oxygen consumption is depressed in patients with lactic acidosis due to biguanide intoxication耗氧乳酸酸中毒患者的抑郁是由于双胍中毒.pdfVIP

Protti et al. Critical Care 2010, 14:R22 /content/14/1/R22 R E S E A R C H Open Access Research Oxygen consumption is depressed in patients with lactic acidosis due to biguanide intoxication 1 1 2 3 4 5 2 Alessandro Protti* , Riccarda Russo , Paola Tagliabue , Sarah Vecchio , Mervyn Singer , Alain Rudiger , Giuseppe Foti , 6 7 1 Anna Rossi , Giovanni Mistraletti and Luciano Gattinoni Abstract Introduction: Lactic acidosis can develop during biguanide (metformin and phenformin) intoxication, possibly as a consequence of mitochondrial dysfunction. To verify this hypothesis, we investigated whether body oxygen consumption (VO2), that primarily depends on mitochondrial respiration, is depressed in patients with biguanide intoxication. Methods: Multicentre retrospective analysis of data collected from 24 patients with lactic acidosis (pH 6.93 ± 0.20; lactate 18 ± 6 mM at hospital admission) due to metformin (n = 23) or phenformin (n = 1) intoxication. In 11 patients, VO was computed as the product of simultaneously recorded arterio-venous difference in O content [C(a-v)O ] and 2 2 2 cardiac index (CI). In 13 additional cases, C(a-v)O2, but not CI, was available. Results: On day 1, VO 2 2 2 was markedly depressed (67 ± 28 ml/min/m ) despite a normal CI (3.4 ± 1.2 L/min/m ). C(a-v)O2 was abnormally lo