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ST-Segment Elevation

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Insights into Electrocardiograms with MCQs

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Abstract

During the early phase of acute myocardial infarction, ECG may not show classical elevation of the ST-segment. All ST-segment elevations are not due to myocardial infarction. Several other conditions can cause ST-segment elevation. Differentiating electrocardiographic features are discussed with representative electrocardiograms. In the context of myocardial infarction, electrocardiographic leads showing ST-segment elevation reflect the site of infarction and the vessel involved. Details of differentiating features are discussed with explanatory diagrams and representative electrocardiograms. Elevation of the ST-segment in some leads suggest a serious condition requiring urgent intervention. These are discussed with explanatory diagrams and representative electrocardiograms. Summary and MCQs at the end of the chapter help in quick revision and self-assessment.

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Authors and Affiliations

  1. Ex Senior professor and head of the department of cardiology, Jawaharlal Nehru Medical College, Ajmer, India

    Sitaram Mittal

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  1. Sitaram Mittal
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Appendices

Summary

  • Beginning of the normal ST-segment is mildly upsloping or isoelectric depending on weather it starts from the end of the S wave or the R wave, respectively. In leads V1 and V2, it may show mild upward convexity. In leads V5 and V6 it may show early uptake (early repolarization variant). Soon after onset, the ST-segment leaves the baseline and merges smoothly with the proximal limb of the T wave. There is no horizontal or isoelectric portion.

  • Diffuse coved ST-segment elevation is seen in coronary vasospasm and Takotsubo cardiomyopathy (stress cardiomyopathy).

  • Coved ST-segment localized to the territory of a coronary artery is seen in transmural injury or ventricular aneurysm. ST-segment elevation of more than 1 mm is considered significant in leads V5 and V6. Elevation of more than 2 mm is considered significant in leads V1, V2, and V3. ST-segment elevation greater in V1 than in V2 suggest occlusion of right coronary artery.

  • ST-segment elevation in leads V1 to V3 is usual in:

    • Occlusion of a septal branch of the left anterior descending coronary artery. ST-segment is coved. It may accompany right bundle branch block.

    • ST-segment may also be elevated in lead V3R in occlusion of conus branch of right coronary artery.

    • Acute pulmonary thromboembolism.

    • Other electrocardiographic findings include sinus tachycardia, right axis deviation, T wave inversion in leads V1 to V4, S wave in lead I, and at times complete right bundle branch block.

    • Left ventricular hypertrophy and left bundle branch block.

ST-segment elevation is upsloping. Elevation of more than 5 mm is considered significant is leads V1 to V3.

  • Hypercalcemia.

ST-segment elevation in leads V1 and V2 is associated with short ST-segment.

  • Hyperkalemia.

ST-segment elevation is associated with tall and peaked T wave.

  • Brugada syndrome.

Incomplete or complete RBBB is associated with prominent J wave simulating elevated ST-segment. Recording in the third intercostal space produces more prominent J wave. Atrial fibrillation can occur. Bradycardia dependent VT/VF can cause sudden death.

  • Cocaine

It can produce Brugada like pattern.

  • Arrhythmogenic right ventricular dysplasia.

It is characterized by RBBB with low amplitude Epsilon wave on the early part of the ST-segment.

  • ST-segment elevation with concavity upward is usual in the following situations:

    • In leads V1 to V3.

As normal variant in

  • Pectus excavatum. rsr’ may be seen in leads V1, V2.

  • Early repolarization.

  • Vagal overdrive—Mild ST-segment elevation is associated with bradycardia and tall T wave.

  • Athletes.

Sinus bradycardia is associated with increased left ventricular voltage and early repolarization pattern in right to mid precordial leads.

  • ST segment elevation in all leads.

  • Hypothermia—It is associated with bradycardia, prolonged PR interval, prolonged QT interval, and prominent J wave (Osborn wave).

  • Acute pericarditis/myopericarditis or myopericardial injury.

Upward concave ST-segment elevation is associated with sinus tachycardia, depression of PR segment, and normal T waves.

By the time pericardial effusion accumulates, T waves tend to become flat. Pericardial constriction is associated with the inversion of T waves.

  • ST-segment elevation in leads V4 to V6.

  • Early repolarization syndrome—It is characterized by ST-segment elevation with upward concavity and slurring of terminal part of the R wave or prominent J wave in lateral and/or inferior leads. T waves are prominent.

  • Left pneumothorax can cause ST-segment elevation with upward concavity in leads V4 to V6.

MCQs

Q1. Earliest ECG change in hyperacute transmural myocardial infarction is:

  1. (a)

    Straight elevation of the ST-segment

  2. (b)

    ST-segment elevation with concavity upward

  3. (c)

    ST-segment elevation with convexity upward

  4. (d)

    Broadening of T wave

Q2. In hyperacute phase of transmural myocardial infarction:

  1. (a)

    ST-segment is elevated from J point

  2. (b)

    R wave amplitude is increased

  3. (c)

    T wave becomes tall and wide

  4. (d)

    All

Q3. In Prinzmetal’s angina:

  1. (a)

    ECG simulates acute transmural myocardial injury

  2. (b)

    ECG normalizes with relief of pain

  3. (c)

    There are wide and deep Q waves

  4. (d)

    T waves are inverted

Q4. Monophasic upright complexes can occur in:

  1. (a)

    Hyperacute phase of myocardial infarction

  2. (b)

    Coronary vasospasm

  3. (c)

    Myocardial ischemia

  4. (d)

    Hyperkalemia

Q5. In pseudonormalization:

  1. (a)

    Q waves are deep and wide

  2. (b)

    ST-segment is isoelectric

  3. (c)

    T waves are symmetrically inverted

  4. (d)

    All

Q6. Takotsubo cardiomyopathy produces:

  1. (a)

    ST-segment elevation in lead aVR

  2. (b)

    Extensive ST-segment depression

  3. (c)

    Extensive T wave inversion

  4. (d)

    All

Q7. ST-segment elevation with concavity upward is seen in:

  1. (a)

    Acute pericarditis

  2. (b)

    Vagotonia

  3. (c)

    Hypothermia

  4. (d)

    All

Q8. ST-segment elevation in leads V1 to V3 is seen in:

  1. (a)

    Massive pulmonary embolism

  2. (b)

    LBBB

  3. (c)

    RBBB

  4. (d)

    Infarction of the interventricular septum

Q9. ST-segment elevation is seen in:

  1. (a)

    LVH

  2. (b)

    Hypokalemia

  3. (c)

    Hypocalcemia

  4. (d)

    Tumors invading myocardium

Q10. Brugada syndrome produces the ST-segment elevation in:

  1. (a)

    Leads V1 and V2

  2. (b)

    Leads V3 and V4

  3. (c)

    Leads V5 and V6

  4. (d)

    Leads II, III, aVF

Q11. Which of the following conditions can produce ST-segment elevation?

  1. (a)

    Trauma to myocardium

  2. (b)

    Myocarditis

  3. (c)

    Left pneumothorax

  4. (d)

    All

Q12. Successful reperfusion is suggested by:

  1. (a)

    ≥70% reduction in ST-segment elevation

  2. (b)

    ≥50% reduction in ST-segment elevation

  3. (c)

    ≥40% reduction in ST-segment elevation

  4. (d)

    ≥30% reduction in ST-segment elevation

Q13. Ventricular aneurysm is suggested by:

  1. (a)

    Persistent ST-segment elevation

  2. (b)

    Deep and broad Q wave

  3. (c)

    Deep and pointed T wave

  4. (d)

    Loss of R wave

Q14. ST-segment elevation in leads I and aVL suggests:

  1. (a)

    Anteroseptal infarction

  2. (b)

    Apical infarction

  3. (c)

    Lateral infarction

  4. (d)

    High lateral infarction

Q15. Posterior infarction produces reciprocal changes in:

  1. (a)

    Leads V2, V3

  2. (b)

    Leads V5, V6

  3. (c)

    Leads I, aVL

  4. (d)

    Leads II, III, aVF

Q16. Tall R wave and tall T wave in lead V2 suggest:

  1. (a)

    Anteroseptal infarction

  2. (b)

    Apical infarction

  3. (c)

    Posterior infarction

  4. (d)

    High lateral infarction

Q17. Inferior infarction produces ST-segment depression in:

  1. (a)

    Leads V1 to V3

  2. (b)

    Leads V4 to V6

  3. (c)

    Leads V7 to V9

  4. (d)

    Leads V3R to V6R

Q18. In the context of inferior infarction, ST-segment elevation in lead V1 suggests concomitant:

  1. (a)

    Anteroseptal infarction

  2. (b)

    Apical infarction

  3. (c)

    High lateral infarction

  4. (d)

    Right ventricular infarction

Q19. In the context of inferior infarction, ST-segment elevation in lead III exceeding that in lead II suggests concomitant:

  1. (a)

    Right ventricular infarction

  2. (b)

    Apical infarction

  3. (c)

    Lateral infarction

  4. (d)

    Posterior infarction

Q20. ST-segment elevation in lead aVR with diffuse ST-segment depression in other leads suggests occlusion of:

  1. (a)

    Left main coronary artery

  2. (b)

    Middle part of the LAD

  3. (c)

    Middle part of LCX

  4. (d)

    Proximal RCA

Q21. ST-segment elevation in leads I, aVL, and V1 to V6 suggests occlusion of:

  1. (a)

    Proximal LAD before diagonal branch

  2. (b)

    Mid LAD

  3. (c)

    Mid circumflex

  4. (d)

    Proximal RCA

Q22. Extensive anterior infarction with inferior infarction suggests occlusion of:

  1. (a)

    Proximal LAD wrapping around the cardiac apex

  2. (b)

    Distal LAD

  3. (c)

    Proximal RCA

  4. (d)

    Proximal PDA

Q23. ST-segment elevation only in leads V2 to V6 suggests occlusion of:

  1. (a)

    LAD before D1

  2. (b)

    LAD after D1 and SI

  3. (c)

    LAD before S1

  4. (d)

    Mid LCX

Q24. In the context of anterior infarction, occlusion of LAD before S1 is suggested by:

  1. (a)

    New RBBB

  2. (b)

    ST-segment elevation in leads V1 and aVR

  3. (c)

    New left anterosuperior fascicular block

  4. (d)

    New left posteroinferior fascicular block

Q25. Left posteroinferior fascicle is supplied by:

  1. (a)

    LAD

  2. (b)

    LAD + LCX

  3. (c)

    LAD + RCA

  4. (d)

    S1 + D1

Q26. ST-segment elevation in leads V1 to V3 suggests occlusion of:

  1. (a)

    Proximal LAD

  2. (b)

    Mid LAD

  3. (c)

    Distal LAD

  4. (d)

    Proximal LCX

Q27. Occlusion of proximal diagonal produces ST-segment elevation in leads:

  1. (a)

    I, aVL

  2. (b)

    V1 to V3

  3. (c)

    V4 to V6

  4. (d)

    V7 to V9

Q28. In the context of inferior infarction, ST-segment elevation in lead I suggests occlusion of:

  1. (a)

    Proximal LCX

  2. (b)

    Mid LAD

  3. (c)

    Proximal RCA

  4. (d)

    Proximal PDA

Q29. In the context of inferior infarction, ST-segment elevation in lead II > that in lead III suggests occlusion of:

  1. (a)

    LCX

  2. (b)

    LAD

  3. (c)

    RCA

  4. (d)

    PDA

Q30. In the context of inferior infarction, T wave inversion in lead V4R suggests occlusion of:

  1. (a)

    Proximal RCA

  2. (b)

    Mid RCA

  3. (c)

    Distal RCA

  4. (d)

    LCX

Q31. Normally the ST-segment may show mild coved elevation in leads:

  1. (a)

    V1, V2

  2. (b)

    V5, V6

  3. (c)

    V7, V8

  4. (d)

    V3R, V4R

Q32. Normally the ST-segment may show early repolarization pattern in leads:

  1. (a)

    V1, V2

  2. (b)

    V3, V4

  3. (c)

    V5, V6

  4. (d)

    V7, V8

Q33. Normally, which part of the ST-segment is isoelectric?

  1. (a)

    Initial

  2. (b)

    Middle

  3. (c)

    Terminal

  4. (d)

    None

Q34. Coronary vasospasm usually produces:

  1. (a)

    Diffuse coved ST-segment elevation

  2. (b)

    Diffuse concave ST-segment elevation

  3. (c)

    Convex ST-segment elevation in leads V5, V6

  4. (d)

    Concave ST-segment elevation in leads V1, V2

Q35. Stress cardiomyopathy usually produces:

  1. (a)

    Diffuse coved ST-segment elevation

  2. (b)

    Coved ST-segment elevation in leads V5, V6

  3. (c)

    Diffuse concave ST-segment elevation

  4. (d)

    Coved ST-segment elevation in leads V3R to V6R

Q36. Normally the ST-segment can show coved elevation of up to 2 mm in leads:

  1. (a)

    V1, V2

  2. (b)

    V3, V4

  3. (c)

    V5, V6

  4. (d)

    V7, V8

Q37. Coved ST-segment elevation greater in V1 than in V2 suggests occlusion of:

  1. (a)

    Right coronary artery

  2. (b)

    Major septal branch of LAD

  3. (c)

    D1

  4. (d)

    OM1

Q38. Sinus tachycardia, right axis deviation, ST-segment elevation with T wave inversion in leads V1 to V4 and S wave in lead 1 suggest the possibility of:

  1. (a)

    Occlusion of conus artery

  2. (b)

    Occlusion of major septal

  3. (c)

    Acute cor pulmonale

  4. (d)

    Chronic cor pulmonale

Q39. In left bundle branch block, ST-segment elevation in leads V1, V2 suggests:

  1. (a)

    Occlusion of conus artery

  2. (b)

    Normal pattern

  3. (c)

    Left ventricular hypertrophy

  4. (d)

    Posterior infarction

Q40. In left bundle branch block, what magnitude of ST-segment elevation in lead V2 is considered abnormal?

  1. (a)

    More than 1 mm

  2. (b)

    More than 3 mm

  3. (c)

    More than 4 mm

  4. (d)

    More than 5 mm

Q41. Which leads can show upsloping ST-segment elevation in left ventricular hypertrophy with ST-segment depression and T wave inversion in leads V5, V6?

  1. (a)

    V3, V4

  2. (b)

    V1, V2

  3. (c)

    I, aVL

  4. (d)

    II, III, aVF

Q42. ST segment elevation in leads V1, V2 with short ST-segment (short Q-T interval) suggests:

  1. (a)

    Left ventricular hypertrophy

  2. (b)

    Hypercalcemia

  3. (c)

    Left bundle branch block

  4. (d)

    Hypocalcemia

Q43. ST-segment elevation with tall peaked T wave suggests:

  1. (a)

    Hypercalcemia

  2. (b)

    Hyperkalemia

  3. (c)

    Hypomagnesemia

  4. (d)

    Hyponatremia

Q44. Right bundle branch block pattern with prominent J wave simulating ST-segment elevation in lead V1, V2 suggests:

  1. (a)

    RBBB with right ventricular hypertrophy

  2. (b)

    RBBB with left ventricular hypertrophy

  3. (c)

    RBBB with right ventricular infarction

  4. (d)

    Brugada syndrome

Q45. Right bundle branch block with ST-segment elevation and additional low voltage wave on the early part of ST-segment suggests:

  1. (a)

    Brugada syndrome

  2. (b)

    Arrhythmogenic right ventricular cardiomyopathy

  3. (c)

    Right lateral accessory pathway

  4. (d)

    Normal variation

Q46. Pectus excavatum can produce:

  1. (a)

    rsr’ pattern in lead V1

  2. (b)

    Mild ST-segment elevation in leads V1, V2

  3. (c)

    Deep S in lead V6

  4. (d)

    All

Q47. Electrocardiogram from an athlete can show:

  1. (a)

    Sinus bradycardia

  2. (b)

    Increased left ventricular voltages in leads V5, V6

  3. (c)

    Early repolarization pattern in right to mid precordial leads

  4. (d)

    None

Q48. Bradycardia with prominent J wave suggest the possibility of:

  1. (a)

    Hypothermia

  2. (b)

    Myxedema

  3. (c)

    Athlete heart

  4. (d)

    All

Q49. Sinus tachycardia with diffuse upward concave ST-segment elevation and elevation of PR segment in lead aVR suggests:

  1. (a)

    Coronary vasospasm

  2. (b)

    Stress cardiomyopathy

  3. (c)

    Acute pericarditis

  4. (d)

    Right ventricular infarction

Q50. Slurring of the terminal part of prominent R in lead V5 with prominent T wave and ST segment elevation with upward concavity suggests:

  1. (a)

    Early repolarization syndrome

  2. (b)

    Chronic severe aortic regurgitation

  3. (c)

    Chronic severe mitral regurgitation

  4. (d)

    Left lateral accessory pathway

Q51. Normal ECG cannot exclude:

  1. (a)

    Acute pericarditis

  2. (b)

    Brugada syndrome

  3. (c)

    Arrhythmogenic right ventricular cardiomyopathy

  4. (d)

    All

Q52. Diffuse concave upward ST-segment elevation in leads other than lead aVR and V1, with normal T wave and depression of PR segment suggests:

  1. (a)

    Acute pericarditis

  2. (b)

    Early repolarization syndrome

  3. (c)

    Cardiac tumor

  4. (d)

    Vagal overdrive

Q53. Sinus tachycardia, low QRS voltage, isoelectric ST-segment with diffuse inverted T wave suggests:

  1. (a)

    Acute pericarditis

  2. (b)

    Pericardial constriction

  3. (c)

    Emphysema

  4. (d)

    Acute cor pulmonale

Q54. Atrial fibrillation with diffuse concave ST-segment elevation and low amplitude positive T wave suggest:

  1. (a)

    Mitral stenosis

  2. (b)

    Mitral regurgitation

  3. (c)

    Acute pericarditis

  4. (d)

    Constrictive pericarditis

Q55. Mild pulmonary embolism produces:

  1. (a)

    ST-segment elevation in leads V1 to V3

  2. (b)

    Deep T inversion in leads V1 to V3

  3. (c)

    S1 Q3 and inverted T3 pattern

  4. (d)

    None

Q56. Acute pericarditis produces:

  1. (a)

    Isoelectric ST-segment

  2. (b)

    Diffuse T wave inversion

  3. (c)

    T wave amplitude less than 5 mm

  4. (d)

    T wave amplitude greater than 5 mm

Q57. ST segment elevation in acute pericarditis is due to:

  1. (a)

    Myocarditis

  2. (b)

    Pericardial effusion

  3. (c)

    Early repolarization

  4. (d)

    All

Q58. Cocaine can produce:

  1. (a)

    ST-segment elevation with concavity upward

  2. (b)

    Brugada pattern

  3. (c)

    Prolongation of QT interval

  4. (d)

    ST-segment depression

1.1 Answers

(1) a (2) d (3) a, b (4) a, b (5) b (6) a (7) d (8) a, b, d (9) a, d (10) a (11) d (12) a (13) a (14) d (15) a (16) c (17) a (18) d (19) a (20) a (21) a (22) a (23) b (24) a, b (25) c (26) b (27) a (28) a (29) a (30) d (31) a (32) c (33) d (34) a (35) a (36) a (37) a (38) c (39) b (40) d (41) b (42) b (43) b (44) d (45) b (46) a, b (47) a, b, c (48) a (49) c (50) a (51) d (52) a (53) b (54) c (55) d (56) c (57) a (58) b, c

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Mittal, S. (2023). ST-Segment Elevation. In: Insights into Electrocardiograms with MCQs. Springer, Singapore. https://doi.org/10.1007/978-981-99-0127-2_40

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  • DOI: https://doi.org/10.1007/978-981-99-0127-2_40

  • Published:

  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-99-0126-5

  • Online ISBN: 978-981-99-0127-2

  • eBook Packages: MedicineMedicine (R0)

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