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Weakness and palpitations after rapid weight loss for a boxing weigh-in

The case

22-year-old man. Weakness and palpitations after rapid weight loss for a boxing weigh-in

He has lost 7 kg in twelve days by restricting food and fluids, inducing vomiting and using stimulant laxatives. He takes no prescribed medication and has no known cardiac history.

On arrival

HR
54
GCS
15
SpO₂ (%)
99
Respiratory rate
16
Temperature (°C)
36.5
Systolic BP (mmHg)
98
Diastolic BP (mmHg)
58

Stage 1 of 2

He feels weak but is alert and talking. His pulse is slow with occasional early beats. A twelve-lead is recorded while intravenous access is obtained.

Tracing 1 of 2 for the quiz “Weakness and palpitations after rapid weight loss for a boxing weigh-in”.
Twelve-lead recorded on arrival, 25 mm/s, 10 mm/mV. Open this tracing in the studio

Observations

HR
54
SpO₂ (%)
99
Respiratory rate
16
Temperature (°C)
36.5
Systolic BP (mmHg)
98
Diastolic BP (mmHg)
58
Which description best fits this tracing?

The tracing shows sinus bradycardia at about 54 beats per minute with low-amplitude, flattened T waves, ST depression visible across the precordial and limb leads, and prominent U waves following the T waves. Tall peaked T waves and QRS widening would point to hyperkalaemia, which is the opposite picture. Diffuse ST elevation with PR depression describes pericarditis, and a short QT with normal T waves suggests hypercalcaemia, neither of which matches.

Which biochemical abnormality is most strongly suggested by this combination?

Flattened T waves, ST depression and prominent U waves are the classic triad of severe hypokalaemia. The history of vomiting, laxative abuse and fluid restriction makes potassium loss overwhelming. Severe hyperkalaemia produces the opposite ECG picture with tall peaked T waves and QRS widening. Isolated hyponatraemia does not produce characteristic ST or T-wave changes, and hypercalcaemia shortens the QT interval rather than prolonging it.

Stage 2 of 2

While the first blood sample is being sent, he says he feels faint and then becomes unresponsive. The monitor records this rhythm. No pulse is palpable.

Tracing 2 of 2 for the quiz “Weakness and palpitations after rapid weight loss for a boxing weigh-in”.
Monitor strip recorded at the moment of deterioration, 25 mm/s, 10 mm/mV. Open this tracing in the studio

Bloods

Sodium (mmol/L)
137
Magnesium (mmol/L)
0.54
Potassium (mmol/L)
2.1
Calcium, adjusted (mmol/L)
2.29
What rhythm does the monitor strip show?

The strip shows a wide-complex tachycardia at about 225 beats per minute with a continuously shifting QRS axis, the complexes waxing and waning in amplitude in the characteristic spindle pattern. This undulating morphology distinguishes torsades de pointes from monomorphic ventricular tachycardia, which has a fixed axis. Ventricular fibrillation is disorganised without repeating complexes, and movement artifact would not produce regular, evolving QRS morphology.

What is the immediate action while he remains pulseless in this rhythm?

Torsades de pointes causing cardiac arrest is a shockable rhythm and the immediate action is unsynchronised defibrillation, following standard cardiac arrest algorithms. Intravenous magnesium is the specific treatment for preventing recurrence but does not replace or precede the shock in a pulseless patient. Synchronised cardioversion requires a reliable R wave to synchronise on, which the shifting axis of torsades does not provide. Amiodarone prolongs the QT interval and is contraindicated in torsades.

Diagnosis

Severe hypokalaemia with prominent U waves progressing to torsades de pointes

Rapid weight loss by vomiting, fluid restriction and laxative abuse depletes potassium, magnesium and total body water. The twelve-lead on arrival already showed the signature of severe hypokalaemia: flattened T waves merging with prominent U waves, ST depression and a prolonged QT/QU interval. These changes lengthen repolarisation and set the stage for torsades de pointes, which is what the monitor captured when he became pulseless.

The immediate treatment of pulseless torsades is defibrillation, exactly as for any cardiac arrest in a shockable rhythm. Intravenous magnesium is the specific antiarrhythmic for torsades but follows the shock, not the other way round. Amiodarone, which itself prolongs the QT, is avoided.

References

  1. Diercks DB, Shumaik GM, Harrigan RA, Brady WJ, Chan TC. Electrocardiographic manifestations: electrolyte abnormalities. J Emerg Med 2004;27(2):153-160.
  2. Soar J, Bottiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support. Resuscitation 2021;161:115-151.
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This tracing was generated, not recorded. It opens in the studio with every dial live.

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