ECG Based Serum Potassium Estimation

Potassium is the most abundant cation found in the human body with concentration levels of approximately 55mEq/Kg body weight [1]. A major portion of this Potassium is found in intracellular compartments (most generously in muscle and bone cells) with concentrations of approximately 150 mmol/L while the concentration of potassium in the extracellular fluid is strictly maintained between 3.5 and 5.5 mmol/L [2]. The exclusive source of Potassium is dietary (approximately 100mEq per day) and counterbalanced by excretion through urine (90%), stool and sweat (10%) [3]. Though the homeostasis of Serum Potassium is maintained heavily by the kidneys [4], the effects of its fluctuations can be felt across the body, most commonly affected tissues being skeletal, cardiac and gastrointestinal muscles [5]. One of the reasons for these widespread effects to Potassium level fluctuations is its involvement as the main ion responsible for the repolarization phase of action potentials in all cells of the body [6].

Due to the effects of Potassium fluctuations in the cardiac muscles, widespread ECG changes are often noted in both Hypokalemia and Hyperkalemia patients. These changes include (Table 1).

Table 1:

Problem Statement

However, these changes only occur after the levels of Serum Potassium have gone up or down, there is no indication to predict when these changes will occur and by extension when and how much of variations in Serum Potassium levels the patient will suffer. Even when the patients start experiencing symptoms, blood tests often take too long to report the fluctuations.

Aim

The aim of this paper is to present a method of Serum Potassium level estimation from ECG tracings.

A multi-centric clinical trial was carried out across 4 hospitals in India with a total patient count of 1306.

Inclusion Criteria

a) Adult patients above 14 years of age.

b) 611 patients of Hyperkalemia.

c) 695 patients of Hypokalemia.

d) In-patient admissions (for ease of follow-ups).

Exclusion Criteria

a) Patients below 14 years of age.

b) Patients without pathologies known to cause Hyperkalemia or Hypokalemia.

c) Patients treated in outpatient departments.

For each patient, we reported blood tests for Serum Potassium and 12-lead ECGs for each patient during admission and after their Potassium levels have stabilised.

Rising Potassium levels

For a rising Serum Potassium (patients being treated for Hypokalemia), every 0.2mV (2 small squares) increase in T-wave height in a 12-lead ECG corresponded with approximately 0.7mEq/L increase in Serum Potassium levels. From this equation, once the initial Potassium level: T-wave proportion was mapped, we were able to calculate the patients’ Potassium levels and verify it with the blood reports later (Figure 1).

Falling Potassium levels

Again, for a reducing Serum Potassium (patients being treated for Hyperkalemia), 0.2mV (2 small squares) decrease in T-wave height corresponded with approximately 0.7mEq/L decrease in Serum Potassium levels. Here also we mapped the initial Potassium level: T-wave proportion and calculated the patients’ Potassium levels and verified it with the blood reports (Figure 2).

From the above calculations it is very obvious that the method of calculating Serum Potassium levels from T-wave heights in ECGs is not only extremely accurate but also non-invasive and less timeconsuming. Utilizations of these equations can be most useful in cardiac monitored beds (e.g. ICU, CCU, HDU etc.) where Potassium levels can be continuously displayed without any extra hardware, any expertise or any invasive procedures. This can help clinicians assess very subtle changes in Serum Potassium levels as and when they occur.

None.

No conflict of Interest.