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T Wave and Ischemia

T wave and ischemia

Depolarization Vector Without Ischemia

Fast depolarization electrical vector in myocardial wall

Propagation of depolarization wavefront in non-ischemic myocardium, R wave formation

Myocardial Depolarization

  • The change in the extracellular space becomes negative
  • It always starts in the endocardium and moves towards the epicardium
  • The extracellular space becomes negative
  • The cardiac vector moves in the direction of depolarization (from endocardium to epicardium)
    • The vector always moves towards the more positive area
  • Depolarization occurs rapidly
    • A narrow R wave appears in the leads that "view" the vector

Repolarization Vector Without Ischemia

Slow repolarization electrical vector in myocardial wall

Propagation of repolarization wavefront in non-ischemic myocardium, T wave formation

Myocardial Repolarization


Physiological T Wave Without Ischemia

Mechanism normal non-ischemic T wave, action potential, endocardium and epicardium depolarization repolarization, concordant T wave with QRS complex

Physiological T Wave

  • Depolarization
    • Spreads to the epicardium
    • Occurs rapidly (creates a narrow R wave)
      • The vector points towards the epicardium (towards the corresponding lead)
  • Repolarization
    • Spreads to the endocardium, as the epicardium starts repolarizing earlier than the endocardium
    • Occurs slowly (creates a wide T wave)
      • The vector also points towards the epicardium (towards the corresponding lead)
  • Physiological T wave is concordant (same polarity as the QRS complex)

Negative T Wave and Subendocardial Ischemia

Subendocardial ischemia, shorter action potential duration in endocardium than epicardium, negative inverted ischemic T wave

Subendocardial Ischemia


Hyperacute T Wave and Subepicardial Ischemia

Hyperacute T wave, subepicardial and transmural ischemia, action potential duration in endocardial and epicardial cells

Subepicardial and Transmural Ischemia

  • Subepicardial ischemia
    • Occurs due to occlusion (blockage) of a coronary artery
    • Progresses to transmural ischemia within a few minutes
  • Action potential duration is shortened in both endocardium and epicardium
    • Both areas are ischemic
  • However, the action potential duration shortens more in the epicardium
    • The epicardium is more sensitive to ischemia than the endocardium
  • Depolarization
    • Occurs similarly to non-ischemic myocardium
    • Depolarization and the vector both point towards the epicardium
  • Repolarization (during the hyperacute phase of STEMI)
    • Lasts for several minutes after occlusion
    • There is a greater shortening of the action potential in the epicardium
    • Proceeds in the same direction as in non-ischemic myocardium
      • However, repolarization starts earlier and occurs faster
    • Results in a hyperacute T wave
      • Lasts for only several minutes after occlusion
      • Is closer to the QRS complex
      • Is peaked (similar to hyperkalemia)
      • Is concordant (same polarity as the QRS complex)

Negative T Wave and Late Transmural Ischemia

T wave later stage subepicardial ischemia, negative inverted T wave

Late Transmural Ischemia



Acute LAD stenosis and subendocardial ischemia of the anterior wall
ECG inverted - negatvie T wave and subendocardial ischemia

Unstable Angina Pectoris

  • Sinus Rhythm
  • Inverted T waves (I, aVL, V2-V6)
  • The patient experienced approximately 10 minutes of angina
    • The patient did not have inverted T waves on previous EKG recordings
  • Indications of 1mm ST elevations in V2-V6
  • However, ST elevations later normalized and troponin levels were repeatedly normal


Hyperacute LAD occlusion subepicardial ischemia
ECG hyperacute anterior STEMI infarction, hyperacute T wave

Hyperacute STEMI of the Anterior Wall


Old anterior STEMI infarction with anterior necrosis
ECG unstable angina pectoris, stenosis proximal left anterior descending artery

Old Anterior STEMI

  • Sinus Rhythm
  • The patient had an Anterior STEMI 2 weeks ago
  • Inverted T waves (V1-V5, aVL)
    • Persist for several weeks after the STEMI infarction

ST Elevation Dynamics in STEMI Infarction

ECG ST elevation evolution in STEMI infarction

STEMI Classification by Stage




Sources

  • ECG from Basics to Essentials Step by Step
  • litfl.com
  • ecgwaves.com
  • metealpaslan.com
  • medmastery.com
  • uptodate.com
  • ecgpedia.org
  • wikipedia.org
  • Strong Medicine
  • Understanding Pacemakers





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Home /

T Wave and Ischemia

T wave and ischemia

Depolarization Vector Without Ischemia

Fast depolarization electrical vector in myocardial wall Propagation of depolarization wavefront in non-ischemic myocardium, R wave formation

Myocardial Depolarization

  • The change in the extracellular space becomes negative
  • It always starts in the endocardium and moves towards the epicardium
  • The extracellular space becomes negative
  • The cardiac vector moves in the direction of depolarization (from endocardium to epicardium)
    • The vector always moves towards the more positive area
  • Depolarization occurs rapidly
    • A narrow R wave appears in the leads that "view" the vector

Repolarization Vector Without Ischemia

Slow repolarization electrical vector in myocardial wall Propagation of repolarization wavefront in non-ischemic myocardium, T wave formation

Myocardial Repolarization

  • The change in the extracellular space becomes positive
  • It begins after complete depolarization
  • Cells of the epicardium start to repolarize earlier than the cells of the endocardium
    • Therefore, repolarization spreads from the epicardium to the endocardium
  • Repolarization is a change in polarity of the extracellular space to positive
  • Thus, the vector points in the opposite direction (toward the epicardium) of the repolarization direction
    • The vector always points towards the more positive area
  • Repolarization occurs more slowly than depolarization
    • A wide T wave appears in the leads that "view" the vector

Physiological T Wave Without Ischemia

Mechanism normal non-ischemic T wave, action potential, endocardium and epicardium depolarization repolarization, concordant T wave with QRS complex

Physiological T Wave

  • Depolarization
    • Spreads to the epicardium
    • Occurs rapidly (creates a narrow R wave)
      • The vector points towards the epicardium (towards the corresponding lead)
  • Repolarization
    • Spreads to the endocardium, as the epicardium starts repolarizing earlier than the endocardium
    • Occurs slowly (creates a wide T wave)
      • The vector also points towards the epicardium (towards the corresponding lead)
  • Physiological T wave is concordant (same polarity as the QRS complex)

Negative T Wave and Subendocardial Ischemia

Subendocardial ischemia, shorter action potential duration in endocardium than epicardium, negative inverted ischemic T wave

Subendocardial Ischemia


Hyperacute T Wave and Subepicardial Ischemia

Hyperacute T wave, subepicardial and transmural ischemia, action potential duration in endocardial and epicardial cells

Subepicardial and Transmural Ischemia

  • Subepicardial ischemia
    • Occurs due to occlusion (blockage) of a coronary artery
    • Progresses to transmural ischemia within a few minutes
  • Action potential duration is shortened in both endocardium and epicardium
    • Both areas are ischemic
  • However, the action potential duration shortens more in the epicardium
    • The epicardium is more sensitive to ischemia than the endocardium
  • Depolarization
    • Occurs similarly to non-ischemic myocardium
    • Depolarization and the vector both point towards the epicardium
  • Repolarization (during the hyperacute phase of STEMI)
    • Lasts for several minutes after occlusion
    • There is a greater shortening of the action potential in the epicardium
    • Proceeds in the same direction as in non-ischemic myocardium
      • However, repolarization starts earlier and occurs faster
    • Results in a hyperacute T wave
      • Lasts for only several minutes after occlusion
      • Is closer to the QRS complex
      • Is peaked (similar to hyperkalemia)
      • Is concordant (same polarity as the QRS complex)

Negative T Wave and Late Transmural Ischemia

T wave later stage subepicardial ischemia, negative inverted T wave

Late Transmural Ischemia



ECG inverted - negatvie T wave and subendocardial ischemia

Unstable Angina Pectoris

  • Sinus Rhythm
  • Inverted T waves (I, aVL, V2-V6)
  • The patient experienced approximately 10 minutes of angina
    • The patient did not have inverted T waves on previous EKG recordings
  • Indications of 1mm ST elevations in V2-V6
  • However, ST elevations later normalized and troponin levels were repeatedly normal
 Acute LAD stenosis and subendocardial ischemia of the anterior wall


ECG hyperacute anterior STEMI infarction, hyperacute T wave

Hyperacute STEMI of the Anterior Wall

 Hyperacute LAD occlusion subepicardial ischemia

ECG unstable angina pectoris, stenosis proximal left anterior descending artery

Old Anterior STEMI

  • Sinus Rhythm
  • The patient had an Anterior STEMI 2 weeks ago
  • Inverted T waves (V1-V5, aVL)
    • Persist for several weeks after the STEMI infarction
 Old anterior STEMI infarction with anterior necrosis

ST Elevation Dynamics in STEMI Infarction

ECG ST elevation evolution in STEMI infarction

STEMI Classification by Stage




Sources

  • ECG from Basics to Essentials Step by Step
  • litfl.com
  • ecgwaves.com
  • metealpaslan.com
  • medmastery.com
  • uptodate.com
  • ecgpedia.org
  • wikipedia.org
  • Strong Medicine
  • Understanding Pacemakers