Acidemic Group Research Articles

Determining the Utility of Metabolic Acidosis for Trauma Patients in the Emergency Department

BackgroundMetabolic acidosis has been proposed as the gold standard to define shock in trauma patients. Other studies determine the presence of shock by use of serum lactate. However, not all medical centers have the ability to utilize point-of-care lactate at bedside. ObjectiveThis study seeks to determine the relationship between serum lactate and metabolic acidemia in trauma patients, and if metabolic acidemia can be used to guide therapy. We hypothesized that acidemia would be strongly correlated with lactate levels and would be associated with activation of massive transfusion (MT) in the presence of shock in trauma. MethodsThis was a prospective observational cohort study, level II evidence; this study aids in decision-making. Setting was a Level I academic, urban trauma center. The study took place from July 1, 2012 to March 1, 2013 and included patients who were ≥18 years old and required trauma team activation. Observations included baseline demographics (age, gender, type of injury), vital signs, point-of-care arterial blood gas, lactate, and need for MT. ResultsOne hundred patients were enrolled over the study period. The average age was 34 years, and 82% were male. Forty patients were acidemic (pH < 7.35), and there was a significant difference in lactate levels between the acidemic and non-acidemic groups (p < 0.002). We found a strong correlation between pH and lactate: rs = −0.38, t = −4.03, p < 0.001. In addition, using a logistic regression, we show that pH was associated with activation of MT (p = 0.002). ConclusionThis is a prospective observational cohort study with level II evidence. This study demonstrates that acidemia was strongly correlated to serum lactate, lactate levels were higher in the acidemic group, and metabolic acidemia was associated with the activation of MT for trauma patients at our institution.

In a Porcine Model of Mixed Acidemia HES 130/0.4 May Support More Stable Hemodynamics during CVVH when Compared to Gelatine

Continuous veno-venous hemofiltration (CVVH) and mixed acidemia often occur simultaneously in critically ill patients. In a previous study in non-acidemic pigs we found that colloids and CVVH interact specifically with respect to hemodynamic stability, with favorable effects for 6% HES 130/0.4 versus 4% gelatine (GEL) infusion. In a porcine model, we investigated whether these colloid-type associated differences are still dominant under acidemic conditions. We utilized 5 groups, a non-acidemic reference group receiving HES130 and CVVH; two acidemic groups receiving HES130 infusion (one with and one without CVVH); and two acidemic groups receiving GEL infusion (one with and one without CVVH). Mixed acidemia (pH ~7.20) was established by low tidal volume ventilation and acid infusion. Stable acidemia/CVVH application was maintained for 3 hours. Hemodynamics and blood gases were recorded. Mixed acidemia led to a significant decrease in MAP and increase in MPAP in all groups. CVVH led to a further decrease in MAP but improved MPAP. During CVVH, HES130 ensured significantly higher MAP, Hb, and DO2 values than GEL infusion. In the groups without CVVH these differences between HES 130/0.4 and GEL were not observed. As in a previous study in non-acidemic pigs, we found a colloid-specific influence of HES130 versus GEL on hemodynamics during CVVH under acidemia. Again, HES130 infusion may lead to favorable effects. In contrast, acidemia without CVVH application was dominant over the impact of a respective colloid. The application of a CVVH seems to be an important trigger for the overall circulatory response to a particular colloid.

Neonatal brain imaging and the identification of metabolic acidemia and hypoxic–ischemic encephalopathy

Objective. To determine the precision with which intrapartum metabolic acidemia and hypoxic–ischemic encephalopathy (HIE) in term and near-term infants can be identified by neonatal brain imaging.Study design. This is a case–control study whose inclusion criteria were neonates born at ≥34 weeks gestation with a cord gas at delivery, suspected neurological abnormalities, and computed tomography (CT) or magnetic resonance (MR) imaging of the brain. Neonates with chromosomal and major congenital malformations were excluded. Brain imaging for neonates with and without metabolic acidemia (pH < 7.0 and base deficit > 12 mM) at birth and HIE were retrospectively reviewed by a neuroradiologist blinded to their clinical course and compared.Results. There were 54 neonates admitted to the NICU at a single university hospital between 1992 and 2006 that met these inclusion criteria of which 27 had metabolic acidemia at birth. There were 16 diagnosed clinically as having HIE at the time of neonatal discharge, 13 from the acidemic group and 3 from the nonacidemic group. Radiological signs of basal ganglia injury were significantly more common in neonates with metabolic acidemia (29.6%, 3.7%, p = 0.02) and HIE (37.5%, 7.9%, p = 0.01). Logistic regression corrected for gestational age showed that radiological signs of basal ganglia injury could identify the presence of HIE with area under the ROC curve of 0.71, sensitivity 37.5%, specificity 92.1%, positive predictive value 66.7%, and negative predictive value of 77.8%.Conclusion. Radiological signs of basal ganglia injury on early neonatal imaging are associated with metabolic acidemia and HIE, but is not precise enough to serve as a gold standard in the identification of these conditions.

Chronic binge ethanol-mediated acidemia reduces availability of glutamine and related amino acids in maternal plasma of pregnant sheep

Heavy drinking during pregnancy can result in fetal alcohol syndrome (FAS), of which, fetal and postnatal growth retardation and central nervous system deficits are cardinal features. Although a number of mechanisms have been proposed, none fully account for these deficiencies. We have previously reported that maternal ethanol exposure (1.75 g/kg) results in transient acidemia in the mother and fetus. Alterations in pH are known to regulate glutamine homeostasis. Therefore, we hypothesized that chronic binge ethanol-mediated acidosis reduces glutamine concentrations in maternal plasma that result in decreases in the circulating levels of amino acids related to glutamine metabolism. Pregnant ewes were divided into three groups: ethanol (1.75 g/kg), saline control, and acidemia (inspired fractional carbon dioxide [CO 2] was manipulated to mimic the maternal arterial pH pattern created by ethanol). The experiment was conducted on three consecutive days followed by four days without treatment beginning on gestational day (GD) 109, continuing to GD 132. Plasma samples were analyzed for nutrients and metabolites using HPLC and spectrophotometric methods. Maternal plasma concentrations of glutamate increased (58%), whereas glutamine, citrulline, and arginine decreased (between 14 and 53%) in response to an acute challenge after the chronic exposure in ethanol-treated ewes. No differences in these amino acid concentrations were noted between the ethanol and acidemic group subjects. Maternal plasma lactate levels increased by ∼100% in response to ethanol, whereas glucose and urea levels did not change in any group. We conclude that maternal chronic binge ethanol consumption results in acidosis-mediated reductions in circulating levels of glutamine and related amino acids that could be responsible for neuronal deficits, altered fetal growth, development, and programming. We also speculate that the consequent increase in fetal glutamate during critical periods of brain development may contribute to the pathogenesis of FAS.

Pulse oximetry during labour—does it give rise to hope?: Value of saturation monitoring in comparison to fetal blood gas status

Objective: Purpose of this presentation is to show the diagnostic power of fetal pulse oximetry in comparison to the other blood gas parameters from fetal blood samplings (FBS). The distribution of saturation readings in acidotic fetuses and normally oxygenated fetuses should be established. Study design: A fetal pulse oximetry system (N400, FS14) was evaluated in a strictly observational study design based on blinded saturation display and on continuous data storing. The investigation was performed on 170 fetuses with non-reassuring fetal heart rate (FHR)-tracings. Since pulse oximetry readings were not available for decision finding, the clinical management was based on electronic fetal monitoring and fetal blood samplings. The oxygen saturation from FBS or umbilical cord blood was measured by blood gas analysers with an integrated hemoximeter (Bayer 865; ABL 625, Radiometer) and biosensors measuring lactate as metabolic component. Out of the 170 cases 17 cases were defined as group of acidemia ( pH umb. art. < 7.16 + BD<−9.4). The distribution of saturation readings and the duration of desaturation periods (in minutes and percentage of total monitoring time SPO 2 below 30%) were determined. ROC curve analysis from FBS preceding delivery compared the diagnostic power of other blood gas parameters with oxygen saturation. The Wilcoxon test for uneven pairs was used. Results: The distribution of oxygen saturation in the normal group of fetuses differs significantly from the acidemic group. The correlation coefficient between both methods to determine oxygen saturation was r=0.66. A specific evaluation of the distribution of SPO 2 shows an overestimation of pulse oximetry in the low range and an underestimation in the high range of saturation. ROC-curve analysis showed a good diagnostic power of lactate in comparison to the oxygen saturation measured by pulse oximetry or by hemoximetry. Conclusions: The advantage of continuous fetal pulse oximetry surveilling the fetus under suspicion of hypoxia appears limited by the poor diagnostic power of the respiratory parameter saturation itself and by the impairment of the precision of the technology.

The effect of profound umbilical artery acidemia in term neonates admitted to a newborn nursery

Objective: To determine whether there were immediate adverse effects of an umbilical artery pH ≤ 7.0 in term and near-term infants. Study Design: All infants triaged to the newborn nursery with an umbilical artery pH ≤ 7.0 from May 1993 through April 1994 ( n = 37) were prospectively identified; 35 of the 37 infants were enrolled and matched with nonacidemic control infants ( n = 35). Organ system dysfunction (neurologic, renal, hepatic, gastrointestinal) was evaluated either clinically or biochemically with selected blood and urine parameters. Results: Acidemic and control groups were similar for pregnancy complications before labor, but acidemic infants were more often delivered by cesarean section (20/35 vs 6/35, p = 0.001). No differences existed between acidemic and control infants in gestational age, birth weight, neurologic evaluations, hearing deficits, feeding tolerance, and hepatic function. The acidemic group had a higher mean serum creatinine than control infants on day 2 of life (0.90 ± 0.34 vs 0.71 ± 0.12 mg/dl, p = 0.005) and a greater number of infants with a urine Chemstrip positive for heme (14/35 vs 3/35, p = 0.005). No differences existed between groups in time to first void, urine specific gravity, and number of infants with microscopic hematuria. Conclusion: Term and near-term infants born with an umbilical artery pH ≤ 7.0 and triaged to the newborn nursery on the basis of a stable appearance in the delivery room do not have clinical manifestations of hypoxia-ischemia in the 48 hours after birth. The higher mean serum creatinine for acidemic compared with control groups is presumably prerenal in origin and results from processes responsible for profound fetal acidemia. Infants with an umbilical artery pH ≤ 7.0 and assessed to be clinically well can be treated similar to nonacidemic infants. (J Pediatr 1998;132:624-9)

Sonography‐guided Fetal Blood Sampling for ph and Blood Gases in Premature Fetuses with Abnormal Fetal Heart Rate Traces

In nine pregnancies, remote from term, with an abnormal Non-Stress Test (NST) and Bio-Physical Profile (BPP) of 3 or above, cordocentesis for fetal blood gas analysis was performed. In seven cases an immediate post-partum blood sample was taken from the fetal cord for a similar analysis. The two tests gave very similar results. The results showed fetal acidemia (pH 7.09-7.19 and B.E. -10-15) in 4 cases, followed by immediate delivery. In the remaining 5 cases, normal blood gases were evident (pH 7.28-7.35); despite the abnormal NST, pregnancy was allowed to continue for 2 to 7 weeks, under close supervision. At birth, 2 out of 9 newborns were deemed by the neonatologist suffering from asphyxia. Both belonged to the acidemic group of women who were managed by immediate cesarean section. The other 5 fetuses, which were managed expectantly, had normal post-partum blood gases or Apgar score; none had asphyxia. Fetal blood gas analysis, on samples obtained by cordocentesis, provides useful information that can assist in the management of premature fetuses suspected of being distressed, according to their heart traces. Normal fetal blood gases can identify those fetuses falsely identified by the NST as in distress and thereby spare them unnecessary premature birth with its known complications.

Arterial pH modulation of regional cerebral blood flow during hyperammonemia in dogs

Acute hyperammonemia at normal arterial pH causes selective increases in midbrain blood flow in dogs. Unexpectedly, further increases occur with hypocapnia. We investigated whether metabolic acidemia and alkalemia modulate the distribution of ammonium across the blood-brain barrier and if, in turn, midbrain blood flow is effectively modulated. In dogs anesthetized with pentobarbital sodium, hyperammonemia (approximately 940 microM) was produced by a 210-min infusion of ammonium acetate. Concurrent infusion of NaHCO3 increased arterial pH to 7.53 +/- 0.02 (SE), whereas HCl infusion decreased pH to 7.11 +/- 0.01. Normocapnia was maintained. Cerebrospinal fluid [HCO3-] increased 5 mM with alkalemia (one-half of the increase in blood) and was unchanged with acidemia. Thus cerebrospinal fluid [H+]/blood [H+] was greater with alkalemia than acidemia. The corresponding ratio for ammonium was likewise greater with alkalemia (0.70 +/- 0.06) than acidemia (0.44 +/- 0.08). Microsphere-determined blood flow to midbrain more than doubled in the alkalemic group but was unchanged in the acidemic group. No other region along the neuraxis or in cerebrum showed increased blood flow in either hyperammonemic group. Alkalemia without hyperammonemia did not increase midbrain blood flow. Thus metabolic acidemia-alkalemia significantly alters ammonium partitioning into cerebrospinal fluid, and this alteration is sufficiently great to exert a specific physiological effect manifested by changes in midbrain blood flow.

Arterial blood gases in acute pulmonary edema

Arterial blood gas and pH measurements in 82 patients with acute pulmonary edema of cardiogenic origin entering the emergency department varied widely and were unpredictable using clinical examination. The mean arterial oxygen tension (PaO2) measured in 71 patients breathing room air was 59 mm Hg. Fourteen of the 82 patients were acidemic; 35, alkalemic and 33 had a pH in the normal range. The acidemic group had markedly lower PaO2, all under 60 mm Hg. Oxygen and furosemide were used in all cases and effectively corrected the hypoxia and reduced pulmonary congestion. Other drugs used included aminophylline (14 patients), morphine sulfate (9 patients) and digoxin (3 patients). Five of the nine patients who received morphine were hypercarbic initially but the CO2 retention did not worsen. No patient died during the initial 48 hours. This study reiterates the importance of directing therapy at ventilatory and cardiac abnormalities and points out the value of arterial blood gas monitoring to assess the initial status, monitor the patient's course, and to select drug therapy.

Cardiovascular responses to hypoxemia and acidemia in fetal lambs

Circulatory responses to hypoxemia and acidemia were studied in 10 fetal lambs in utero with gestational ages of 122 to 142 days. Vinyl catheters were placed in fetal and maternal vessels, and the fetuses were studied 2 to 5 days postoperatively. Fetal heart rate, arterial pressure,Po2,Pco2, and pH were measured during a control period and while the standing ewe breathed 6 per cent oxygen and 3 per cent carbon dioxide through a plastic bag over its head. Fetal cardiac output and distribution and absolute organ blood flows were calculated from injections of 15μ nuclide-labeled microspheres, during the control and hypoxemic states. One group of 5 fetuses only became hypoxemic (meanPo2 12 and mean pH 7.36), but the other 5 fetuses also developed acidemia (meanPo2 12 and mean pH 7.28). Fetal arterialPco2 values were normal throughout. During hypoxemia, fetal arterial pressure increased, and fetal heart rate decreased. Although cardiac output fell in all but one fetus, the decrease was significant only in the acidemic group. Blood flow to the fetal body decreased in all, but the change was significantly greater in the acidemic group. Umbilical blood flow was maintained in all fetuses during hypoxemia. The per cent distribution of cardiac output to the placenta rose from 41 to 48 per cent and from 41 to 57 per cent in the hypoxemic and acidemic groups, respectively. Blood flow to the brain, heart, and adrenals increased two- to three-fold in all fetuses during hypoxemia while pulmonary, renal, splenic, gut, and carcass flows decreased. The changes were of greater magnitude in fetuses with combined hypoxemia and acidemia. These studies quantitate the fetal circulatory changes that occur in unanesthetized fetal lambs in utero during maternal hypoxemia.