Good evening, hope you’re all doing well! Thank you for all of the peer discussions so far this year, CPD events with @PreHospECG and on-going learning support; a fantastic start to 2016.
I have never really looked into the electrophysiological depths of ST changes presented on an ECG. What actually causes ST elevation on an ECG in the presence of Myocardial Infarction? What causes reciprocal ST changes or ST depression in the place of ischaemia? I have never even considered asking these questions until recently; so I set out to find an answer.
It does seem that there are a variety of explanations for the reasoning behind ST elevation/depression in the place of infarction and/or ischaemia. There are also discussions that the ST segment does not in fact represent infarction at all, and that diagnostic infarction is solely linked to pathological Q waves. I couldn’t agree more. The ST segment is purely linked with ischaemia and changes to the surrounding tissue of likely infarct.
Key Points to Understand
- An electrical vector travelling towards a positive electrode will cause a positive deflection on an ECG.
- An electrical vector travelling away from a positive electrode will cause a negative deflection on an ECG.
- ST Elevation on an ECG represents a transmural ischaemia (meaning, across the entirety of the heart wall), which is associated with a supply ischaemia; therefore coronary occlusion.
- ST Depression on an ECG represents a non-transmural ischaemia, which is associated with a subendocardial ischaemia; therefore coronary stenosis.
- ECG monitors automatically adjust the isoelectric baseline in accordance to the TQ resting interval of the cardiac cycle, specific to each electrode.
There are many theories for what causes ST Elevation and Depression; two of which are the ‘Diastolic Current of Injury’ and the ‘Systolic Current of Injury’. For this article I will be looking at the Diastolic Current of Injury, and how the TQ interval is effectively electrical diastole in the cardiac cycle.
The coronary arteries are located in the subepicardium, which is the inner part of the ventricular wall. Myocardial Ischaemia is more often than not, related to the ‘cellular hypoxia’ of the subepicardial tissue. When coronary blood flow is insufficient to supply the work of the hearts muscular tissue (the myocardium), cellular hypoxia begins. Prolonged cellular hypoxia (ischaemia) can lead to tissue death (infarction) and total loss of electrical activity. Subendocardial ischaemia is generally caused by coronary stenosis (the narrowing of the coronary arteries), for example due to fatty deposits (atheroma) lining the inner walls of the vessels.
Hypoxic conditions, or ischaemic conditions, lead to a diminished intracellular concentration of ATP due to a lack of blood supply. Think of supply and demand! The loss of ATP leads to decreasing activity of ATP-dependant mechanisms, such as the sodium-potassium pump. The sodium-potassium pump normally transports potassium into the cell, and sodium out of the cell, managing action potential due to ion concentrations intra and extracellularly. Decreased activity of the sodium-potassium pump leads to an increase of extracellular potassium ions, meaning a more positive environment outside of the cell, and a more negative environment inside of the cell. The normal resting cell is therefore said to be more positive (+++) than that of the resting ischaemic cell (+), due to the decreased function of the sodium-potassium pump.
A non-transmural ischaemia, or more specifically a subendocardial ischaemia, will present with ST Depression. The region of ischaemic tissue will be in a constant state of partial depolarisation. Due to this, during the repolarisation and resting period of the cardiac cycle (the TQ period), electrical activity travels towards a positive electrode causing TQ elevation. This is because there is normal functioning cardiac tissue surrounding the ischaemic region, that is actively able to utilise sodium-potassium pumps and to continue action potentials. As said before, the ECG monitor adapts to the TQ interval and makes this interval the ‘isoelectric baseline’ on that specific electrode. Due to this, the ST segment appears to be lowered (ST depression) due to baseline adaptation from the ECG monitor. See the representation below which brilliantly depicts how the TQ section (in red) is elevated, therefore when brought to the 0 mV isoelectric baseline, the ST segment appears as depression. The reason that the ST segment itself is not elevated or depressed in this state, is that the NET change in electrical activity practically ‘cancels’ itself out, due to electrical activity both moving towards/away from the positive electrode. It is the NET movement of electrical activity, a vector, that causes ECG deflection changes in presentation.
A transmural ischaemia, meaning an ischaemia that spreads the entire wall in a region of the heart, will present with ST Elevation. The transmural region is depolarised during the cardiac repolarisation and resting phase (the TQ interval), yet the electrical activity can only travel away from the positive electrodes due to the ischaemic region spanning the entirety of the hearts wall. As said before, electrical activity moving away from a positive electrode, causes a negative deflection on an ECG. As the transmural ischaemic region is depolarised during the resting and repolarisation phase, the TQ interval is negatively deflected. Again, the TQ interval is adjusted to be the isoelectric baseline of the specific electrode, therefore the ST segment appears elevated. See the representation below which brilliantly depicts how the TQ section (in red) is depressed, therefore when brought to the 0 mV isoelectric baseline, the ST segment appears as elevated. The reason that the ST segment is not elevated or depressed in this state, again, is because that the NET change in electrical activity practically ‘cancels’ itself out. The appearance of ST elevation is solely due to the readjustment of the TQ interval isoelectric baseline, due to transmural ischaemia.
The other main theory, the ‘Systolic Current of Injury’ discusses how there is no voltage gradient between ischaemic and normally functioning cardiac tissues, but that ischaemic myocytes repolarise earlier in the cardiac cycle (therefore T waves are superimposed on the QRS complex, giving an appearance of ST elevation). Both models are theories that have not yet been fully proven or clarified, yet they give more of an understanding to an interpretation as to why ST changes are seen.