Effect of extracorporeal carbon dioxide removal on respiratory quotient measured by indirect calorimetry: Unravelling the mystery.

NEW FINDINGS: What is the main observation in this case? Several studies have reported progressive hypoxaemia once extracorporeal carbon dioxide removal is started in patients with hypercapnic respiratory failure, possibly attributable to an altered respiratory quotient. What insights does it reveal? In this quality control report, we show that the respiratory quotient exhibits only minimal alteration when extracorporeal carbon dioxide removal is started and assume that the progressive hypoxaemia is attributable to an increase in intrapulmonary shunt. ABSTRACT: The use of extracorporeal carbon dioxide removal (ECCO2 R) has been proposed in patients with acute respiratory distress syndrome to achieve lung-protective ventilation and in patients with selective hypercapnic respiratory failure. However, several studies have reported progressive hypoxaemia, as expressed by a need to increase the inspired oxygen fraction (Fi O2 ) to maintain adequate oxygenation or by a decrease in the ratio of arterial oxygen tension (Pa O2 ) to Fi O2 once ECCO2 R is started. We present the case of a patient who was admitted to the intensive care unit for a coronavirus disease 2019 pneumonia and who was intubated because of hypercapnic respiratory insufficiency. Extracorporeal carbon dioxide removal was started, and the patient subsequently developed progressive hypoxaemia. To test whether the hypoxaemia was attributable to the ECCO2 R, blood samples were taken in different settings: (1) 'no ECCO2 R', blood flow 150 ml/min with a ECCO2 R gas flow of 0 L/min; and (2) 'with ECCO2 R', blood flow 400 ml/min with gas flow 12 L/min. We measured Pa O2 , alveolar oxygen tension, Pa O2 /Fi O2 , alveolar-arterial oxygen tension difference, arterial carbon dioxide tension and the respiratory quotient (RQ) by indirect calorimetry in each setting. The RQ was 0.60 without ECCO2 R and 0.57 with ECCO2 R. The alveolar oxygen tension was 220.4 mmHg without ECCO2 R and increased to 240.3 mmHg with ECCO2 R, whereas Pa O2 /Fi O2 decreased from 177 to 171. Our study showed only a minimal change in RQ when ECCO2 R was started. We were the first to measure the RQ directly, before and after the initiation of ECCO2 R, in a patient with hypercapnic respiratory failure.

Signs of post-traumatic hypovolemia on abdominal CT and their clinical importance: A systematic review.

PURPOSE: Our aim was to assess the findings of hypovolemia on abdominal CT that are most frequently seen in blunt abdominal trauma patients. When possible, we assessed the correlation of these CT signs with clinical outcome. METHODS: MEDLINE, CENTRAL and EMBASE were systematically searched. Two reviewers independently screened and included articles and performed the data-extraction. Primary outcomes of interest were the frequency of each sign and its correlation with mortality. Secondary outcomes were need for intervention, transfusion need, intensive care unit admission rate and length of stay. RESULTS: A flat inferior vena cava and an inferior vena cava halo, a diminished aortic calibre, shock bowel, altered enhancement of the liver, pancreas, adrenals, kidneys, spleen and gallbladder, peripancreatic fluid and splenic volume changes have been described in the setting of hypovolemic trauma patients to constellate a CT hypovolemic shock complex. It is argued that vascular signs represent the true hypovolemic state and the visceral signs represent hypoperfusion. There is no consensus on the frequency or clinical relevance of these signs, which at least partly can be explained by the heterogeneity in study design, study population, scanning protocols and outcome parameters. Available evidence suggests a good predictive value for occult shock and a higher mortality rate when a flat inferior vena cava is present. Evidence regarding the other signs is scarce. CONCLUSIONS: The hypovolemic shock complex is an entity of both vascular and visceral CT signs that can be seen in blunt trauma patients. It can offer guidance to a swift primary imaging survey in the acute trauma setting, allowing the radiologist to alert the treating physicians to possible pending hypovolemic shock.

Performance of an active inspired hypoxic guard.

Current hypoxic guards systems fail to maintain the inspired O2 concentration (FIO2) ≥ 21 % across the entire fresh gas flow (FGF) range when a second carrier gas is used (N2O or air). We examined the performance of the Maquet O2 Guard(®), a smart hypoxic guard that increases O2 delivery if an inspired hypoxic mixture is formed. After obtaining IRB approval and informed consent, 12 ASA I-II patients were enrolled. During anesthesia with sevoflurane in O2/air, the O2 Guard(®) was tested by administering O2/air at the following delivered hypoxic guard limits [expressed as (total FGF in L min(-1); FDO2 in %)] for 4 min each: [0.3;67], [0.4;50], [0.6;34], [0.8;25], [1.0;21], [1.2;21], [1.5;21], [2;21], [3;21], and [5;21]. The following data were collected: (1) time from FIO2 = 30 to 20 %; (2) time from FIO2 = 20 % to O2 Guard(®) activation; (3) time from O2 Guard(®) activation to FIO2 = 25 %; (4) FGF and FDO2 used by the O2 Guard. If SpO2 was <90 % for 10 s or longer at any time, the patient was excluded. Three patients were excluded for low SpO2. The incidence of FIO2 < 21 % was 100 % within the 1-2 L min(-1) FGF range. The O2 Guard(®) was activated within 20 s after FIO2 became 20 %, except in one patient where FIO2 oscillated between 20 and 21 %. FDO2 was increased to 60 % and FGF to 1 L min(-1) (the latter only if it was lower than 1 L min(-1) prior to activation of the O2 Guard). FIO2 increased to 25 % within 55 s after O2 Guard activation in all patients. The O2 Guard(®), an active inspired hypoxic guard, rapidly reverses and limits the duration of inspired hypoxic episodes when the delivered hypoxic guard fails to do so.