Myocardial Infarction

The heart needs an oxygenated blood supply in order to function in the same way as the rest of the body. The coronary arteries supply the surface of the heart muscle with this oxygenated blood, so when the lumen of one or more of these vessels becomes occluded, the required oxygen supply may not be sufficient to adequately oxygenate the myocytes that facilitate the contracting of the organ.

When the supply oxygen via blood flow is insufficient to the needs of the muscle, tissue oxygen levels will decline, leading to cellular hypoxia. If this hypoxic state is prolonged, it can result in cell death. This, in turn, will lead to a loss of electrical function within the cardiac muscle.


  1. Intramyocardial perfusion defect
  2. Diastolic dysfunction
  3. Systolic dysfunction
  4. Increased LVEDP
  5. ECG changes
  6. Symptoms
  7. Infarct

Hypoxia that is remedied fairly quickly, or simply not as severe as that previously described, will result in electrical and mechanical changes in the heart.

Effectively, insufficient myocardial oxygen supply leads to cellular inflammation and injury, which results in infarction.

These heart attacks are categorised as unstable angina,  STEMI and NSTEMI, which are covered here.


  • Fatigue
  • Chest pain/discomfort
    • Often constant for 30-60 minutes
    • Radiation to ulnar left arm, neck, shoulder and jaw
    • Usually described as sharp, squeezing, aching or burning
  • Malaise


  • Cardiac biomarkers
    • Troponin; only increase during myocardial necrosis
    • Effective in both STEMI and NSTEMI 
    • Creatine kinase; increase within 3-12 hours of chest pain onset

and at least ONE of the following:

  • Typical signs and symptoms
  • Pathological Q waves on the ECG
  • ST elevation or depression
  • Previous stenting

ECG Diagnosis

  • ECG is the most important asset in early assessment of a suspected MI, being cited as confirmatory in 80% of all cases.
    • Cardiac biomarkers are not instantly assessable, so ECG is crucial
  • The first hours and days following an MI produce changes on the ECG
    1. Hyperacute T waves
    2. ST changes
    3. Negative T waves
    4. Pathological Q waves


  • L-R: The progression of ST changes and Q wave formation in STEMI

ST segment changes result from what is known as the injury current. This is generated by the discrepancy between the areas of non-ischaemic myocardium and ischaemic myocardium. They occur during the resting and plateau phase of the ventricular action potential, i.e. the ST segment.

The supply/demand between muscle and oxygen determines the direction of ST segment transformation on the ECG

  • Decreased supply: Transmural ischaemia
    • ST segment elevation toward affected region
  • Increased demand: Subendocardial ischaemia
    • ST segment depression away from entire LV
    • Reproducible with exertion
    • Angina

Localising the MI

MI Localisation