey P. (2023). "Posterior Myocardial Ischemia". StatPearls. StatPearls Publishing. Archived from the original on 24 January 2024. Retrieved 21 January 2024.
  7. 7.0 7.1 "Type-1 Myocardial Infarction". EMCrit Project. Archived from the original on 15 November 2023. Retrieved 22 January 2024.
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  9. Smith SW, Whitwam W (February 2006). "Acute coronary syndromes". Emerg. Med. Clin. North Am. 24 (1): 53–89, vi. doi:10.1016/j.emc.2005.08.008. PMID 16308113.
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  11. 11.0 11.1 11.2 11.3 11.4 gpnotebook.co.uk > ECG changes in myocardial infarction Archived 2005-09-11 at the Wayback Machine Retrieved on June 16, 2010
  12. Brady WJ, Perron AD, Martin ML, Beagle C, Aufderheide TP (January 2001). "Cause of ST segment abnormality in ED chest pain patients". Am J Emerg Med. 19 (1): 25–8. doi:10.1053/ajem.2001.18029. PMID 11146012.
  13. 13.0 13.1 Wang K, Asinger RW, Marriott HJ (November 2003). "ST-segment elevation in conditions other than acute myocardial infarction". N. Engl. J. Med. 349 (22): 2128–35. doi:10.1056/NEJMra022580. PMID 14645641.
  14. Brady WJ, Chan TC, Pollack M (January 2000). "Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy". J Emerg Med. 18 (1): 71–8. doi:10.1016/S0736-4679(99)00178-X. PMID 10645842.
  15. Brady WJ, Perron AD, Chan T (April 2001). "Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians". Acad Emerg Med. 8 (4): 349–60. doi:10.1111/j.1553-2712.2001.tb02113.x. PMID 11282670.
  16. Smith, Clay (22 May 2020). "Differentiating STEMI from Pericarditis". JournalFeed. Archived from the original on 2 June 2023. Retrieved 29 December 2023.
  17. David A. Morrow; Elliott M. Antman; Andrew Charlesworth; Richard Cairns; Sabina A. Murphy; James A. de Lemos; Robert P. Giugliano; Carolyn H. McCabe; Eugene Braunwald (2000). "TIMI Risk Score for ST-Elevation Myocardial Infarction: A Convenient, Bedside, Clinical Score for Risk Assessment at Presentation: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy". Circulation. 102 (17): 2031–7. doi:10.1161/01.cir.102.17.2031. PMID 11044416.
  18. David A. Morrow; Elliott M. Antman; Andrew Charlesworth; Richard Cairns; Sabina A. Murphy; James A. de Lemos; Robert P. Giugliano; Carolyn H. McCabe; Eugene Braunwald (2000). "The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI: A Method for Prognostication and Therapeutic Decision Making". JAMA. 284 (7): 835–42. doi:10.1001/jama.284.7.835. PMID 10938172.
  19. Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum A, Goodman SG, Flather MD, Anderson FA Jr, Granger CB (2006). "Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE)". BMJ. 333 (7578): 2153–8. doi:10.1136/bmj.38985.646481.55. PMC 1661748. PMID 17032691.
  20. Backus BE, Six AJ, Kelder JC, Bosschaert MA, Mast EG, Mosterd A, Veldkamp RF, Wardeh AJ, Tio R, Braam R, Monnink SH, van Tooren R, Mast TP, van den Akker F, Cramer MJ, Poldervaart JM, Hoes AW, Doevendans PA (2013). "A prospective validation of the HEART score for chest pain patients at the emergency department". Circulation. 168 (3): 2153–8. doi:10.1016/j.ijcard.2013.01.255. PMID 23465250.
  21. 21.0 21.1 Cannon CP at al. Management of Acute Coronary Syndromes. p. 175. New Jersey: Humana Press, 1999. ISBN 0-89603-552-2.
  22. Selker HP, Zalenski RJ, Antman EM, et al. (January 1997). "An evaluation of technologies for identifying acute cardiac ischemia in the emergency department: executive summary of a National Heart Attack Alert Program Working Group Report". Ann Emerg Med. 29 (1): 1–12. doi:10.1016/S0196-0644(97)70297-X. PMID 8998085.
  23. Masoudi FA, Magid DJ, Vinson DR, et al. (October 2006). "Implications of the failure to identify high-risk electrocardiogram findings for the quality of care of patients with acute myocardial infarction: results of the Emergency Department Quality in Myocardial Infarction (EDQMI) study". Circulation. 114 (15): 1565–71. doi:10.1161/CIRCULATIONAHA.106.623652. PMID 17015790.

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