A 69-year-old man was admitted for elective coronary artery bypass grafting. He had a history of chronic hypotension that caused him to have occasional dizziness upon standing and at the time of his exercise test he was noted to have low blood pressure. Subsequent coronary angiography showed poor left ventricular function but, due to his low blood pressure, he was not started upon Angiotensin Converting Enzyme inhibitors. During pre-operative assessment, his left brachial blood pressure was measured as 82/44 mmHg using a sphygmomanometer. When the left radial artery was subsequently cannulated prior to surgery, it showed a pressure of 85/50 mmHg which corresponded to a pressure of 88/54 mmHg measured at the same time noninvasively on the right arm. However, on review prior to the induction of anaesthesia, it was noted that at cardiac catheterisation the pressure measured in the aorta had been 178/88 mmHg and so a femoral arterial line was inserted. This measured a pressure of 165/85 mmHg. During the operation and cardiopulmonary bypass (CPB) the femoral arterial line was used for pressure monitoring and the mean arterial pressure (MAP) was maintained at 85 mmHg. This pressure was higher than we would normally use during CPB but it equated with a mean pressure in the radial artery of 55 mmHg. His postoperative course was uneventful and he recovered with no neurological problems. A postdischarge Duplex scan showed no flow to either common internal or external carotid arteries, the subclavian arteries were damped and the only patent arterial supply to the brain was a markedly enlarged right vertebral artery. Subsequent CT angiography showed that the left brachiocephalic artery was occluded with the distal subclavian filling by collaterals. It is well recognised that following the onset of CPB a pressure gradient may develop between the radial and femoral arteries [1]. Because the femoral pressure equates more consistently with the aortic pressure, it is increasingly used to monitor blood pressure of patients undergoing cardiac surgery. In our patient, a significant gradient existed even before surgery was begun but it was only appreciated when both the femoral and the radial arterial pressures were measured simultaneously prior to the induction of anaesthesia. If, as is common practice, a femoral arterial line had been used from the outset, then a lower mean arterial pressure would have been maintained during bypass. Since a large fixed gradient already existed between the femoral and the radial arteries, a lower femoral pressure would have produced a very low radial pressure but this would have gone unnoticed. Fortunately, the simultaneous monitoring of a radial and femoral arterial pressure revealed a large femoral–radial pressure gradient, and alerted us to bilateral subclavian arterial disease and the possibility of carotid disease. By assuming a correlation between radial MAP and cerebral perfusion pressure and maintaining the radial MAP at 55 mmHg during CPB, we achieved a cerebral perfusion pressure adequate to prevent detectable cerebral injury. If femoral lines are being routinely used to monitor blood pressure during cardiac surgery, or indeed other major surgery, then we would recommend that the pressure in the upper limbs be assessed noninvasively to exclude a significant femoral–radial pressure gradient. The presence of a large gradient may reflect impaired cerebral circulation and would be an indication for maintaining higher femoral pressures throughout the procedure.