Normotension (as in the present case) or low BP with attenuated response to vasopressors is possible in BS due to increased renal prostaglandin E2 levels, in spite of the activation of the renin-angiotensin-aldosterone axis.[2, 6] Hypokalemia, hypovolemia and positive pressure ventilation can add to haemodynamic instability.[9] Metabolic alkalosis may get corrected with the correction of hypokalemia. This evidence concerns the gene REN and Hypokalemia.