Research Article Lactate Arterial-Central Venous Gradient among COVID-19 PatientsinICU:APotentialToolintheClinicalPractice Giuseppe Nardi , 1 Gianfranco Sanson , 2 Lucia Tassinari, 1 Giovanna Guiotto, 3 Antonella Potalivo, 1 Jonathan Montomoli, 1 andFernandoSchiraldi 4 1 Dept. of Anaesthesia and Intensive Care, Infermi Hospital, Viale Settembrini 2, 47921 Rimini, Italy 2 Clinical Dept. of Medical, Surgical and Health Sciences, University of Trieste, Strada Di Fiume 447, 34149 Trieste, Italy 3 Dept of Emergency Medicine, AORN San Pio, Via Pacevecchia 53, 82100 Benevento, Italy 4 Emergency Dept San Paolo Hospital, Via Terracina, 80125 Naples, Italy Correspondence should be addressed to Giuseppe Nardi; 4doctornardi@gmail.com Received 24 April 2020; Revised 16 June 2020; Accepted 3 August 2020; Published 25 September 2020 Academic Editor: Timothy E. Albertson Copyright © 2020 Giuseppe Nardi et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. e aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference. Methods. A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T 0 ) and 24 hours after canakinumab administration (T 1 ). Results. At T 0 , 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07–0.25). In the 13 patients undergoing canakinumab administration, at T 1 , Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T 0 : median 0.24, IQR 0.09–0.31 mmol/L; T 1 : median −0.01, IQR −0.08–0.04 mmol/L; p � 0.002). Con- clusion. A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies. 1.Background e role of serial lactate determinations in critically ill pa- tients is well agreed and may be useful in tailoring the therapy in many different diseases [1–3]. ere is consensus about the two mainly observed forms of raised blood lactate concentration: lactic acidosis due to O 2 -demand/DO 2 mismatch [4] and hyperlactatemia with near-normal arterial pH, the latter being substantially linked to hypermetabolic stress, or inherited disease [5]. In physiological conditions, arterial blood lactate con- centration is equal to or lower than central venous blood lactate concentration (Delta a-cv lactate, normal value ≤ 0 mmol/L) [6]. Less is known about the meaning of a Delta a-cv lactate reversal (a-cv difference > 0 mmol/L), which could reflect a derangement in the mitochondrial meta- bolism of lung cells induced by inflammation or other uncoupling mediators, likely to be responsible for the large lung parenchymal disruption (acute respiratory distress syndrome- (ARDS-) like) [7]. Indeed, De Backer et al. [8] Hindawi Critical Care Research and Practice Volume 2020, Article ID 4743904, 5 pages https://doi.org/10.1155/2020/4743904