An essential player in maintenance of electrolyte balance and blood pressure, ACE2 is regarded by many as the principal counter‐regulatory arm in the axis of renin–angiotensin‐aldosterone system (RAAS; Santos, Ferreira, & Simões e Silva, 2008). Upon infection, SARS‐CoV‐2 binds ACE2. This results in degradation of ACE2, which subsequently dampens the counter‐effect of ACE2 on RAAS. The final effect of ACE2 in an otherwise healthy adult is to increase reabsorption of sodium and the reciprocal excretion of potassium ions (K+). The concomitant re‐uptake of water with sodium reabsorption prompts an increase in blood pressure (Weir & Rolfe, 2010). Potassium is the predominant intracellular ion, that is majorly involved in regulation of cell membrane polarity. Too low levels of K+ in blood, known as hypokalemia, can result in cellular hyper‐polarity. A hyper‐polarized cell membrane tends to be depolarized faster than normal, causing aberrancy in the function of cardiac cells (Bielecka‐Dabrowa et al., 2012).