A 25 year old male well known to your ED for Cannabis hyperemesis syndrome, presents after numerous syncope during the day. He has an episode of loss of consciousness in ED while monitored and is found to e going into Torsades de Pointe.

Metabolic Alkalosis – pH 7.47 HCO3 36mmol/l

Expected PCO2 = 0.7 X HCO3 + 20 = 46mmHg

Lactate borderline high, severely low potassium and moderately low sodium and chloride

The above VBG shows a fully compensated metabolic alkalaemia associated with a severe hypokalaemia and moderate hyponatraemia and hypochloraemia

In this clinical setting the hypochloraemic metabolic alkalosis is due to vomiting and volume contraction.  Other causes to consider would be diuretic use and hyperaldosteronism, however in this case the sodium is low. (in hyperaldosteronism there is hypokalaemia and a mild hypernatraemia).  Bicarbonate retention in hypochloraemia and hypokalaemia can also be a cause for the alkalosis.  Recall CLEVERPD for other causes of metabolic alkalosis – these are unlikely in this case. The hypokalaemia results in prolonged QT leading to torsades, and there is likely an underlying hypomagnesemia

For Torsades to be diagnosed the patient has to have evidence of both polymorphic VT and QT prolongation

The management of Torsades

• If pulseless – follow ALS pulseless VT algorithm – Shock 200J
• If in extremis – synchronised cardioversion
• MgSO4 5mmol over 10min followed by 20mmol over 4 hours
• Replace electrolytes – potassium and calcium
• In case of heart block or bradycardia – over drive pacing, adrenalin or isoprenaline infusion.
• Alkalinisation if due to sodium channel blockade