Nursing care
Hypokalaemia vs hyperkalaemia: ECG changes, muscle findings and first priorities
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated October 2026
Short answer
Low potassium flattens T waves, depresses ST segments and produces prominent U waves; high potassium causes peaked T waves, then a lengthening PR interval, loss of P waves and widening QRS. Both can cause muscle weakness and dangerous arrhythmias, so the nursing priority for either is cardiac monitoring, prompt reporting and safe replacement or removal as prescribed.
Read the T wave first
The most differentiating feature on a rhythm strip is the T wave. In hypokalaemia, T waves flatten or invert, the ST segment sags, and a U wave appears after the T wave and grows as potassium falls. In hyperkalaemia, early T waves become tall, narrow and peaked.
As hyperkalaemia worsens, the PR interval lengthens, P waves flatten and disappear, and the QRS widens until it may merge into a sine-wave pattern before ventricular fibrillation or asystole. ECG changes do not track the potassium level reliably, so a normal-looking strip does not mean a high result is safe.
Compare muscle and bowel findings
Both imbalances can cause muscle weakness, which is why weakness alone does not identify the direction. Hypokalaemia commonly brings muscle cramps, fatigue, reduced bowel movement or ileus, and in severe cases paralysis that can involve respiratory muscles. Constipation and abdominal distension in a patient on diuretics are classic clues. Checking bowel sounds and asking about bowel habits can therefore support the assessment.
Hyperkalaemia is often silent until the heart is affected, although some patients report weakness, tingling or ascending flaccid paralysis. Because symptoms can be absent, the nurse treats a markedly high result as a potential emergency even when the patient feels well, while confirming that the sample was not haemolysed.
Link each result to its likely cause
Low potassium usually reflects loss or a shift into cells: loop and thiazide diuretics, vomiting, diarrhoea or laxative misuse, insulin treatment, and low magnesium, which makes potassium harder to correct. Patients taking digoxin are especially vulnerable, because even mild hypokalaemia increases the risk of digoxin-related arrhythmias.
High potassium usually reflects reduced kidney excretion or release from cells: kidney injury or chronic kidney disease, ACE inhibitors, angiotensin receptor blockers and potassium-sparing diuretics, metabolic acidosis, and tissue breakdown such as burns or crush injury. A falsely high result can come from red cell damage during a difficult blood draw. Reviewing the medication list and kidney function together usually explains the result.
Set the nursing priority for each
For hypokalaemia, priorities include cardiac monitoring when the level is significantly low, reviewing diuretics and digoxin, checking magnesium, and giving replacement exactly as prescribed. Intravenous potassium is diluted, given by infusion at a controlled rate under local policy, and never as a direct push. Watch the infusion site and urine output. Teach patients on diuretics to report cramps, weakness or palpitations.
For hyperkalaemia, the priority is protecting the heart: place the patient on a cardiac monitor, report promptly and prepare for prescribed treatment. Intravenous calcium stabilises the heart muscle without lowering potassium, insulin with glucose shifts potassium into cells and requires glucose monitoring, and other therapies remove potassium from the body. Hold potassium supplements pending review.
Reason through a hypothetical laboratory alert
Imagine a hypothetical client with chronic kidney disease taking an ACE inhibitor whose potassium returns markedly high. They feel well, and their scheduled potassium-rich supplement is due. The options are to give the supplement because the client is asymptomatic, recheck the level in the morning, or place the client on a monitor and notify the prescriber.
Monitoring and notifying the prescriber is the strongest response, because hyperkalaemia can cause arrhythmias without warning symptoms. The supplement should be held pending review. A morning recheck delays action, although the prescriber may request a repeat sample if haemolysis is suspected. The kidney disease and ACE inhibitor make a true elevation plausible.
Sources and further reading
MSD Manual Professional: Hypokalemia. Causes including diuretics, GI losses, insulin and hypomagnesaemia, weakness, cramps, ileus and paralysis, ST and T changes with U waves, digoxin risk and controlled IV replacement.
MSD Manual Professional: Hyperkalemia. Renal, medication, acidosis and cell-breakdown causes, pseudohyperkalaemia from haemolysis, progressive ECG changes, and calcium, insulin with glucose and removal therapies.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our dosage calculation and lab values practice questions are the closest set to what this page covers.
Common questions
What ECG change is most associated with hypokalaemia?
Flattened T waves with a prominent U wave, often with ST depression. The U wave becomes more noticeable as potassium falls further.
Why is calcium given in hyperkalaemia if it does not lower potassium?
Intravenous calcium stabilises the heart muscle membrane and reduces arrhythmia risk while other treatments shift potassium into cells or remove it from the body.
Can intravenous potassium be given as a push?
No. Intravenous potassium must be diluted and infused at a controlled rate according to policy. A direct push can cause fatal arrhythmias.
More on dosage calculation and lab values