Rapid Changes in Arterial Carbon Dioxide Levels Caused by Extracorporeal Membrane Oxygenation. The Temptation of a Fascinating Technology.
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ABSTRACT:
SUBMITTER: Karagiannidis C
PROVIDER: S-EPMC7301726 | biostudies-literature | 2020 Jun
REPOSITORIES: biostudies-literature
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Rapid Changes in Arterial Carbon Dioxide Levels Caused by Extracorporeal Membrane Oxygenation. The Temptation of a Fascinating Technology.
Karagiannidis Christian C Windisch Wolfram W Bein Thomas T
American journal of respiratory and critical care medicine 20200601 12
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Project description:Acute brain injury (ABI) occurs frequently in patients receiving venoarterial extracorporeal membrane oxygenation (VA-ECMO). We examined the association between peri-cannulation arterial carbon dioxide tension (PaCO 2 ) and ABI with granular blood gas data. We retrospectively analyzed adult patients who underwent VA-ECMO at a tertiary care center with standardized neuromonitoring. Pre- and post-cannulation PaCO 2 were defined as the mean of all PaCO 2 values in the 12 hours before and after cannulation, respectively. Peri-cannulation PaCO 2 drop (∆PaCO 2 ) equaled pre- minus post-cannulation PaCO 2 . ABI included intracranial hemorrhage (ICH), ischemic stroke, hypoxic-ischemic brain injury, cerebral edema, seizure, and brain death. Univariable logistic regression analysis was performed for the presence of ABI. Out of 129 VA-ECMO patients (median age = 60, 63% male), 43 (33%) patients experienced ABI. Patients had a median of 11 (interquartile range: 8-14) peri-cannulation PaCO 2 values. Comparing patients with and without ABI, pre-cannulation (39 vs. 42 mm Hg; p = 0.38) and post-cannulation (37 vs. 36 mm Hg; p = 0.82) PaCO 2 were not different. However, higher pre-cannulation PaCO 2 (odds ratio [OR] = 2.10; 95% confidence interval [CI] = 1.10-4.00; p = 0.02) and larger ∆PaCO 2 (OR = 2.69; 95% CI = 1.18-6.13; p = 0.02) were associated with ICH. In conclusion, in a cohort with granular arterial blood gas (ABG) data and a standardized neuromonitoring protocol, higher pre-cannulation PaCO 2 and larger ∆PaCO 2 were associated with increased prevalence of ICH.
| S-EPMC9477972 | biostudies-literature
Project description:ObjectivesThe manipulation of arterial carbon dioxide tension is associated with differential mortality and neurologic injury in intensive care and cardiac arrest patients; however, few studies have investigated this relationship in patients on venoarterial extracorporeal membrane oxygenation. We investigated the association between the initial arterial carbon dioxide tension and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiac arrest and refractory cardiogenic shock.DesignRetrospective cohort analysis of adult patients recorded in the international Extracorporeal Life Support Organization Registry.SettingData reported to the Extracorporeal Life Support Organization from all international extracorporeal membrane oxygenation centers during 2003-2016.PatientsAdult patients (≥ 18 yr old) supported with venoarterial extracorporeal membrane oxygenation.InterventionsNone.Measurements and main resultsA total of 7,168 patients had sufficient data for analysis at the initiation of venoarterial extracorporeal membrane oxygenation, 4,918 of these patients had arterial carbon dioxide tension data available at 24 hours on support. The overall in-hospital mortality rate was 59.9%. A U-shaped relationship between arterial carbon dioxide tension tension at extracorporeal membrane oxygenation initiation and in-hospital mortality was observed. Increased mortality was observed with a arterial carbon dioxide tension less than 30 mm Hg (odds ratio, 1.26; 95% CI, 1.08-1.47; p = 0.003) and greater than 60 mm Hg (odds ratio, 1.28; 95% CI, 1.10-1.50; p = 0.002). Large reductions (> 20 mm Hg) in arterial carbon dioxide tension over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outcome (odds ratio, 1.63; 95% CI, 1.03-2.59; p = 0.04), independent of the initial arterial carbon dioxide tension.ConclusionsInitial arterial carbon dioxide tension tension was independently associated with mortality in this cohort of venoarterial extracorporeal membrane oxygenation patients. Reductions in arterial carbon dioxide tension (> 20 mm Hg) from the initiation of extracorporeal membrane oxygenation were associated with neurologic complications. Further prospective studies testing these associations are warranted.
| S-EPMC7393440 | biostudies-literature
Project description:Extracorporeal membrane oxygenation (ECMO) is a technique widely used worldwide to improve gas exchange. Changes in ECMO settings affect both oxygen and carbon dioxide. The impact on oxygenation can be followed closely by continuous pulse oximeter. Conversely, carbon dioxide equilibrates much slower and is not usually monitored directly.We investigated the time to stabilization of arterial carbon dioxide partial pressure (PaCO2) following step changes in ECMO settings in 5 apnoeic porcine models under veno-venous ECMO support with polymethylpentene membranes. We collected sequential arterial blood gases at a pre-specified interval of 50 min using a sequence of standardized blood and sweep gas flow combinations.Following the changes in ECMO parameters, the kinetics of carbon dioxide was dependent on sweep gas and ECMO blood flow. With a blood flow of 1500 mL/min, PaCO2 takes longer than 50 min to equilibrate following the changes in sweep gas flow. Furthermore, the sweep gas flow from 3.0 to 10.0 L/min did not significantly affect PaCO2. However, with a blood flow of 3500 mL/min, 50 min was enough for PaCO2 to reach the equilibrium and every increment of sweep gas flow (up to 10.0 L/min) resulted in additional reductions of PaCO2.Fifty minutes was enough to reach the equilibrium of PaCO2 after ECMO initiation or after changes in blood and sweep gas flow with an ECMO blood flow of 3500 ml/min. Longer periods may be necessary with lower ECMO blood flows.
| S-EPMC4703593 | biostudies-other
Project description:The primary objective was to investigate the association between partial pressure of carbon dioxide (PaCO2) change after extracorporeal membrane oxygenation (ECMO) initiation and neurologic outcome in neonates treated for respiratory failure. A retrospective analysis of the Extracorporeal Life Support Organization (ELSO) database including newborns supported by ECMO for respiratory indication during 2015-2020. The closest Pre-ECMO (Pre-ECMO PaCO2) and at 24 hours after ECMO initiation (H24 PaCO2) PaCO2 values allowed to calculate the relative change in PaCO2 (Rel Δ PaCO2 = [H24 PaCO2 - Pre-ECMO PaCO2]/Pre-ECMO PaCO2). The primary outcome was the onset of any acute neurologic event (ANE), defined as cerebral bleeding, ischemic stroke, clinical or electrical seizure, or brain death during ECMO. We included 3,583 newborns (median age 1 day [interquartile range {IQR}, 1-3], median weight 3.2 kg [IQR, 2.8-3.6]) from 198 ELSO centers. The median Rel Δ PaCO2 value was -29.9% [IQR, -46.2 to -8.5]. Six hundred nine (17%) of them had ANE (405 cerebral bleedings, 111 ischemic strokes, 225 seizures, and 6 brain deaths). Patients with a decrease of PaCO2 > 50% were more likely to develop ANE than others (odds ratio [OR] 1.78, 95% confidence interval [CI], 1.31-2.42, p < 0.001). This was still observed after adjustment for all clinically relevant confounding factors (adjusted OR 1.94, 95% CI, 1.29-2.92, p = 0.001). A significant decrease in PaCO2 after ECMO start is associated with ANE among neonates requiring ECMO for respiratory failure. Cautious PaCO2 decrease should be considered after start of ECMO therapy.
| S-EPMC10044589 | biostudies-literature
Project description:Mechanical ventilation (MV) represents a lifesaving treatment for patients with respiratory failure, but it could be harmful through the development of ventilator-induced lung injury (VILI). In patients with acute respiratory distress syndrome (ARDS), protective MV strategies with low tidal volume to minimize VILI have been demonstrated to reduce lung injury and mortality. However, they can be limited by the emergence of uncontrolled hypercapnia. Similarly, in COPD patients, noninvasive MV failure often is associated with a progressive rise in arterial CO2 and need for endotracheal intubation, with higher risk of hospital mortality. Minimally invasive extracorporeal CO2 removal systems (ECCO2R) theoretically can remove the entire amount of the CO2 produced in the body per minute. In ARDS patients, ECCO2R may further reduce the risk of VILI ensuring ultraprotective MV and avoiding hypercapnia. In patients with exacerbation of COPD, ECCO2R may help to avoid intubation or facilitate weaning from invasive MV. In intensive care unit, concomitant renal and respiratory failure with MV is one of the strongest risk factors for hospital mortality. Combining ECCO2R and renal replacement therapy may support respiratory and renal functions and limit the side effects of MV. However, the need for systemic anticoagulation and the related risk of bleeding still represent a concern for a wider application of ECCO2R devices. In conclusion, ECCO2R is an effective support therapy to MV to limit its invasiveness and side effects, but its efficacy and safety must be proven in well-designed clinical trials. Objectives This chapter will:1 Explain the physiology of CO2 removal during extracorporeal support.2 Describe potential clinical applications of extracorporeal CO2 removal systems (ECCO2R) support therapy in patients with acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD) as well as in those with acute kidney injury requiring renal replacement therapy.
| S-EPMC7969728 | biostudies-literature
Project description:BackgroundCentral nervous system (CNS) injury following initiation of veno-venous extracorporeal membrane oxygenation (VV-ECMO) is common. An acute decrease in partial pressure of arterial carbon dioxide (PaCO2) following VV-ECMO initiation has been suggested as an etiological factor, but the challenges of diagnosing CNS injuries has made discerning a relationship between PaCO2 and CNS injury difficult.MethodsWe conducted a prospective cohort study of adult patients undergoing VV-ECMO for acute respiratory failure. Arterial blood gas measurements were obtained prior to initiation of VV-ECMO, and at every 2-4 h for the first 24 h. Neuroimaging was conducted within the first 7-14 days in patients who were suspected of having neurological injury or unable to be examined because of sedation. We collected blood biospecimens to measure brain biomarkers [neurofilament light (NF-L); glial fibrillary acidic protein (GFAP); and phosphorylated-tau 181] in the first 7 days following initiation of VV-ECMO. We assessed the relationship between both PaCO2 over the first 24 h and brain biomarkers with CNS injury using mixed methods linear regression. Finally, we explored the effects of absolute change of PaCO2 on serum levels of neurological biomarkers by separate mixed methods linear regression for each biomarker using three PaCO2 exposures hypothesized to result in CNS injury.ResultsIn our cohort, 12 of 59 (20%) patients had overt CNS injury identified on head computed tomography. The PaCO2 decrease with VV-ECMO initiation was steeper in patients who developed a CNS injury (- 0.32%, 95% confidence interval - 0.25 to - 0.39) compared with those without (- 0.18%, 95% confidence interval - 0.14 to - 0.21, P interaction < 0.001). The mean concentration of NF-L increased over time and was higher in those with a CNS injury (464 [739]) compared with those without (127 [257]; P = 0.001). GFAP was higher in those with a CNS injury (4278 [11,653] pg/ml) compared with those without (116 [108] pg/ml; P < 0.001). The mean NF-L, GFAP, and tau over time in patients stratified by the three thresholds of absolute change of PaCO2 showed no differences and had no significant interaction for time.ConclusionsAlthough rapid decreases in PaCO2 following initiation of VV-ECMO were slightly greater in patients who had CNS injuries versus those without, data overlap and absence of relationships between PaCO2 and brain biomarkers suggests other pathophysiologic variables are likely at play.
| S-EPMC11335840 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-10-15 | GSE182609 | GEO
Project description:Venoarterial extracorporeal membrane oxygenation (VA-ECMO) provides temporary cardiac and respiratory support and has emerged as an established salvage intervention for patients with hemodynamic compromise or shock. It is thereby used as a bridge to recovery, bridge to permanent ventricular assist devices, bridge to transplantation, or bridge to decision. However, weaning from VA-ECMO differs between centers, and information about standardized weaning protocols are rare. Given the high mortality of patients undergoing VA-ECMO treatment, it is all the more important to answer the many questions still remaining unresolved in this field Standardized algorithms are recommended to optimize the weaning process and determine whether the VA-ECMO can be safely removed. Successful weaning as a multifactorial process requires sufficient recovery of myocardial and end-organ function. The patient should be considered hemodynamically stable, although left ventricular function often remains impaired during and after weaning. Echocardiographic and invasive hemodynamic monitoring seem to be indispensable when evaluating biventricular recovery and in determining whether the VA-ECMO can be weaned successfully or not, whereas cardiac biomarkers may not be useful in stratifying those who will recover. This review summarizes the strategies of weaning of VA-ECMO and discusses predictors of successful and poor weaning outcome.
| S-EPMC7230450 | biostudies-literature
Project description:IntroductionPatients on veno-arterial extracorporeal membrane oxygenation (V-A ECMO) support are at a high risk of hemorrhagic complications, including upper gastrointestinal bleeding (UGIB). The objective of this study was to evaluate the incidence and impact of this complication in V-A ECMO patients.Materials and methodsA retrospective single-center study (2013-2017) was conducted on V-A ECMO patients, excluding those who died within 24 h. All patients with suspected UGIB underwent esophagogastroduodenoscopy (EGD) and were analyzed and compared to the remainder of the cohort, from the initiation of ECMO until 5 days after explantation.ResultsA total of 150 V-A ECMO cases (65 after cardiac surgery and 85 due to medical etiology) were included. 90% of the patients received prophylactic proton pump inhibitor therapy and enteral nutrition. Thirty-one patients underwent EGD for suspected UGIB, with 16 confirmed cases of UGIB. The incidence was 10.7%, with a median occurrence at 10 [7-17] days. There were no significant differences in clinical or biological characteristics on the day of EGD. However, patients with UGIB had significant increases in packed red blood cells and fresh frozen plasma needs, mechanical ventilation duration and V-A ECMO duration, as well as in length of intensive care unit and hospital stays. There was no significant difference in mortality. The only independent risk factor of UGIB was a history of peptic ulcer (OR = 7.32; 95% CI [1.07-50.01], p = 0.042).ConclusionUGIB occurred in at least 1 out of 10 cases of V-A ECMO patients, with significant consequences on healthcare resources. Enteral nutrition and proton pump inhibitor prophylaxis did not appear to protect V-A ECMO patients. Further studies should assess their real benefits in these patients with high risk of hemorrhage.
| S-EPMC11222359 | biostudies-literature
Project description:BackgroundAcute brain injury (ABI) remains common after extracorporeal cardiopulmonary resuscitation (ECPR). Using a large international multicenter cohort, we investigated the impact of peri-cannulation arterial oxygen (PaO2) and carbon dioxide (PaCO2) on ABI occurrence.MethodsWe retrospectively analyzed adult (≥18 years old) ECPR patients in the Extracorporeal Life Support Organization registry from 1/2009 through 12/2020. Composite ABI included ischemic stroke, intracranial hemorrhage (ICH), seizures, and brain death. The registry collects 2 blood gas data pre- (6 hours) and post- (24 hours) cannulation. Blood gas parameters were classified as: hypoxia (<60mm Hg), normoxia (60-119mm Hg), and mild (120-199mm Hg), moderate (200-299mm Hg), and severe hyperoxia (≥300mm Hg); hypocarbia (<35mm Hg), normocarbia (35-44mm Hg), mild (45-54mm Hg) and severe hypercarbia (≥55mm Hg). Missing values were handled using multiple imputation. Multivariable logistic regression analysis was used to assess the relationship of PaO2 and PaCO2 with ABI.ResultsOf 3,125 patients with ECPR intervention (median age=58, 69% male), 488 (16%) experienced ABI (7% ischemic stroke; 3% ICH). In multivariable analysis, on-ECMO moderate (aOR=1.42, 95%CI: 1.02-1.97) and severe hyperoxia (aOR=1.59, 95%CI: 1.20-2.10) were associated with composite ABI. Additionally, severe hyperoxia was associated with ischemic stroke (aOR=1.63, 95%CI: 1.11-2.40), ICH (aOR=1.92, 95%CI: 1.08-3.40), and in-hospital mortality (aOR=1.58, 95%CI: 1.21-2.06). Mild hypercarbia pre-ECMO was protective of composite ABI (aOR=0.61, 95%CI: 0.44-0.84) and ischemic stroke (aOR=0.56, 95%CI: 0.35-0.89).ConclusionsEarly severe hyperoxia (≥300mm Hg) on ECMO was a significant risk factor for ABI and mortality. Careful consideration should be given in early oxygen delivery in ECPR patients who are at risk of reperfusion injury.
| S-EPMC10050131 | biostudies-literature