Arterial Base Deficit Research Articles

A comparison of central venous and arterial base deficit as a predictor of survival in acute trauma

Background The arterial base deficit has been demonstrated to be a marker of shock and predictive of survival in injured patients. The venous blood, however, may better reflect tissue perfusion. Its usefulness in trauma is unknown. We compared central venous with arterial blood gas analysis to determine which was a better predictor of survival in injured patients. Methods A prospective, nonrandomized series of acutely injured patients was investigated. Patients who had an arterial blood gas analysis for acid-base determination had a simultaneous central venous blood gas analysis and routine blood tests. Patient demographics, Injury Severity Score, and survival past 24 hours were recorded. Arterial and venous blood samples were analyzed for pH, P co 2, P o 2, HCO 3, hemoglobin-oxygen saturation, base deficit, and lactate. Results One hundred patients were enrolled. There were 76 survivors and 24 nonsurvivors. Wilcoxon rank sum test and multivariate logistic regression were used for each recorded variable; only central venous base deficit was predictive of survival past 24 hours ( P = .0081). Specifically, arterial base deficit was not predictive of survival past 24 hours. Conclusion In a prospective series of acutely injured patients, central venous base deficit, not arterial base deficit, was predictive of survival past 24 hours.

Predictors of necrotizing enterocolitis in preterm growth-restricted neonates

The purpose of this study was to test the hypothesis that multivessel fetal Doppler imaging provides enhanced prediction of necrotizing enterocolitis (NEC) in preterm placental insufficiency. Placental-based growth-restricted fetuses (abdominal circumference <5%, abnormal umbilical artery [UA] Doppler imaging) were examined. UA, middle cerebral artery, ductus venosus, and umbilical vein (UV) were evaluated prenatally and were assessed for their ability to predict NEC in neonates who were delivered at <37 weeks of gestation. Thirty-nine of 404 neonates (9.7%) experienced NEC. Among these, the mortality rate was 15.4% (6/39 neonates; odds ratio, 2.7; 95% CI, 1.03-7.11). NEC cases had higher UA Doppler indices prenatally (P = .023), lower gestational ages and birthweight at delivery (P < .0001, respectively), 5-minute Apgar scores of <7, and higher umbilical cord artery base deficit (P < .01, respectively). NEC was more likely after prenatal UV pulsations (odds ratio, 2.4; 95% CI, 1.13-5.14; P = .028) and severe cardiovascular abnormality (composite variable incorporating UA- absent or reversed end diastolic velocity, absent or reversed ductus venosus a-wave, or UV pulsations; odds ratio, 2.1; 95% CI, 1.06-4.05; P = .029) Logistic regression revealed birthweight and base deficit as the main contributors of NEC (r(2) = 0.20; P < .0001). Receiver operating characteristic analyses revealed birthweight of <790 g (sensitivity, 74.4%; specificity, 72.9%; P < .0001) and gestational age of < or =32.2 weeks (sensitivity, 94.9%; specificity, 45.8%; P < .0001) as optimal cut-offs that provide an odds ratio for NEC of 8.2 (95% CI, 3.9-17.6; P < .0001). Placental disease predisposes the severely growth-restricted neonate to necrotizing enterocolitis. Even when arterial and venous Doppler variables are taken into consideration, birthweight remains the predominant risk factor for NEC. Further research should focus on the critical transition to neonatal life to identify relevant triggers in predisposed neonates.

Improved Markers for Burn Wound Perfusion in the Severely Burned Patient: The Role for Tissue and Gastric Pco2

Improved markers of resuscitation are needed in patients with severe burn injuries. In previous animal and human work, we showed 1) wound hypoperfusion plays a role in burn depth progression, 2) that there are periods of repetitive ischemia and reperfusion which correlate closely to wound hypoperfusion, and 3) that wound and splanchnic bed CO2 measurements are dependent on the adequacy of resuscitation. We and others believe that current markers for resuscitation, urine output (U/O), and mean arterial pressure (MAP), lag behind in reflecting wound perfusion. In this study, we explore whether gastric and tissue tonometry are better in reflecting minute-to-minute changes in wound perfusion in humans. During the 48-hour experimental period, burn wound, gastric, and arterial pH, Pco2, and PaO2 were measured every 6 seconds using a Paratrend 7 monitor in four patients with life threatening burns. Slopes of change were analyzed and a proportion derived relative to pooled data on 5-minute intervals. Serum lactate, U/O, and MAP were recorded. Laser Doppler Imager (LDI) scans were performed on burn areas every 4 hours, allowing real-time determination of burn perfusion. Resuscitation followed current clinical guidelines. All four patients eventually succumbed, one doing so during the observation period. In the remaining three, U/O and MAP goals were met within 2 hours of resuscitation. Our analysis shows cyclic changes in burn wound pH, CO2, and PaO2, gastric CO2, and PaO2, and arterial base deficit (all P < .005). LDI showed cyclic changes in perfusion (P < .0001) which closely mimic the changes in wound pH, gastric CO2, and arterial base deficit. These changes preceded changes in U/O, MAP, and lactate. Although U/O, MAP, and serum lactate reflect changes in burn wound perfusion, they lag behind other markers. Tissue pH and CO2 and gastric CO2 seem to be more timely related to changes in actual burn perfusion.

Early Coagulopathy After Traumatic Brain Injury: The Role of Hypoperfusion and the Protein C Pathway

Early coagulopathy after traumatic brain injury (TBI) is thought to be the result of injury-mediated local release of tissue factor, although the precise mechanisms that cause hypoperfusion and early systemic coagulopathy in TBI patients are unknown. We have previously reported that early systemic coagulopathy after trauma is present only when tissue injury is associated with severe hypoperfusion leading to the activation of the protein C pathway. However, the role of hypoperfusion as an important mechanism for the development of coagulopathy early after TBI is unclear. The objective of the present study was to determine the importance of hypoperfusion and protein C activation in causing early coagulopathy in TBI patients. We performed a prospective cohort study including patients with isolated brain injury admitted to a single trauma center. Blood was drawn on average 32 minutes after injury. Plasma samples were assayed for protein C and thrombomodulin by standard laboratory techniques. Routine coagulation measures (prothrombin time, partial thromboplastin time) and arterial blood gas analysis were performed concurrently. Severe hypoperfusion was evidenced by the presence of an arterial base deficit greater than 6. Thirty-nine TBI patients were included in the study during a 15-month period. TBI patients without concurrent hypoperfusion (n = 28) did not develop an early coagulopathy after trauma, no matter the severity of injury. In contrast, patients with TBI who also had severe hypoperfusion (BD >6) (n = 11) were coagulopathic early after injury. Indeed, these patients had higher prothrombin time and partial thromboplastin time, compared with those with TBI and a BD <6 (17.6 +/- 3.6 vs. 14.3 +/- 2.3, p < 0.005; and 43.13 +/- 18.3 vs. 27.4 +/- 3.8, p < 0.0001). Unactivated protein C levels were lower in the TBI group with BD >6 (56 +/- 32 vs. 85 +/- 35, p = 0.03) and thrombomodulin levels were significantly higher (48 +/- 26 vs. 35 +/- 10, p = 0.04). Without hypoperfusion, there was no effect of increasing brain injury on protein C pathway or fibrinolysis pathway mediators. TBI alone does not cause early coagulopathy, but must be coupled with hypoperfusion to lead to coagulation derangements, associated with the activation of the protein C pathway. This novel finding has significant implications for the treatment of coagulopathy after severe brain injury.

A French randomized controlled trial of ST-segment analysis in a population with abnormal cardiotocograms during labor

The purpose of this study was to assess whether knowledge of ST-segment analysis was associated with a reduction in operative deliveries for nonreassuring fetal status (NRFS) or with a need for at least 1 scalp pH during labor. Seven hundred ninety-nine women at term with abnormal cardiotocography or meconium-stained amniotic fluid (7%) were assigned randomly to the intervention group (cardiotocography + STAN) or the control group (cardiotocography) in 2 university hospitals in Strasbourg, France. Scalp pH testing was optional in both groups. Abnormal neonatal outcome was pH <7.05 or umbilical cord blood artery base deficit of >12 or a 5-min Apgar score of <7 or neonatal intensive care unit admission or convulsions or neonatal death. Study power was 80% for the detection of a prespecified reduction from 50%-40% in operative delivery for NRFS. The operative delivery (cesarean or instrumental) rate for NRFS did not differ between the 2 groups: 33.6% (134/399) in the cardiotocography + STAN analysis group vs 37% (148/400) in the cardiotocography group (relative risk, 0.91; 95% CI, 0.75-1.10). The rate of operative delivery for dystocia was also similar in both groups. The percentage of women whose fetus had at least 1 scalp pH measurement during labor was substantially lower in the group with ST-segment analysis: 27% compared with 62% (relative risk, 0.44; 95% CI, 0.36-0.52). Neonatal outcomes did not differ significantly between groups. In a population with abnormal cardiotocography in labor, cardiotocography combined with ST-segment analysis was not associated with a reduction in operative deliveries for NRFS. The proportion of infants without scalp pH sampling during labor increased substantially, however.

LETTER TO THE EDITOR

Sir, We read with interest the study of Valenzuela et al., which evaluates the reliability of cord blood analysis at birth 1. Analysis was carried out immediately after clamping of the cord at birth, and latency periods of 60 and 120 min. No significant changes were found in pH, while pCO2 was significantly lower after 60 and 120 min. The authors conclude that these changes are modest, and that acid base data obtained with delay are still reliable. We do not agree with the conclusion. In cord blood analysis, pCO2 is a key parameter, since it is used in combination with pH to calculate the base deficit (BD). Calculation of the BD is a pre-requisite when distinguishing between respiratory and metabolic acidosis 2. Furthermore, cord artery pH and BD are incorporated as a main criteria for definition of intrapartum asphyxia 3. Thus, an evaluation of reliability has to include the BD, as it represents an essential part of cord blood analysis at birth. The study found that the mean pCO2 was 10.46 mmHg (1.39 kPa) lower after 60 min compared to the sample analysed immediately. Given a pH of 7.29, this corresponds to an increase of 4.3 mmol/l in the mean BD calculated, according to Siggaard-Andersens reference charts 4, e.g. a false high BD is calculated. Analysis of cord blood after 60 min could generate a higher frequency of metabolic acidosis. In consequence, a diagnosed metabolic acidosis would not be reliable as an indicator for the quality of intra partum monitoring. In contrast to the authors, we find that the results support that timing of the cord blood analysis is of clinical importance, and measurements obtained with a delay of 60 min or more might lead to misinterpretation, and should be considered as invalid.

Identifying traumatic brain injury in patients with isolated head trauma: are arterial lactate and base deficit as helpful as in polytrauma?

Background: Increase in lactate (LAC) within the central nervous system after head trauma is an established marker of traumatic brain injury (TBI). Objective: To investigate the utility of arterial base...

Relationship between Intertwin Delivery Interval and Metabolic Acidosis in the Second Twin

This study sought to assess the relationship between intertwin delivery interval (ITDI) and metabolic acidosis in the second twin at birth using a retrospective twin delivery cohort from a tertiary-level teaching hospital. Twin births were identified from an obstetrical database during a 10-year period from 1994 to 2004. Mean arterial cord pH and base deficit among different ITDIs were compared by analysis of variance. Logistic regression models were used to estimate effects of ITDI on metabolic acidosis. The incidence of metabolic acidosis in the second twin was defined as pH < 7.0, and base deficit was defined as >or= 12 mmol/L at birth. After excluding those pregnancies with both twins delivered by cesarean section, birthweight less than 750 g of either twin, antepartum death of either twin, or second twins with missing cord arterial pH, we had 310 twin pairs left for final analysis. Mean pH was significantly lower and base deficit significantly higher for second twin after ITDI exceeded 60 minutes. The incidence of metabolic acidosis increased with increasing ITDI (chi2 test for linear trend, P = 0.02) and the risk of metabolic acidosis (odds ratio, 22.6; 95% confidence interval, 2.5 to 494.1) was increased in the second twins with ITDI longer than 60 minutes compared with those with ITDI less than 15 minutes. The incidence of metabolic acidosis increases with increasing ITDI and there is a statistically significant increased risk of neonatal acidosis after longer than 60 minutes compared with less than 15 minutes of ITDI.

ACOG Committee Opinion No. 348: Umbilical Cord Blood Gas and Acid-Base Analysis

Umbilical cord blood gas and acid-base assessment are the most objective determinations of the fetal metabolic condition at the moment of birth. Moderate and severe newborn encephalopathy, respiratory complications, and composite complication scores increase with an umbilical arterial base deficit of 12-16 mmol/L. Moderate or severe newborn complications occur in 10% of neonates who have this level of acidemia and the rate increases to 40% in neonates who have an umbilical arterial base deficit greater than 16 mmol/L at birth. Immediately after the delivery of the neonate, a segment of umbilical cord should be double-clamped, divided, and placed on the delivery table. Physicians should attempt to obtain venous and arterial blood cord samples in circumstances of cesarean delivery for fetal compromise, low 5-minute Apgar score, severe growth restriction, abnormal fetal heart rate tracing, maternal thyroid disease, intrapartum fever, or multifetal gestation.

Continuous Muscle Tissue Oxygenation in Critically Injured Patients: A Prospective Observational Study

Despite normalization of vital signs, critically injured patients may remain in a state of occult underresuscitation that sets the stage for sepsis, organ failure, and death. A continuous, sensitive, and accurate measure of resuscitation after injury remains elusive. In this pilot study, we evaluated the ability of two continuous measures of peripheral tissue oxygenation in their ability to detect hypoperfusion: the Licox polarographic tissue oxygen monitor (PmO2) and the InSpectra near-infrared spectrometer (StO2). We hypothesized that deltoid muscle tissue oxygenation measurements could detect patients in "occult shock" who are at increased risk for post-injury complications. The study was designed to (1) define values for PmO2 and StO2 in patients who by all standard measures appeared to be clinically resuscitated; (2) evaluate the relationship between PmO2, StO2 and other physiologic variables including mean arterial pressure (MAP), lactate and base deficit (BD); and (3) examine the relationship between early low tissue oxygen values and the subsequent development of infections and organ dysfunction. Licox probes were inserted into the deltoid muscle of critically injured patients after initial surgical and radiologic interventions, and transcutaneous StO2 monitors were applied over the same muscle bed. PmO2, StO2, and standard physiologic data were collected continuously using a multimodal bioinformatics system. Twenty-eight critically injured patients were enrolled in this study at admission to the intensive care unit (ICU). For patients who appeared to be well resuscitated (defined as MAP > or = 70 mm Hg, heart rate [HR] < or = 110 bpm, BD > or = -2, and partial pressure of arterial oxygen (PaO2) = 80 and 150 mm Hg), the mean PmO2 was 34 +/- 11 mm Hg and StO2 was 63 +/- 27%. There was a strong relationship between PmO2 and BD (p < 0.001) but no significant relationship between StO2 and BD. The relationship between PmO2 and StO2 was weak but statistically significant. Early low values of both PmO2 and StO2 identified patients at risk for infectious complications or multiple organ failure (MOF). In patients who were well resuscitated by standard continuous parameters (HR and MAP), low PmO2 during the first 24 hours after admission (PmO2 < or = 25 for at least 2 hours) was strongly associated with the development of infectious complications (Odds Ratio = 16.5, 95% CI 1.49 to 183, p = 0.02). PmO2 is a responsive, reliable and continuous monitor of changes in base deficit. Initial low values for either PmO2 or StO2 were associated with post-injury complications. PmO2 monitoring may be useful in identifying patients in the state of occult underresuscitation who remain at risk for developing infection and MOF.

Serum bicarbonate may replace the arterial base deficit in the trauma intensive care unit

Objective Arterial base deficit (BD) is a commonly used marker of injury severity and endpoint of resuscitation but requires an arterial puncture and blood gas analysis. Serum bicarbonate (HCO 3) is routinely obtained as part of the chemistry panel on most admissions. We hypothesized that serum HCO 3 strongly correlates with arterial BD and provides equivalent predictive information. Methods All trauma ICU admissions from 1996 to 2004 with simultaneously obtained serum chemistry panels and arterial blood gases were identified. Correlation between BD and HCO 3 was analyzed by using linear regression, and predictive abilities for acidoses and mortality were compared using the area under the respective receiver operating characteristic curve (AUC). Separate analyses were done for the entire dataset and the subset of ICU admission laboratory values. Results We identified 3,102 patients with 50,311 matched pairs of laboratory data. Serum HCO 3 showed a significant linear correlation with BD for all laboratory sets ( r = 0.85, P < .01) and admission laboratory values only ( r = 0.80, P < .01). Serum HCO 3 reliably predicted the presence of significant metabolic acidoses (BD >5), with an AUC of 0.96 ( P < .01), which clearly outperformed pH (AUC = 0.83), anion gap (AUC = 0.7), and lactate (AUC = 0.73). The mean admission BD among survivors was 2.5 versus 5.2 for nonsurvivors ( P < .01), and the mean HCO 3 was 17.7 versus 19.8 ( P < .01). The admission HCO 3 identified nonsurvivors as accurately as BD (AUCs of 0.66 and 0.68) and more accurately than either pH (AUC = 0.53) or anion gap (AUC = 0.6). Conclusion Serum HCO 3 measurement shows a strong linear correlation and similar predictive ability compared with the arterial BD. Serum HCO 3 may be safely and accurately substituted for arterial BD measurement in critically injured patients.

Use of Serum Bicarbonate Measurement in Place of Arterial Base Deficit in the Surgical Intensive Care Unit

Serum bicarbonate (HCO(3)) measurement may accurately and reliably be substituted for the arterial base deficit (BD) assay in the surgical intensive care unit (ICU). Retrospective criterion standard analysis. Surgical ICU in a tertiary care facility. Consecutive sample of non-trauma-related surgical ICU admissions from January 1996 to January 2004 with simultaneously obtained serum HCO(3) and arterial BD levels. Correlation between HCO(3) and BD at admission and during the ICU stay; predictive value of serum HCO(3) for significant metabolic acidosis and ICU mortality. The study included 2291 patients with 26 063 sets of paired laboratory data. The mean +/- SD age was 52 +/- 16 years and mean ICU stay was 5.8 +/- 9.8 days. There were 174 ICU deaths (8%). Serum HCO(3) levels showed significant correlation with arterial BD levels both at admission (r = 0.85, R(2) = 0.72, P<.001) and throughout the ICU stay (r = 0.88, R(2) = 0.77, P<.001). Serum HCO(3) reliably predicted the presence of significant metabolic acidosis (BD > 5) with an area under the receiver operating characteristic curve (AUC) of 0.93 at admission and 0.95 overall (both P<.001), outperforming pH (AUC, 0.80), anion gap (AUC, 0.70), and lactate (AUC, 0.70). The admission serum HCO(3) level predicted ICU mortality as accurately as the admission arterial BD (AUCs of 0.68 and 0.70, respectively) and more accurately than either admission pH or anion gap. Serum HCO(3) provides equivalent information to the arterial BD and may be used as an alternative predictive marker or guide to resuscitation. Low HCO(3) levels should prompt immediate metabolic acidosis evaluation and management.

Prehospital hemoglobin-based oxygen carrier resuscitation attenuates postinjury acute lung injury

Crystalloid infusion has been the standard prehospital fluid resuscitation in the United States for the past 35 years, but the emergence of a safe and effective hemoglobin-based oxygen carrier (HBOC) may change that practice. The purpose of this in vivo study is to simulate an existing multicenter prehospital trial of HBOC versus crystalloid to determine the effects in a controlled 2-event construct of postinjury multiple organ failure. Rats underwent hemorrhagic shock (30 mm Hg x 45 min) and were resuscitated over 2 hours in a clinically relevant design: 2 x volume of shed blood (SB) using normal saline (NS) in the first 30 minutes; 1/2 volume of SB in the next 30 minutes; another 2 x SB volume with NS over the remaining 60 minutes. Study groups represented alternative fluid strategies during the first hour of resuscitation: (1) Inhospital SB (standard resuscitation), (2) Inhospital HBOC, (3) Prehospital SB, and (4) Prehospital HBOC. Global physiologic response was assessed via tissue oxygenation (near infrared spectroscopy) and arterial base deficit, and pulmonary response, via lung polymorphonuclear neutrophil accumulation and vascular permeability. Prehospital HBOC resuscitation provided the most efficient recovery of tissue oxygenation and correction of base deficit, had the greatest reduction in pulmonary polymorphonuclear neutrophil accumulation, and abrogated acute lung injury. Prehospital SB and Inhospital HBOC regimens afforded intermediate lung protection, compared with standard resuscitation. The findings in this controlled in vivo study suggest prehospital HBOC resuscitation improves the recovery from postshock oxygen debt and reduces postinjury organ dysfunction.

Anaesthesia for Caesarean section and neonatal acid‐base status: a meta‐analysis*

Spinal anaesthesia is generally preferred for Caesarean section. Its superiority for the baby is often assumed. Umbilical artery acid-base status provides a valid index of fetal welfare. Twenty-seven studies reporting neonatal acid-base data with different types of anaesthesia were used to compare umbilical artery or vein pH and base deficit, using random-effect meta-analysis. Cord pH was significantly lower with spinal than with both general (difference: -0.015; 95% CI -0.029 to -0.001; 13 studies, 1272 subjects) and epidural anaesthesia (difference -0.013; 95% CI -0.024 to -0.002; 11 studies, 828 subjects). Larger doses of ephedrine contributed to the latter effect (p = 0.023). Sixteen studies reported a base deficit, which was significantly higher for spinal than for general (difference 1.109; 95% CI 0.434-1.784 mEq.l(-1); seven studies, 695 subject) and epidural anaesthesia (difference 0.910; 95% CI 0.222-1.598 mEq.l(-1); seven studies, 497 subjects). Spinal anaesthesia cannot be considered safer than epidural or general anaesthesia for the fetus.

Variables Predicting Trauma Patient Survival Following Massive Transfusion

The literature contains little information regarding demographic or transfusion-related factors associated with survival following massive blood transfusion in trauma patients. The objective of this study was to describe patient, transfusion, and laboratory variables contributing to survival in this population during the first and second days after arrival at the hospital. A secondary objective was to identify costs associated with massive blood transfusion. A 7-year, retrospective review of 13,005 consecutive trauma patient records yielded a sample of 46 who were transfused with > or =50 units of blood products in the first postinjury day. Descriptive statistics were computed to describe the sample, transfusion data, and laboratory values. Logistic regression was used to predict survival using selected patient characteristics, laboratory data, and transfusion characteristics for both the first and second days. Overall survival among this group who received massive transfusion was 63%. No significant differences were found between survivors and nonsurvivors in age, sex, type of trauma, or amount of any of the blood components administered on Day 1. Nonsurvivors had higher Injury Severity Scores and shorter ICU and hospital lengths of stay. Controlling for other variables, only arterial base deficit levels made a significant unique contribution to predicting survival. The volume of blood transfused on Day 2 did not contribute to survival prediction. The average cost of blood transfusion was more than 49,000 US dollars per survivor and 51,000 US dollars per nonsurvivor. Defining medical futility based solely on the volume of blood products transfused currently is unjustified. The search for other early indicators of survival in the trauma population must continue.

Umbilical Artery Blood Gas Parameters in Neonates With Early-Onset Seizures Who Die

Hypoxic–ischemic encephalopathy is diagnosed when newborn infants have certain neurologic abnormalities, including early-onset seizures, within 24–48 hours of admission to neonatal intensive care. The American College of Obstetricians and Gynecologists defines hypoxia severe enough to cause hypoxic–ischemic encephalopathy as a group of findings including a pH below 7.0; an Apgar score of 0–3 for longer than 5 minutes; neurologic sequelae; and cardiovascular, gastrointestinal, hematologic, pulmonary, or renal dysfunction. Early-onset seizures are the clearest indicator of moderate to severe disease with hypoxic–ischemic encephalopathy. Infants with this disorder are also at increased risk of cerebral palsy and neonatal death. This study sought to relate umbilical artery blood gas parameters to mortality in 47 infants at 32 or more weeks gestation who were admitted with early-onset seizures secondary to hypoxic–ischemic encephalopathy. Fourteen of 47 newborn infants admitted to the study died of complications related to hypoxic–ischemic encephalopathy. Maternal demographic factors were comparable regardless of whether the infant died or survived. Active resuscitation was attempted in all instances. There were no significant differences between infants who died and those who survived with respect to umbilical artery blood values of pH, base deficit, PCO2, or oxygen saturation. Levels of PO2 were significantly higher in neonates who died than in survivors (18.4 vs. 12.3). Neither umbilical artery blood pH nor base deficit predicted neonatal deaths in the present study of infants having hypoxic–ischemic encephalopathy and early-onset seizures. A high PO2 in newborn infants who subsequently die may reflect an impaired inability to extract oxygen from the blood. The question of whether patterns of change in PCO2 predict the development of neonatal encephalopathy awaits further investigation.

Chronic implantation of transit-time flow probes on the ascending aorta of rodents.

This study describes the implantation of transit-time flow probes on the ascending aorta of rats while minimizing the risk of postoperative complications. Special emphasis is placed on our new method of rat intubation as well as the production of materials necessary for the implantation procedure such as endotracheal tubes and heparin bonded vessel catheters. The effects of these devices on the response to acute hypoxia were studied in rats following a 5-7 day recovery from the implantation procedure. Systemic and microvascular measurements were made on instrumented rats (n = 5) and non-instrumented controls (n = 3) that were ventilated with 21%, 15%, 10%, 8% and 5% oxygen. Arterial pressure, PO(2), lactate, and base deficit were not different between the implanted and control animals at any inspired oxygen concentration. Microvascular flow in the primary arterioles of the spinotrapezius muscle was also similar between the two groups at all inspired oxygen concentrations. We conclude that this novel methodology facilitates the measurement of whole body oxygen delivery in resting and haemodynamically-stressed rats.

Umbilical artery blood gas parameters in neonates with early onset seizures who die

To relate umbilical artery blood gas parameters to mortality among neonates with hypoxic-ischaemic encephalopathy related to early onset seizures. Population cohort study. British Columbia Women's Hospital. Forty-seven infants at >or=32 weeks of gestation admitted to NICU with early onset seizures secondary to hypoxic-ischaemic encephalopathy with umbilical artery blood gases done at delivery. Patients were divided into two groups: (1) Infants with neonatal seizures who survived, and (2) infants with neonatal seizures who died related to hypoxic-ischaemic encephalopathy complications. Comparison of umbilical artery pH, PO(2), PCO(2), base deficit was done between the two groups with Student's t tests. Umbilical artery pH, PO(2), PCO(2) and base deficit. The PO(2) was significantly higher in the group that expired (18.36 +/- 9.15 vs 12.33 +/- 7.51). There were no significant differences in any other blood gas parameters between the groups. Neither the umbilical artery pH nor base deficit is predictive of neonatal death in infants with hypoxic-ischaemic encephalopathy with seizures. The finding of a high PO(2) in neonates who died may indicate an inability of those infants to efficiently extract oxygen from blood.

The influence of vacuum extractor on fetal oxygenation and newborn status.

The aim of this study was to determine the effects of vacuum extractor assisted delivery on fetal oxygenation and acid-base balance. Sixty-one women were enrolled in the present study. The subjects were divided into two groups. Group A, consisting of 39 women, had normal vaginal deliveries. Group B, consisting of 22 women, underwent a vacuum extractor assisted vaginal delivery. Fetal arterial oxygen saturation (SpO2) monitoring was used in all women after full cervical dilatation. After delivery, umbilical artery pH, pCO2, pO2 and base deficit (BDecf) levels were determined in all neonates. The mean FSpO2 value in Group A was 51.53+/-5.87% and in Group B 48.03+/-6.39% (p<0.03). The mean cord pH value in fetuses of Group A was 7.26+/-0.05, and in Group B 7.17+/-0.09. There was also a significant difference between the two groups with regards to mean pO2, pCO2 and BDecf values. Vacuum assisted vaginal delivery was associated with lower fetal arterial oxygen saturation levels as well as lower cord blood pH values compared to those seen after unassisted vaginal delivery. Although decreased, however, the above parameters remained within normal ranges.

The 2003 Carl A Moyer Award: real-time metabolic monitors, ischemia-reperfusion, titration endpoints, and ultraprecise burn resuscitation.

Real-time metabolic monitoring of varied vascular beds provides the raw data necessary to conduct ultraprecise burn shock resuscitation based on second-by-second assessment of regional tissue perfusion. It also illustrates shortcomings of current clinical practices. Arterial base deficit was continuously monitored during 11 clinical resuscitations of patients suffering burn shock using a Paratrend monitor. Separately, in a 30% TBSA rat burn model (N = 70), three Paratrend monitors simultaneously recorded arterial blood gas and tissue pCO2 of the burn wound and colonic mucosa during resuscitation at 0, 2, 4, 6, and 8 ml/kg/%TBSA. Paratrend data were analyzed in conjunction with previously reported laser Doppler images of actual burn wound capillary perfusion. With current clinical therapy, continuous monitoring of arterial base deficit revealed repetitive cycles of resolution/worsening/resolution during burn shock resuscitation. In the rat model, tissue pCO2 in both burn wounds and splanchnic circulation differed depending on the rate of fluid resuscitation (P <.01 between sham and 0 ml/kg/%TBSA and between 2 ml/kg/%TBSA and 4 ml/kg/%TBSA). Burn wound pCO2 values correlated well with laser Doppler determination of actual capillary perfusion (rho = -.48, P <.01). The following conclusions were reached: 1). Gratuitous and repetitive ischemia-reperfusion-ischemia cycles plague current clinical therapy as demonstrated by numerous "false starts" in the resolution of arterial base deficit; 2). in a rat model, real-time monitoring of burn wound and splanchnic pCO2 demonstrate a dose-response relationship with rate of fluid administration; and 3). burn wound and splanchnic pCO2 are highly correlated with direct measurement of burn wound capillary perfusion by laser Doppler imager. Either technique can serve as a resuscitation endpoint for real-time feedback-controlled ultraprecise resuscitation.