Myocardial Infarction

Myocardial Infarction ECG

Myocardial infarction or MI refers to a heart attack when one or more than one coronary artery is occluded obstructing blood flow to the distal artery. The occlusion of the coronary artery resulting from the rupture of an atheromatous plaque. In Small portion of patients, Mi may be due to emboli or coronary spasm in normal coronary arteries or vasculitis. This article deals all about the myocardial infarction ECG. The characteristics of ECG changes may be seen in a condition other than acute MI.

The incident rate of myocardial infarction (MI) is 5/1000 per year (UK). The diagnosis of MI is based on the presence of at least 2 out of 3 of typical history, myocardial infarction ECG, and cardiac enzyme rise.

Myocardial Infarction ECG findings

The electrocardiogram (ECG) is used to assess cardiac rhythm and conduction. The myocardial infarction ECG is the main test used in the diagnosis of myocardial infarction and also in the myocardial ischaemia.

The physiological basis of myocardial infarction ECG recording is the fact that electrical depolarization of myocardial tissue produces a small dipole current, which can be detected by electrode pairs on the body surface. These signals are augmented and either printed or visible on a monitor.

During sinus rhythm, the SA node triggers atrial depolarisation, producing P wave. Depolarisation proceeds casually through Av node, which is too small to produce a depolarization wave detectable from the body surface.

The bundle of His, bundle branches and Purkinje system are then actuated, initiating ventricular myocardial depolarization, which produces the QRS complex. The muscle mass of ventricles is much larger than that of the atria, so the QRS complex is larger than P waves.

The interval between the onset of the P wave and the onset of the QRS complex is termed as the ‘PR interval” and largely reflects the duration of AV nodal conduction. Injury to left-right bundle branch delays ventricular depolarisation, widening QRS complex.

Selective agony of one of the left fascicles affects the electrical axis. Repolarastion is slower and spreads from the epicardium to endocardium. Atrial repolarisation does not cause a detectable signal but ventricular repolarisation produces the T wave. The OT interval represents the total duration of ventricular depolarisation and repolarisation.

The abnormalities of cardiomyocyte electrophysiological conduction are common following bouts of myocardial ischaemia. These abnormalities are reflected in the myocardial infarction ECG and are used to detect myocardial infarctions and distinguish between the subtypes of Non-ST elevated myocardial infarction and ST elevated Myocardial infarction.

Non-ST elevated Myocardial infarction

Non-ST elevated Myocardial infarctions result in acute depression of the ST segment or inversion of the T wave. Essentially, the elevation of the ST segment does not occur. Over time the electrophysiological abnormalities return to normal.

ST elevated Myocardial infarction

ST elevated Myocardial infarctions are characterized by early elevations of the ST segment which persist for 1-2 days following infarction. In some cases, the Q wave of the QRS complex may become enhanced several hours after MI and this may reflect the development of a transmural infarct. However, Because there are several hours of lag before Q wave enhancement develops, Q waves are not frequently used for diagnostic purposes.

Criteria for diagnosis of an acute Myocardial Infarction (MI)

Apprehension of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin (cTn)), with at least one value above the 99th cantile upper reference limit (URL) and with at least one of the following:

  1. Symptoms of ischaemia
  2. New or presumed new significant DT segment-T waves (ST-T) changes or new left bundle branch block (LBBB)
  3. Development of pathological Q waves in the myocardial infarction ECG
  4. Radiological demonstration of new loss of viable myocardium or new regional wall motion abnormality
  5. Assimilation of an intracoronary thrombus by angiography or postmortem

The cardiac death is a manifestation with expressive of myocardial ischaemia and infringes new ischaemic ECG changes or new LBBB, but cardiac death occurred before cardiac biomarkers were accomplished, or before cardiac marker appraisal would be increased.

Percutaneous coronary arbitration (PCI)-affiliated MI is arbitrarily defined by the elevation of cTn values (>5×99th centile URL) in patients with methodical precedent values (≤99th centile URL) or a rise of cTn values >20% if the baseline values are elevated and are constant or decreasing. In addition, either

  • Symptoms of suggestive myocardial ischaemia, or
  • New ischaemic ECG changes, or
  • Angiographic findings consistent with procedural complications, or
  • Imaging exhibition of new loss of viable myocardium or new regional wall motion abnormality are required

Thrombosis named as stent thrombosis affiliated with MI when encounter by coronary angiography or postmortem in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one appraisal above the 99th centile URL.

CABG(Coronary artery bypass grafting )-related Myocardial infarction is arbitrarily fenced by elevation of cardiac biomarker amount (>10×99th centile URL) in patients with normal baseline cTn amount (≤ 99th centile URL). In addition either

  • Recent pathological Q waves or new LBBB, or
  • Angiographic documented new graft or new coronary artery occlusion, or
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality is required during episodes of ischaemia.

Careful assessment and risk stratification are important because of these guide the use of more complex pharmacological and interventional treatment which can improve outcome.

Conclusion

Myocardial infarction (MI) is a term used for an event of a heart attack which is due to the formation of plagues in the interior walls of arteries. This causes a reduction in blood flow to the heart and injures heart muscles because of the lack of oxygen supply.

In a myocardial infarction transmural ischemia develops. In the first hours and days after the onset of an MI, several changes can be observed on the Myocardial infraction ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative Twaves and finally pathologic Q waves develop. This is all; about myocardial infarction ECG.

Disclaimer

All of the information in this article is meant for educational purposes only.

 

Dr Aadarsh Yadav

Dr Adarsh Yadav is a registered medical expert currently is a medical officer at the department of paediatrics at Scheer memorial Adventist hospital, kavre, Nepal. He had been a very well trained medical practitioner, and apart from his medical practice, he had been a member of different health camps organizing blood donation camps in Bangladesh just during his internship.

5 Comments

  1. Good day! Do you use Twitter? I’d like to follow you if that would be ok.
    I’m definitely enjoying your blog and look forward to new posts.

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