ECG is the summated recording of individual myocyte electrical activity from the body surface .The single cell action potential represent the classical description of ionic flows within and outside the cardiac myocyte. ECG is nothing but the electrical recording of systematic flow of ionic currents. When one looks at qrs complex we should mentally see the Na ions getting in .When the ST/QT segment begins the calcium enters ( Some chloride also ) and K + begins to leave cells .As we look at the sharp or blunted T waves we are actually looking at potassium channel activity.
The phase 0 is the rapid inflow of sodium ions into the cell. Contrary to this , during the repolarisation of myocytes the efflux of potassium from the cells occur more slowly .This , along with slow calcium influx create the sustained dome of action potential .The phase 3 begins with a rapid efflux of k+ which corresponds to inscription of T waves.Phase 4 occurs in diastolic depolariation .
Note : *Na exit from cells occur very fast ( Which is not mentioned in the diagram .This again is an important event . Pharmacologically Na channel manipulation is often done .All class 1 anti arrhythmic drugs block this channel.
It’s obvious , T wave genesis is greatly influensed by k+ dynamics.A tall t wave indicate high intracellular concentration of k and efflux of K + further slowed down as reduced gradient acrosss the cell membrane.This results in tall t waves.There is a fairly good correlation between K+ levels and T wave amplitude.Similarly when there is hypokalemia , there is inversion of T waves with associated with prolongation of QT interval.
While T waves are linked to K + , the QRS complex is closely linked to Na + concentration , but still sodium levels rarely alter the QRS complex why ?
Hyponatremia is a common electrolytic disorder , especially in elderly and in patients who are over treated with diuretics. Dilutional hyponatremia due to excess free water is a common finding in CHF.While ECG is very helpful to diagnose hyperkalemia , it is rarely useful in hypo or hypernatremia.
This is primarily due to two reasons .The Na induced depolarisation is a very fast event ( Max 80ms) . K+ efflux is a slow event up to 400 ms . Unlike K + , Na+ can not prolong the QT interval however low it’s levels are . This is due to the fact Sodium channels have a huge gradient across the cell even if the serum sodium levels fall. Further, Na is an extra cellular cation and has little influence within the myocyte. But , occasionally wide qrs complex or aberrant conduction , bundle branch defects are observed due to hypo or hypernatremia .The exact mechanism is not known.
Conduction defects and electrolytes
Similarly K+ ions have major effects on SA node and AV node .It can depress them , though reversibly it can have serious consequences. It is very rare for Na+ to have any major effect on conduction tissues. Multiple electrolytic defects with associated acidosis can have variable effect on ECG morphology .Abnormal calcium and magnesium levels can have serious effects of cardiac excitabillty.
Note : *Na exit from cells occur very fast ( Which is not mentioned in the diagram ) .This again is an important event . Pharmocologically Na channel manipulation is done with all class 1 anti arrhythmic drugs act on this channel.