Peaked T waves in a patient taking digoxin
A 68-year-old man with chronic kidney disease (eGFR 25 mL/min/1.73 m²) is admitted with nausea, palpitations and muscle weakness. He takes digoxin 0.25 mg daily for heart failure and has had gastroenteritis for three days. Investigations show serum K+ 6.9 mmol/L (reference 3.5–5.0), Na+ 134 mmol/L, creatinine 3.1 mg/dL, and a digoxin level above the therapeutic range. The ECG shows tall peaked T waves, PR prolongation and a QRS duration of 130 ms. Intracellular K+ is taken as 140 mmol/L and body temperature as 37 °C, where RT/F ≈ 26.7 mV. A junior doctor, remembering that digoxin toxicity is classically associated with low potassium, proposes giving 20 mmol KCl. The registrar instead orders intravenous calcium gluconate and an insulin–glucose infusion while potassium is monitored.
1. Using the Nernst equation, calculate the potassium equilibrium potential at extracellular K+ of 4.0 and 6.9 mmol/L, and state the expected effect on the resting membrane potential.
Read the worked answer
EK = (RT/F) ln([K+]out/[K+]in) = 26.7 ln([K+]out/140).
- At 4.0 mmol/L: ln(4.0/140) = ln 0.0286 = −3.56, so EK = 26.7 × (−3.56) = −95 mV.
- At 6.9 mmol/L: ln(6.9/140) = ln 0.0493 = −3.01, so EK = 26.7 × (−3.01) = −80 mV.
The change is about +15 mV, i.e. a less negative EK. Because the resting membrane potential is dominated by potassium permeability (with a small sodium leak pulling it above EK), the resting potential shifts in the same direction, from roughly −90 mV towards roughly −75 mV. The direction is the key point: raising extracellular potassium reduces the concentration gradient, so potassium's outward driving force falls and the membrane depolarises. This is the opposite of what happens in hypokalaemia, where the resting potential becomes more negative.
2. Explain how this change in resting potential produces the ECG findings and why giving KCl would be dangerous.
Read the worked answer
A resting potential of about −75 mV instead of −90 mV keeps a fraction of voltage-gated Na+ channels in the inactivated state, because inactivation is set by sustained depolarisation. On stimulation fewer Na+ channels are available, so phase 0 is slower and smaller, conduction velocity falls, and the QRS widens - matching the 130 ms QRS and the PR prolongation. Peaked T waves reflect the altered repolarisation that accompanies the changed potassium gradient. Slow and uneven conduction favours re-entry, which is why hyperkalaemia causes ventricular arrhythmias and can progress to a sine-wave pattern and asystole.
Giving 20 mmol KCl would raise extracellular K+ further, depolarise the membrane more, and inactivate still more Na+ channels - it could precipitate cardiac arrest. Digoxin adds to the problem because it inhibits Na+/K+-ATPase, the very pump needed to keep potassium inside cells. The junior doctor has confused a true association (hypokalaemia predisposes to digoxin toxicity) with this patient's actual emergency, which is hyperkalaemia.
3. Justify the choice of calcium gluconate and of insulin–glucose as two different kinds of treatment.
Read the worked answer
They act at different levels and are not alternatives.
- Calcium gluconate acts within minutes on the myocardium. Raising extracellular Ca2+ raises the threshold for excitation and opposes the depolarising effect of hyperkalaemia, so the ECG changes reverse and the risk of arrhythmia falls. It moves no potassium at all; it treats the membrane, not the number.
- Insulin–glucose stimulates Na+/K+-ATPase and drives potassium into cells, lowering serum K+ over roughly 15–30 minutes. Glucose is included to prevent hypoglycaemia from the insulin. This redistributes potassium but does not remove it from the body.
In renal failure neither measure eliminates potassium, so dialysis or a potassium binder is eventually required. The correct sequence is membrane stabilisation first when ECG changes are present, then intracellular shifting, then elimination - and monitoring for rebound hyperkalaemia as the insulin effect wears off.