Peripheral venous blood gases and pulse-oximetry in acute cardiogenic pulmonary oedema

Background: The role of venous blood gases as an alternative to arterial blood gases in patients with severe acute heart failure has not been established. Objective: To assess the correlation between arterial and peripheral venous blood gases together with pulse-oximetry (SpO2), as well as to estimate arterial values from venous samples in the first hours upon admission of patients with acute cardiogenic pulmonary oedema. Methods: Simultaneous venous and arterial blood samples were extracted on admission and over the next 1, 2, 3, 4, and 10 hours. SpO2 was also registered at the same intervals. Results: A total of 178 pairs of samples were obtained from 34 consecutive patients with acute cardiogenic pulmonary oedema. Arterial and venous blood gases followed a parallel course in the first hours, showing high correlation rates at all time intervals. Venous samples underestimated pH (mean difference −0.028) and overestimated CO2 (+5.1 mmHg) and bicarbonate (+1 mEq/l). Conversely, SpO2 tended to underestimate SaO2 (mean±SD: 93.1±9.1 vs. 94.2±8.4). Applying simple mathematical formulae based on these differences, arterial values were empirically calculated from venous samples, showing acceptable agreement in the Bland−Altman test. Likewise, a venous pH 51.3 mmHg, and bicarbonate <22.8 mEq/l could fairly identify arterial acidosis, either respiratory or metabolic, with a test accuracy of 92, 68, and 91%, respectively. Conclusions: In patients with cardiogenic pulmonary oedema, arterial blood gas disturbances may be estimated from peripheral venous samples. By monitoring SpO2 simultaneously, arterial punctures could often be avoide

Pitfalls in Interpreting Umbilical Cord Blood Gases and Lactate at Birth

Acid-base status in umbilical cord blood is an objective measure of the fetus’ exposure to and ability to handle hypoxia. The objective of this thesis was to clarify some of the methodological pitfalls in interpreting umbilical cord blood gases and lactate values at birth. Study I pinpoints the methodological confounding in calculating base deficit (BD) with algorithms used in different brands of blood gas analyzers and reports the consequences for diagnosing metabolic acidosis (MA) at birth. Neonatal MA rates cannot be compared between maternity units or between scientific articles where different fetal compartments (blood or extracellular fluid) and different algorithms for calculating BD have been used. Study II addresses the issue of possible diagnostic discrepancies when acid-base parameter value decimals are rounded off. A drift of a dichotomy parameter value cut-off due to decimal rounding will result in a shift in distribution of negative and positive cases in a population sample. The findings warrant a discussion on standardization of round-off rule and the number of decimals for a specific analyte result. Study III demonstrates that delayed cord blood sampling with intact pulsations affects umbilical acid-base values and hematological parameters in both vaginal and cesarean deliveries. The changes were more marked after vaginal delivery. A change towards acidemia and lactemia can be explained by the hidden acidosis phenomenon, i.e. a surge into the central circulation of peripherally trapped acid metabolites when the newborn starts to breathe. Study IV shows that clinical characteristics have a significant influence on the distribution of veno-arterial and arterio-venous gradients (Δ values) in umbilical cord blood. Validation criteria based on fixed ΔpH and ΔpCO2 values may then exclude correct samples of clinical outliers. Lactate cannot be used for validation of umbilical cord blood samples. A negative ΔpO2 value indicates delayed cord blood sampling or mix-up of samples and is the only certain validation criterion

Arteriovenous Blood Metabolomics: A Readout of Intra-Tissue Metabostasis.

The human circulatory system consists of arterial blood that delivers nutrients to tissues, and venous blood that removes the metabolic by-products. Although it is well established that arterial blood generally has higher concentrations of glucose and oxygen relative to venous blood, a comprehensive biochemical characterization of arteriovenous differences has not yet been reported. Here we apply cutting-edge, mass spectrometry-based metabolomic technologies to provide a global characterization of metabolites that vary in concentration between the arterial and venous blood of human patients. Global profiling of paired arterial and venous plasma from 20 healthy individuals, followed up by targeted analysis made it possible to measure subtle (&lt;2 fold), yet highly statistically significant and physiologically important differences in water soluble human plasma metabolome. While we detected changes in lactic acid, alanine, glutamine, and glutamate as expected from skeletal muscle activity, a number of unanticipated metabolites were also determined to be significantly altered including Krebs cycle intermediates, amino acids that have not been previously implicated in transport, and a few oxidized fatty acids. This study provides the most comprehensive assessment of metabolic changes in the blood during circulation to date and suggests that such profiling approach may offer new insights into organ homeostasis and organ specific pathology

Lactate: brain fuel in human traumatic brain injury: a comparison with normal healthy control subjects.

We evaluated the hypothesis that lactate shuttling helps support the nutritive needs of injured brains. To that end, we utilized dual isotope tracer [6,6-(2)H2]glucose, that is, D2-glucose, and [3-(13)C]lactate techniques involving arm vein tracer infusion along with simultaneous cerebral (arterial [art] and jugular bulb [JB]) blood sampling. Traumatic brain injury (TBI) patients with nonpenetrating brain injuries (n=12) were entered into the study following consent of patients' legal representatives. Written and informed consent was obtained from control volunteers (n=6). Patients were studied 5.7±2.2 (mean±SD) days post-injury; during periods when arterial glucose concentration tended to be higher in TBI patients. As in previous investigations, the cerebral metabolic rate for glucose (CMRgluc, i.e., net glucose uptake) was significantly suppressed following TBI (p&lt;0.001). However, lactate fractional extraction, an index of cerebral lactate uptake related to systemic lactate supply, approximated 11% in both healthy control subjects and TBI patients. Further, neither the CMR for lactate (CMRlac, i.e., net lactate release), nor the tracer-measured cerebral lactate uptake differed between healthy controls and TBI patients. The percentages of lactate tracer taken up and released as (13)CO2 into the JB accounted for 92% and 91% for control and TBI conditions, respectively, suggesting that most cerebral lactate uptake was oxidized following TBI. Comparisons of isotopic enrichments of lactate oxidation from infused [3-(13)C]lactate tracer and (13)C-glucose produced during hepatic and renal gluconeogenesis (GNG) showed that 75-80% of (13)CO2 released into the JB was from lactate and that the remainder was from the oxidation of glucose secondarily labeled from lactate. Hence, either directly as lactate uptake, or indirectly via GNG, peripheral lactate production accounted for ∼70% of carbohydrate (direct lactate uptake+uptake of glucose from lactate) consumed by the injured brain. Undiminished cerebral lactate fractional extraction and uptake suggest that arterial lactate supplementation may be used to compensate for decreased CMRgluc following TBI