Author Response: The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (PCO2 Gap) during Resuscitation Affects ICU Outcomes: A Prospective Observational Study.

How to cite this article: Tiwari AM, Zirpe KG, Kulkarni AP. Author Response: The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (PCO2 Gap) During Resuscitation Affects ICU Outcomes: A Prospective Observational Study. Indian J Crit Care Med 2024;28(7):710.

The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (pCO2 Gap) during Resuscitation Affects ICU Outcomes: A Prospective Observational Study.

How to cite this article: Sundarsingh V, Kumar M, Rodrigues PR. The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (pCO2 Gap) during Resuscitation Affects ICU Outcomes: A Prospective Observational Study. Indian J Crit Care Med 2024;28(7):709.

CO2 gap changes compared with cardiac output changes in response to intravenous volume expansion and/or vasopressor therapy in septic shock.

Background: The difference in partial pressure of carbon dioxide (PCO2) between mixed or central venous blood and arterial blood, known as the ∆PCO2 or CO2 gap, has demonstrated a strong relationship with cardiac index during septic shock resuscitation. Early monitoring of the ∆PCO2 can help assess the cardiac output (CO) adequacy for tissue perfusion. Objectives: To investigate the value of ∆PCO2 changes in early septic shock management compared with CO. Methods: This observational prospective study included 76 patients diagnosed with septic shock admitted to Cairo University Hospital's Critical Care Department between December 2020 and March 2022. Patients were categorised by initial resuscitation response, initial ∆PCO2 and 28-day mortality. The primary outcome was the relationship between the ∆PCO2 and CO changes before and after initial resuscitation, with secondary outcomes including ICU length of stay (LOS) and 28-day mortality. Results: Peri-resuscitation ∆PCO2 changes predicted a ≥15% change in the cardiac index (CI) (area under the curve (AUC) 0.727; 95% CI 0.614 - 0.840) with 66.7% sensitivity and 62.8% specificity. The optimal ∆PCO2 change cut-off value was <-1.85, corresponding to a <-22% threshold for a 15% cardiac index increase. The PCO2 gap ratio (gap/gap ratio of T1- PCO2 gap to T0 -PCO2 gap) also predicted a ≥15% change in cardiac index (AUC 745; 95% CI 0.634 - 0.855) with 63.6% sensitivity and 79.1% specificity. The optimal CO2 gap/gap ratio cut-off value was <0.71. A significant difference in 28-day mortality was noted based on the gap/gap ratio. Conclusion: Peri-resuscitation ∆PCO2 and the gap/gap ratio are useful non-invasive bedside markers for predicting changes in CO and preload responsiveness. Contribution of the study: The current study provides an insight to the PCO2 gap changes during and after early resuscitation of septic shock patients, which correlate to cardiac output changes and might also serve as a fluid responsiveness indicator.

Evaluating the efficacy of a standardized 4 mL/kg fluid bolus technique in critically ill patients with elevated PvaCO2: secondary analysis of two prospective studies.

Background: Limiting the fluid bolus (FB) volume may attenuate side effects, including hemodilution and increased filling pressures, but it may also reduce hemodynamic responsiveness. The minimum volume to create hemodynamic effects is considered to be 4 mL/kg. In critically ill patients, the hemodynamic effects of FB with this volume have not been adequately investigated and compared to higher quantities. We hypothesized that a standardized FB approach using 4 mL/kg has comparable hemodynamic and metabolic effects to the common practice of physician-determined FB in critically ill patients. Methods: We conducted post hoc analysis of two trials in non-selected critically ill patients with central venous-to-arterial CO2 tension (PvaCO2) >6 mmHg and no acute bleeding. All patients received crystalloids either at a physician-determined volume and rate or at 4 mL/kg pump-administered at 1.2 L/h. Cardiac index (CI) was calculated with transthoracic echocardiogram, and arterial and venous blood gas samples were assessed before and after FB. Endpoints were changes in CI and oxygen delivery (DO2) >15%. Results: A total of 47 patients were eligible for the study, 15 of whom received physician-determined FB and 32 of whom received standardized FB. Patients in the physician-determined FB group received 16 (12-19) mL/kg at a fluid rate of 1.5 (1.5-1.9) L/h, compared to 4.1 (3.7-4.4) mL/kg at a fluid rate of 1.2 (1.2-1.2) L/h (p < 0.01) in the standardized FB group. The difference in CI elevations between the two groups was not statistically significant (8.8% [-0.1-19.9%] vs. 8.4% [0.3-23.2%], p = 0.76). Compared to physician-determined FB, the standardized FB technique had similar probabilities of increasing CI or DO2 by >15% (odds ratios: 1.3 [95% CI: 0.37-5.18], p = 0.66 and 1.83 [95% CI: 0.49-7.85], p = 0.38). Conclusion: A standardized FB protocol (4 mL/kg at 1.2 L/h) effectively reduced the volume of fluid administered to critically ill patients without compromising hemodynamic or metabolic effects.

The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (PCO2 Gap) during Resuscitation Affects ICU Outcomes: A Prospective Observational Study.

Introduction: The usual methods of perfusion assessment in patients with shock, such as capillary refill time, skin mottling, and serial serum lactate measurements have many limitations. Veno-arterial difference in the partial pressure of carbon dioxide (PCO2 gap) is advocated being more reliable. We evaluated serial change in PCO2 gap during resuscitation in circulatory shock and its effect on ICU outcomes. Materials and methods: This prospective observational study included 110 adults with circulatory shock. Patients were resuscitated as per current standards of care. We recorded invasive arterial pressure, urine output, cardiac index (CI), PCO2 gap at ICU admission at 6, 12, and 24 hours, and various patient outcomes. Results: Significant decrease in PCO2 gap was observed at 6 h and was accompanied by improvement in serum lactate, mean arterial pressure, CI and urine output in (n = 61). We compared these patients with those in whom this decrease did not occur (n = 49). Mortality and ICU LOS was significantly lower in patients with low PCO2 gap, while more patients with high PCO2 gap required RRT. Conclusion: We found that a persistently high PCO2 gap at 6 and 12 h following resuscitation in patients with shock of various etiologies, was associated with increased mortality, need for RRT and increased ICU LOS. High PCO2 gap had a moderate discriminative ability to predict mortality. How to cite this article: Zirpe KG, Tiwari AM, Kulkarni AP, Vaidya HS, Gurav SK, Deshmukh AM, et al. The Evolution of Central Venous-to-arterial Carbon Dioxide Difference (PCO2 Gap) during Resuscitation Affects ICU Outcomes: A Prospective Observational Study. Indian J Crit Care Med 2024;28(4):349-354.

Can perioperative pCO2 gaps predict complications in patients undergoing major elective abdominal surgery randomized to goal-directed therapy or standard care? A secondary analysis.

The difference between venous and arterial carbon dioxide pressure (pCO2 gap), has been used as a diagnostic and prognostic tool. We aimed to assess whether perioperative pCO2 gaps can predict postoperative complications. This was a secondary analysis of a multicenter RCT comparing goal-directed therapy (GDT) to standard care in which 464 patients undergoing high-risk elective abdominal surgery were included. Arterial and central venous blood samples were simultaneously obtained at four time points: after induction, at the end of surgery, at PACU/ICU admission, and PACU/ICU discharge. Complications within the first 30 days after surgery were recorded. Similar pCO2 gaps were found in patients with and without complications, except for the pCO2 gap at the end of surgery, which was higher in patients with complications (6.0 mmHg [5.0-8.0] vs. 6.0 mmHg [4.1-7.5], p = 0.005). The area under receiver operating characteristics curves for predicting complications from pCO2 gaps at all time points were between 0.5 and 0.6. A weak correlation between ScvO2 and pCO2 gaps was found for all timepoints (ρ was between - 0.40 and - 0.29 for all timepoints, p < 0.001). The pCO2 gap did not differ between GDT and standard care at any of the selected time points. In our study, pCO2 gap was a poor predictor of major postoperative complications at all selected time points. Our research does not support the use of pCO2 gap as a prognostic tool after high-risk abdominal surgery. pCO2 gaps were comparable between GDT and standard care. Clinical trial registration Netherlands Trial Registry NTR3380.

Hypoperfusion context as a predictor of 28-d all-cause mortality in septic shock patients: A comparative observational study.

BACKGROUND: As per the latest Surviving Sepsis Campaign guidelines, fluid resuscitation should be guided by repeated measurements of blood lactate levels until normalization. Nevertheless, raised lactate levels should be interpreted in the clinical context, as there may be other causes of elevated lactate levels. Thus, it may not be the best tool for real-time assessment of the effect of hemodynamic resuscitation, and exploring alternative resuscitation targets should be an essential research priority in sepsis. AIM: To compare the 28-d mortality in two clinical patterns of septic shock: hyperlactatemic patients with hypoperfusion context and hyperlactatemic patients without hypoperfusion context. METHODS: This prospective comparative observational study carried out on 135 adult patients with septic shock that met Sepsis-3 definitions compared patients with hyperlactatemia in a hypoperfusion context (Group 1, n = 95) and patients with hyperlactatemia in a non-hypoperfusion context (Group 2, n = 40). Hypoperfusion context was defined by a central venous saturation less than 70%, central venous-arterial PCO2 gradient [P(cv-a)CO2] ≥ 6 mmHg, and capillary refilling time (CRT) ≥ 4 s. The patients were observed for various macro and micro hemodynamic parameters at regular intervals of 0 h, 3 h, and 6 h. All-cause 28-d mortality and all other secondary objective parameters were observed at specified intervals. Nominal categorical data were compared using the χ2 or Fisher's exact test. Non-normally distributed continuous variables were compared using the Mann-Whitney U test. Receiver operating characteristic curve analysis with the Youden index determined the cutoff values of lactate, CRT, and metabolic perfusion parameters to predict the 28-d all-cause mortality. A P value of < 0.05 was considered significant. RESULTS: Patient demographics, comorbidities, baseline laboratory, vital parameters, source of infection, baseline lactate levels, and lactate clearance at 3 h and 6 h, Sequential Organ Failure scores, need for invasive mechanical ventilation, days on mechanical ventilation, and renal replacement therapy-free days within 28 d, duration of intensive care unit stay, and hospital stay were comparable between the two groups. The stratification of patients into hypoperfusion and non-hypoperfusion context did not result in a significantly different 28-d mortality (24% vs 15%, respectively; P = 0.234). However, the patients within the hypoperfusion context with high P(cv-a)CO2 and CRT (P = 0.022) at baseline had significantly higher mortality than Group 2. The norepinephrine dose was higher in Group 1 but did not achieve statistical significance with a P > 0.05 at all measured intervals. Group 1 had a higher proportion of patients requiring vasopressin and the mean vasopressor-free days out of the total 28 d were lower in patients with hypoperfusion (18.88 ± 9.04 vs 21.08 ± 8.76; P = 0.011). The mean lactate levels and lactate clearance at 3 h and 6 h, CRT, P(cv-a)CO2 at 0 h, 3 h, and 6 h were found to be associated with 28-d mortality in patients with septic shock, with lactate levels at 6 h having the best predictive value (area under the curve lactate at 6 h: 0.845). CONCLUSION: Septic shock patients fulfilling the hypoperfusion and non-hypoperfusion context exhibited similar 28-d all-cause hospital mortality, although patients with hypoperfusion displayed a more severe circulatory dysfunction. Lactate levels at 6 h had a better predictive value in predicting 28-d mortality than other parameters. Persistently high P(cv-a)CO2 (> 6 mmHg) or increased CRT (> 4 s) at 3 h and 6 h during early resuscitation can be a valuable additional aid for prognostication of septic shock patients.

Veno-arterial CO2 difference and lactate for prediction of early mortality after cardiac arrest.

Patients admitted to intensive care after cardiac arrest are at risk of circulatory shock and early mortality due to cardiovascular failure. The aim of this study was to evaluate the ability of the veno-arterial pCO2 difference (∆pCO2 ; central venous CO2 - arterial CO2 ) and lactate to predict early mortality in postcardiac arrest patients. This was a pre-planned prospective observational sub-study of the target temperature management 2 trial. The sub-study patients were included at five Swedish sites. Repeated measurements of ∆pCO2 and lactate were conducted at 4, 8, 12, 16, 24, 48, and 72 h after randomization. We assessed the association between each marker and 96-h mortality and their prognostic value for 96-h mortality. One hundred sixty-three patients were included in the analysis. Mortality at 96 h was 17%. During the initial 24 h, there was no difference in ∆pCO2 levels between 96-h survivors and non-survivors. ∆pCO2 measured at 4 h was associated with an increased risk of death within 96 h (adjusted odds ratio: 1.15; 95% confidence interval [CI]: 1.02-1.29; p = .018). Lactate levels were associated with poor outcome over multiple measurements. The area under the receiving operating curve to predict death within 96 h was 0.59 (95% CI: 0.48-0.74) and 0.82 (95% CI: 0.72-0.92) for ∆pCO2 and lactate, respectively. Our results do not support the use of ∆pCO2 to identify patients with early mortality in the postresuscitation phase. In contrast, non-survivors demonstrated higher lactate levels in the initial phase and lactate identified patients with early mortality with moderate accuracy.

Ratio of carbon dioxide veno-arterial difference to oxygen arterial-venous difference is not associated with lactate decrease after fluid bolus in critically ill patients with hyperlactatemia: results from a prospective observational study.

BACKGROUND: High ratio of the carbon dioxide veno-arterial difference to the oxygen arterial-venous difference (PvaCO2/CavO2) is associated with fluid bolus (FB) induced increase in oxygen consumption (VO2). This study investigated whether PvaCO2/CavO2 was associated with decreases in blood-lactate levels FB in critically ill patients with hyperlactatemia. METHODS: This prospective observational study examined adult patients in the intensive care unit (ICU) with lactate levels > 1.5 mmol/L who received FBs. Blood-lactate levels were measured before and after FB under unchanged metabolic, respiratory, and hemodynamic conditions. The primary outcome was blood-lactate levels after FB. Significant decreases in blood-lactate levels were considered as blood-lactate levels < 1.5 mmol/L or a decrease of more than 10% compared to baseline. RESULTS: The study enrolled 40 critically ill patients, and their median concentration of blood lactate was 2.6 [IQR:1.9 - 3.8] mmol/L. There were 27 (68%) patients with PvaCO2/CavO2 ≥ 1.4 mmHg/ml, and 10 of them had an increase in oxygen consumption (dVO2) ≥ 15% after FB, while 13 (32%) patients had PvaCO2/CavO2 < 1.4 mmHg/ml before FB, and none of them had dVO2 ≥ 15% after FB. FB increased the cardiac index in patients with high and low preinfusion PvaCO2/CavO2 (13.4% [IQR: 8.3 - 20.2] vs. 8.8% [IQR: 2.9 - 17.4], p = 0.34). Baseline PvaCO2/CavO2 was not found to be associated with a decrease in blood lactate after FB (OR: 0.88 [95% CI: 0.39 - 1.98], p = 0.76). A positive correlation was observed between changes in blood lactate and baseline PvaCO2/CavO2 (r = 0.35, p = 0.02). CONCLUSIONS: In critically ill patients with hyperlactatemia, PvaCO2/CavO2 before FB cannot be used to predict decreases in blood-lactate levels after FB. Increased PvaCO2/CavO2 is associated with less decrease in blood-lactate levels.

Treatment of Hyperlactatemia in Acute Circulatory Failure Based on CO2-O2-Derived Indices: Study Protocol for a Prospective, Multicentric, Single, Blind, Randomized, Superiority Study (The LACTEL Study).

Background: Hyperlactatemia is a biological marker of tissue hypoperfusion with well-known diagnostic, prognostic, and therapeutic implications in shock states. In daily clinical practice, it is difficult to find out the exact mechanism underlying hyperlactatemia. Central venous to arterial CO2 difference (pCO2 gap) is a better parameter of tissue hypoperfusion than the usual ones (clinical examination and mixed venous saturation). Furthermore, the ratio between the pCO2 gap and p(v-a)CO2/C(a-v)O2 may be a promising indicator of anaerobic metabolism, allowing for the identification of different causes of tissue hypoxia and hyperlactatemia. The main aim of the study is to demonstrate that initial hemodynamic resuscitation based on an algorithm integrating the pCO2 gap and p(v-a)CO2/C(a-v)O2 ratio vs. usual clinical practice in acute circulatory failure improves lactate clearance. Methods: LACTEL is a randomized, prospective, multicentric, controlled study. It compares the treatment of hyperlactatemia using an algorithm based on the pCO2 gap and P(v-a)CO2/C(a-v)O2 ratio vs. usual clinical practice in acute circulatory failure. A total of 90 patients were enrolled in each treatment group. The primary endpoint is the number of patients with a lactate clearance of more than 10% 2 h after inclusion. Lactate levels were monitored during the first 48 h of treatment as hemodynamic parameters, biological markers of organ failure, and 28-day mortality. Discussion: pCO2 derivate indices may be of better interest than routine clinical indices to differentiate causes of hyperlactatemia and diagnose anaerobiosis. LACTEL results will provide clinical insights into the role of these indices in the early hemodynamic management of acute circulatory failure in the ICU. Clinical Trial Registration: www.clinicaltrials.gov; identifier: NCT05032521.

PCO2 gap, its ratio to arteriovenous oxygen content, ScvO2 and lactate in high-risk abdominal surgery patients: An observational study.

BACKGROUND: The difference between arterial and central venous carbon dioxide partial pressure (PCO2 gap), a marker of oxygen delivery (DO2) and oxygen consumption (VO2) adequacy, has been evaluated as a promising prognostic tool in intensive care unit (ICU) patients. We therefore sought to study the association between intraoperative PCO2 gap and postoperative complications (POC) in the perioperative setting of elective major abdominal surgery. METHODS: We conducted a single-centre prospective observational study. All adult patients who underwent major planned abdominal surgery were eligible. PCO2 gap was measured every 2 h during surgery, at ICU admission and repeated 12 h and 24 h later. Severe POC within 28 days after surgery were defined as complications graded 3 or more according to Clavien-Dindo classification. Following a univariate analysis, a multivariable analysis using a logistic regression model was performed. RESULTS: Ninety patients were included and divided into two groups according to the occurrence of POC. No significant difference was found between groups regarding baseline characteristics at inclusion. Thirty-nine (43%) patients developed postoperative complications. The median [IQR] intraoperative PCO2 gap was significantly higher in patients who had complications (6.5 [5.5-7.3] mmHg) compared to those who did not (5.0 [3.9-5.8] mmHg; p < 0.001). The area under the receiver operating characteristic curve for occurrence of POC was 0.78 for the PCO2 gap. After multivariable analysis, PCO2 gap was found independently associated with POC (OR: 14.9, 95% CI [4.68-60.1], p < 0.001) with a threshold value of 6.2 mmHg. The duration of surgery (OR: 1.01, 95% CI [1.00; 1.01], p = 0.04) and the need for vasoactive support during surgery (OR: 5.76, 95% CI [1.72; 24.1], p = 0.006) were also independently associated with POC. CONCLUSION: Intraoperative PCO2 gap is a relevant predictive factor of severe postoperative complications in high-risk elective surgery patients. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03914976.

An increase in skin blood flow induced by fluid challenge is associated with an increase in oxygen consumption in patients with circulatory shock.

PURPOSE: To investigate whether an increase in skin blood flow (SBF) after fluid challenge was associated with an increase in oxygen consumption (VO2) in patients with circulatory shock. MATERIALS AND METHODS: We studied 62 patients with shock who required fluid challenge. Using laser Doppler, we measured finger SBF at basal temperature (SBFBT) and after a thermal challenge test (SBFTCT), before and after a fluid challenge (500 ml of Plasmalyte®). In fluid responders (i.e., increase in cardiac index ≥15%), VO2 responders (VO2R) were those with a ≥15% increase in VO2. RESULTS: Of the 62 patients, 33 were fluid responders and 16 of these were VO2R. At baseline, VO2R had lower SBFBT (21[14-52] vs 83[24-116] PU, p = 0.03) and SBFTCT (2.1[1.2-3.3] vs 4.4[2.2-5.6] PU/°C, p = 0.02) than VO2 non-responders (VO2NR); hemodynamic variables were not significantly different. The increase in SBFBT (∆SBFBT) after fluid challenge was greater in VO2R than in VO2NR (141[83-174] vs 57[17-150]%, p = 0.03). Areas under the curves for baseline SBFTCT (0.83 ± 0.07 [0.68-0.98]) and ∆SBFBT (0.90 ± 0.05 [0.75-1.0]) to predict ∆VO2 ≥ 15% were higher than for other variables. CONCLUSION: A lower baseline SBFTCT and a greater ∆SBFBT can identify patients in whom VO2 will increase after fluid challenge, suggesting an improvement in cellular metabolism.

How can CO2-derived indices guide resuscitation in critically ill patients?

Assessing the adequacy of oxygen delivery with oxygen requirements is one of the key-goal of haemodynamic resuscitation. Clinical examination, lactate and central or mixed venous oxygen saturation (SvO2 and ScvO2, respectively) all have their limitations. Many of them may be overcome by the use of the carbon dioxide (CO2)-derived variables. The venoarterial difference in CO2 tension ("ΔPCO2" or "PCO2 gap") is not an indicator of anaerobic metabolism since it is influenced by the oxygen consumption. By contrast, it reliably indicates whether blood flow is sufficient to carry CO2 from the peripheral tissue to the lungs in view of its clearance: it, thus, reflects the adequacy of cardiac output with the metabolic condition. The ratio of the PCO2 gap with the arteriovenous difference of oxygen content (PCO2 gap/Ca-vO2) might be a marker of anaerobiosis. Conversely to SvO2 and ScvO2, it remains interpretable if the oxygen extraction is impaired as it is in case of sepsis. Compared to lactate, it has the main advantage to change without delay and to provide a real-time monitoring of tissue hypoxia.

Usefulness of venous-to-arterial partial pressure of CO2 difference to assess oxygen supply to demand adequacy: effects of dobutamine.

The central venous O2 saturation value and lactic acid levels are part of the diagnostic and therapeutic work up of patients in shock. These usual indicators of tissue hypoxia don't fully describe the adequacy of tissue perfusion. There is ample evidence that supplementing this data with the venous-to-arterial partial pressure of CO2 (PCO2) difference (ΔPCO2) complements the clinician's tools when treating patients with shock. Based on a modified Fick equation as it applies to CO2, in patients in a steady state, the ΔPCO2 reflects the cardiac output (CO). This observation has been shown to be of clinical value in resuscitating patients in shock. Moreover, the ΔPCO2 can be used to titrate inotropes, and differentiate the hemodynamic from the metabolic effect of dobutamine.

Capillary refill time variation induced by passive leg raising predicts capillary refill time response to volume expansion.

BACKGROUND: A peripheral perfusion-targeted resuscitation during early septic shock has shown encouraging results. Capillary refill time, which has a prognostic value, was used. Adding accuracy and predictability on capillary refill time (CRT) measurement, if feasible, would benefit to peripheral perfusion-targeted resuscitation. We assessed whether a reduction of capillary refill time during passive leg raising (ΔCRT-PLR) predicted volume-induced peripheral perfusion improvement defined as a significant decrease of capillary refill time following volume expansion. METHODS: Thirty-four patients with acute circulatory failure were selected. Haemodynamic variables, metabolic variables (PCO2gap), and four capillary refill time measurements were recorded before and during a passive leg raising test and after a 500-mL volume expansion over 20 min. Receiver operating characteristic curves were built, and areas under the curves were calculated (ROCAUC). Confidence intervals (CI) were performed using a bootstrap analysis. We recorded mortality at day 90. RESULTS: The least significant change in the capillary refill time was 25% [95% CI, 18-30]. We defined CRT responders as patients showing a reduction of at least 25% of capillary refill time after volume expansion. A decrease of 27% in ΔCRT-PLR predicted peripheral perfusion improvement with a sensitivity of 87% [95% CI, 73-100] and a specificity of 100% [95% CI, 74-100]. The ROCAUC of ΔCRT-PLR was 0.94 [95% CI, 0.87-1.0]. The ROCAUC of baseline capillary refill time was 0.73 [95% CI, 0.54-0.90] and of baseline PCO2gap was 0.79 [0.61-0.93]. Capillary refill time was significantly longer in non-survivors than in survivors at day 90. CONCLUSION: ΔCRT-PLR predicted peripheral perfusion response following volume expansion. This simple low-cost and non-invasive diagnostic method could be used in peripheral perfusion-targeted resuscitation protocols. TRIAL REGISTRATION: CPP Lyon Sud-Est II ANSM: 2014-A01034-43 Clinicaltrial.gov, NCT02248025 , registered 13th of September 2014.

Gastric feeding intolerance is not caused by mucosal ischemia measured by intragastric air tonometry in the critically ill.

BACKGROUND: Gastric mucosal ischemia may be a risk factor for gastrointestinal intolerance to early feeding in the critically ill. AIMS: To study intragastric PCO2 air tonometry and gastric residual volumes (GRV) before and after the start of gastric feeding. METHODS: This is a two-center study in intensive care units of a university and teaching hospital. Twenty-nine critically ill, consecutive and consenting patients scheduled to start gastric feeding were studied after insertion of a gastric tonometry catheter and prior to and after start of gastric feeding (500 ml over 1 h), when clinically indicated. RESULTS: Blood gasometry and intragastric tonometry were performed prior to and 2 h after gastric feeding. The intragastric to arterial PCO2 gap (normal <8 mm Hg) was elevated in 41% of patients prior to feeding and measured (mean ± standard deviation) 13 ± 20 and 16 ± 23 mm Hg in patients with normal (<100 ml, 42 ± 34 ml, n = 19) and elevated GRV (250 ± 141 ml, n = 10, P = 0.75), respectively. After feeding, the gradient did not increase and measured 27 ± 25 and 23 ± 34 mm Hg, respectively (P = 0.80). CONCLUSION: Gastric mucosal ischemia is not a major risk factor for intolerance to early gastric feeding in the critically ill.