Clinical Notes : Cardiology

149. ECG STEMI - posterior

ECG - Posterior STEMI

Clinical significance of Posterior ST Elevation Myocardial Infarction

MI is myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand.

This is usually caused by occlusion in the coronary arteries. ST-elevation myocardial infarction (STEMI) is suspected when a patient presents with persistent ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history.

 

Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.

  • Isolated posterior MI is less common (3-11% of infarcts).

  • Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.

  • Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.

 

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral STEMI.

How to spot posterior infarction

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.

Posterior MI is suggested by the following changes in V1-3:

  • Horizontal ST depression

  • Tall, broad R waves (>30ms)

  • Upright T waves

  • Dominant R wave (R/S ratio > 1) in V2

 

In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.

 
 

Typical appearance of posterior infarction in V2

Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).

Explanation of the ECG changes in V1-3

The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:

  • ST elevation becomes ST depression

  • Q waves become R waves

  • Terminal T-wave inversion becomes an upright T wave

 

The progressive development of pathological R waves in posterior infarction (the “Q wave equivalent”) mirrors the development of Q waves in anteroseptal STEMI

 

This picture illustrates the reciprocal relationship between the ECG changes seen in STEMI and those seen with posterior infarction.

The previous image (depicting posterior infarction in V2) has been inverted.

See how the ECG now resembles a typical STEMI!

Posterior leads

Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below):

  • V7 – Left posterior axillary line, in the same horizontal plane as V6.

  • V8 – Tip of the left scapula, in the same horizontal plane as V6.

  • V9 – Left paraspinal region, in the same horizontal plane as V6

 

Posterior lead placement V7, V8, V9

The degree of ST elevation seen in V7-9 is typically modest – note that only 0.5 mm of ST elevation is required to make the diagnosis of posterior MI!

 

Example 1a : Inferolateral STEMI. Posterior extension (anterior leads)

Inferolateral STEMI. Posterior extension is suggested by:

  • Horizontal ST depression in V1-3

  • Tall, broad R waves (> 30ms) in V2-3

  • Dominant R wave (R/S ratio > 1) in V2

  • Upright T waves in V2-3

Inferolateral STEMI. Posterior extension. (anterior leads) 

 

Example 1b : Inferolateral STEMI. Posterior extension (posterior leads)

The same patient, with posterior leads recorded:

  • Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall, making this an inferior-lateral-posterior STEMI (= big territory infarct!).

Inferolateral STEMI. Posterior extension. (posterior leads)

Example 2a : Poterior STEMI (anterior leads)

In this ECG, posterior MI is suggested by the presence of:

  • ST depression in V2-3

  • Tall, broad R waves (> 30ms) in V2-3

  • Dominant R wave (R/S ratio > 1) in V2

  • Upright terminal portions of the T waves in V2-3

 

The ECG changes extend out as far as V4, which may reflect superior-medial misplacement of the V4 electrode from its usual position

 

Poterior STEMI (anterior leads)

Example 2b : Poterior STEMI (poterior leads)

The same patient, with posterior leads recorded:

  • Posterior infarction is diagnosed based on the presence of ST segment elevation >0.5mm in leads V7-9.

  • Note that there is also some inferior STE in leads III and aVF (but no Q wave formation) suggesting early inferior involvement

 

Poterior STEMI (Poterior leads)

Example 3a : Chest pain (anterior leads)

Patient presenting with chest pain

 

Chest pain (anterior leads)

Example 3b : Chest pain (anterior leads) 30 minutes later

An ECG of the same patient taken 30 minutes later:

  • There is now some ST elevation developing in V6.

  • With the eye of faith there is perhaps also some early ST elevation in the inferior leads (lead III looks particularly abnormal)

 

Chest pain (anterior leads) 30 minutes later

Example 3c : Chest pain (anterior leads) posterior leads

Posterior infarction is confirmed by the presence of ST elevation >0.5mm in leads V7-9

 

Chest pain (anterior leads) posterior lead

Example 4a : Inferior STEMI (extensive)

Patient presenting with central chest pain

 

Inferior STEMI (extensive)

Flip ECG, confirm V2 STEMI changes of posterior AMI

 

Example 4b : Inferior STEMI (extensive)

The same patient with posterior leads (V8,9) recorded:

Inferior STEMI (extensive) Posterior leads

 

Management

Refer A+E

In OOH settings where delay in transfer to A+E is inevitable : 

  • aspirin

    • 300 mg orally immediately, followed by 75 mg once daily

  • oxygen

    • Supplemental oxygen is indicated only if oxygen saturation is less than 90%

  • morphine

    • 2-4 mg intravenously every 5-15 minutes until adequate pain control is achieved

  • glyceryl trinitrate

    • if not hypotensive :

      • 0.3 to 1 mg sublingually every 5 minutes,

      • maximum 3 doses

    • if hypertensive or heart failure

      • 5 micrograms/minute intravenously initially,

      • increase by 5-20 microgram/minute increments every 3-5 minutes according to response,

      • maximum 200 micrograms/minute

 
LITFL.jpg
BMJ Best Practice.png

Life in the Fast Lane

Austalian Emergency Medicine website. 

View/Access

ST-elevation myocardial infarction

BMJ Best Practice

Last reviewed : March 2019

Last updated : September 2018

View/Access

 

CPD Quiz and Certificate

This activity attracts 1,0 CPD point

Scroll down the box above to view its entire content

All users who successfully complete the quiz are e-mailed a copy of their personalised CPD certificate.