Degree Of Hypercapnia Research Articles

Factors Affecting the Length of Hospital Stay in Hypercapnic Respiratory Failure

Background/Objectives: Hypercapnic respiratory failure (HRF) is a primary cause of admittance to the intensive care unit (ICU). This study aimed to investigate the factors that affect the length of hospital stay in HRF patients. Methods: This study was designed as a retrospective, cross-sectional analysis of patients who were admitted to the ICU because of HRF between 2022 and 2024. The demographic and clinical characteristics of the patients and laboratory results were recorded. The Charlson Comorbidity Index (CCI) was calculated. The relationship between these parameters and the length of hospital stay was assessed. Results: A total of 138 patients were included in the study. The average length of hospital stay was 11.45 days, and 37% of the patients were included in the long-term hospitalization group. The degree of hypercapnia was not associated with the length of hospital stay. It was determined that the patients’ albumin levels and CCI were significant determinants of the length of hospital stay. The combined assessment of these two parameters was found to be superior compared to their separate evaluations. Conclusions: In our study, hypoalbuminemia and a higher CCI were identified as predictors of a prolonged ICU stay in HRF patients. Albumin levels of <3.25 g/dL and CCI scores of ≥5 were linked to longer stays, with this combined evaluation offering greater predictive value. These factors can guide patient management.

Evaluation of CO2 removal rate of ECCO2R for a renal replacement therapy platform in an experimental setting.

A critical parameter of extracorporeal CO2 removal (ECCO2R) applications is the CO2 removal rate (VCO2). Low-flow venovenous extracorporeal support with large-size membrane lung remains undefined. This study aimed to evaluate the VCO2 of a low-flow ECCO2R with large-size membrane lung using a renal replacement therapy platform in an experimental animal model. Twelve healthy pigs were placed under mechanical ventilation and connected to an ECCO2R-CRRT system (surface area = 1.8 m2; OMNIset®, BBraun, Germany). Respiratory settings were reduced to induce two degrees of hypercapnia. VCO2 was recorded under different combinations of PaCO2 (50-69 or 70-89 mm Hg), extracorporeal blood flow (ECBF; 200 or 350 mL/min), and gas flow (4, 6, or 10 L/min). VCO2 increased with ECBF at all three gas flow rates. In severe hypercapnia, the increase in sweep gas flow from 4 to 10 L/min increased VCO2 from 86.38 ± 7.08 to 96.50 ± 8.71 mL/min at an ECBF of 350 mL/min, whereas at ECBF of 200 mL/min, any increase was less effective. But in mild hypercapnia, the increase in sweep gas flow result in significantly increased VCO2 at two ECBF. VCO2 increased with PaCO2 from 50-69 to 70-89 mm Hg at an ECBF of 350 mL/min, but not at ECBF of 200 mL/min. Post-membrane lung PCO2 levels were similar for different levels of premembrane lung PCO2 (p = 0.08), highlighting the gas exchange diffusion efficacy of the membrane lung in gas exchange diffusion. In severe hypercapnia, the reduction of PaCO2 elevated from 11.5% to 19.6% with ECBF increase only at a high gas flow of 10 L/min (p < 0.05) and increase of gas flow significantly reduced PaCO2 only at a high ECBF of 350 mL/min (p < 0.05). Low-flow venovenous extracorporeal ECCO2R-CRRT with large-size membrane lung is more efficient with the increase of ECBF, sweep gas flow rate, and the degree of hypercapnia. The influence of sweep gas flow on VCO2 depends on the ECBF and degree of hypercapnia. Higher ECBF and gas flow should be chosen to reverse severe hypercapnia.

DIFFERENCES IN OUTCOMES OF COPD EXACERBATIONS WITH DEGREE OF HYPERCAPNIA: AN OBSERVATIONAL PERSPECTIVE

DIFFERENCES IN OUTCOMES OF COPD EXACERBATIONS WITH DEGREE OF HYPERCAPNIA: AN OBSERVATIONAL PERSPECTIVE

Effects of Carbon Dioxide and Temperature on the Oxygen-Hemoglobin Dissociation Curve of Human Blood: Implications for Avalanche Victims.

Completely avalanche-buried patients are frequently exposed to a combination of hypoxia and hypercapnia with a risk of normothermic cardiac arrest. Patients with a long burial time and an air pocket are exposed to a combination of hypoxia, hypercapnia, and hypothermia which may lead to the development of the “triple H syndrome”. This specific combination has several pathophysiological implications, particularly on the cardiovascular system and oxygen transport (oxygen supply and oxygen consumption). To examine the effects on hemoglobin oxygen affinity, we investigated venous blood samples from 15 female and 15 male healthy subjects. In a factorial design of four different carbon dioxide partial pressure (PCO2) levels (20, 40, 60, and 80 mmHg) and five different temperature levels (13.7°C, 23°C, 30°C, 37°C, and 42°C), 30 unbuffered whole blood samples were analyzed in a newly developed in vitro method for high-throughput oxygen dissociation curve (ODC) measurements. P50s, Hill coefficients, CO2-Bohr coefficients, and temperature coefficients were analyzed using a linear mixed model (LMM). Mean P50 at baseline (37°C, 40 mmHg PCO2) was 27.1 ± 2.6 mmHg. Both CO2-Bohr (p < 0.001) and temperature coefficients (p < 0.001) had a significant effect on P50. The absolute CO2 effect was still pronounced at normothermic and febrile temperatures, whereas at low temperatures, the relative CO2 effect (expressed by CO2-Bohr coefficient; p < 0.001, interaction) was increased. The larger impact of PCO2 on oxygen affinity at low temperature may be caused by the competition of 2,3-BPG with PCO2 and the exothermic binding characteristic of 2,3-BPG. In a model of an avalanche burial, based on published data of CO2 levels and cooling rates, we calculated the resulting P50 for this specific condition based on the here-reported PCO2 and temperature effect on ODC. Depending on the degree of hypercapnia and hypothermia, a potentially beneficial increase in hemoglobin oxygen affinity in the hypoxic condition might ensue.

Hypercapnia in Advanced Chronic Obstructive Pulmonary Disease: A Secondary Analysis of the National Emphysema Treatment Trial.

Hypercapnia develops in one third of patients with advanced chronic obstructive pulmonary disease (COPD) and is associated with increased morbidity and mortality. Multiple factors in COPD are thought to contribute to the development of hypercapnia including increased carbon dioxide (CO2) production, increased dead space ventilation, and the complex interactions of deranged respiratory system mechanics, inspiratory muscle overload and the ventilatory control center in the brainstem. However, these factors have not previously been systematically analyzed in a large, well-characterized population of severe COPD patients. This is a secondary analysis of the clinical, physiologic and imaging data from the National Emphysema Treatment Trial (NETT). All patients with complete baseline data for the key predictor variables were included. An inclusive list of 32 potential predictor variables were selected a priori based on consensus of the investigators and literature review. Stepwise variable selection yielded 10 statistically significant associations in multivariate regression. A total of 1419 patients with severe COPD were included in the analysis; mean age 66.4 years (standard deviation 6.3), 38% females, and 422 (29.7%) had baseline hypercapnia. Key variables associated with hypercapnia were low resting partial pressure of oxygen in blood, low minute ventilation (Ve), high volume of exhaled carbon dioxide, low forced expiratory volume in 1 second, high residual volume, lower % emphysema on chest computed tomography, use of oxygen, low ventilatory reserve (high Ve/maximal voluntary ventilation), and not being at high altitude. Low diffusing capacity for carbon monoxide showed a positive association with hypercapnia in univariate analysis but a negative correlation in multivariate analysis. Measures of dyspnea and quality of life did not associate with degree of hypercapnia in multivariable analysis. Hypercapnia in a well-characterized cohort with severe COPD and emphysema is chiefly related to poor lung mechanics, high CO2 production, and a reduced ventilatory capability. Hypercapnia is less impacted by gas exchange abnormalities or the presence of emphysema.

Anesthesia differentially modulates neuronal and vascular contributions to the BOLD signal

Most studies involving BOLD fMRI in basic neuroscience research are conducted with anesthetized animals. This study investigates neural and hemodynamic activity through a combination of experiments comprising BOLD fMRI, optical calcium recordings and ASL in vivo. Patch clamp experiments of neurons were conducted to evaluate electrophysiological correlates of neural activity in vitro. Various anesthetic conditions embracing numerous anesthetic depths evoked by different concentrations of isoflurane (ISO) and different degrees of hypercapnia under a constant stimulus were investigated. We observed that different anesthetic conditions had major impact on the results obtained, particularly that anesthesia could cause a massive divergence of different experimental modalities.In ventilated animals, robust BOLD responses were detectable even with relatively deep anesthesia, while in non-ventilated animals, BOLD responses were not detectable under these conditions. This was most likely due to hypercapnia caused by respiratory depression, as in ventilated animals administered CO2 had the same effect. This observation agreed with measurements of perfusion, which showed that inhaled CO2 increased perfusion significantly, while ISO did not.In optical calcium measurements, higher concentrations of ISO decreased spontaneous neural activity, but not stimulus-evoked responses. This observation was explained by a generally lower excitability of neurons under ISO, which suppressed spontaneous activity, and consequently left more neurons available to fire synchronously in response to a stimulus. Interpreting this phenomenon as an integrated signal of independent single neurons was supported by patch clamp experiments as the number of action potentials (APs) per stimulus was decreased by addition of CO2. Addition of ISO on the other hand had no significant effect.Our results provide an explanation on the cellular level for anesthesia-dependent observations in previous studies of task-induced BOLD and resting state connectivity. They further inform selection of the adequate anesthetic regimen for a given combination of modalities.

Obstructive sleep apnoea in children: perioperative considerations

Obstructive sleep apnoea (OSA) has become a major public health concern as its incidence and severity have increased in tandem with the obesity epidemic. In children, OSA is now recognized as a common disorder and can be associated with significant morbidity. OSA belongs to a spectrum of diagnoses known as sleep-related breathing disorders in which the airway is completely (apnoea) or partially (hypopnoea) occluded during sleep despite continued respiratory efforts. This airway obstruction can cause abnormal gas exchange leading to hypoxaemia, hypercapnia, sleep fragmentation, and their attendant physiological and behavioural consequences. The degrees of hypercapnia, hypoxaemia, and upper airway airflow reduction are the primary factors determining the severity of OSA. In young children, adenotonsillar hypertrophy is the most common anatomical abnormality associated with OSA, and adenotonsillectomy is, therefore, the most common surgical intervention. Perioperative complications associated with adenotonsillectomy are more common in children with severe OSA. A thorough understanding of the pathophysiology of OSA, careful and complete preoperative assessment, meticulous intraoperative and postoperative management, and early recognition of potential perioperative complications are essential to optimization of outcomes. The safe anaesthetic management of a child with OSA requires an anaesthetic technique tailored to the underlying aetiology and severity of OSA and the surgical procedure. This review focuses on the epidemiology, pathogenesis, and diagnosis of OSA, and the state-of-the-art and future directions in the perioperative management of children with OSA.

Ventricular performance during exercise in patients with chronic obstructive pulmonary disease (COPD)

We assessed ventricular performance during exercise in 16 COPD patients and 8 normal control subjects by means of radionuclide equilibrium angiography using technetium-99m as a tracer. Supine exercise on a bicycle ergometer was performed until symptom-limited exhaustion. Data were accumulated for 300 heart beats at rest and 150 heart beats during exercise. We used the standard voxel count method to calculate the ventricular volumes. Age, FEV1.0%, %VC, PaO2 and PaCO2 of the COPD patients were 63 +/- 8 yr, 46 +/- 11%, 69 +/- 18%, 68 +/- 11 Torr and 44 +/- 7 Torr (mean +/- SD), respectively. Systolic dysfunction of both the left and right ventricles was well confirmed in the present study. In 12 patients who also underwent hemodynamic studies, resting total pulmonary vascular resistance index (TPVRI) and mean pulmonary artery pressure (Ppa) significantly correlated with right ventricular end-systolic volume index (RVESVI) obtained by RI angiography; gamma = 0.769 (p less than 0.01) and gamma = 0.631 (p less than 0.05), respectively. A significant relationship was also observed between left ventricular dysfunction and the degree of hypercapnia. In response to exercise testing, 10 of 16 patients exhibited insufficient augmentation of stroke volume, and both left and right end-diastolic volumes decreased in half of 10 patients. It is suggested that cardiac function may be disturbed by mechanical factors such as pulmonary hyperinflation in COPD patients.

Assessment of local changes of cerebral perfusion and blood concentration by near infrared spectroscopy and ultrasound contrast densitometry

The objective of this study is to correlate regional cerebral blood concentration measurements made with near infrared spectroscopy to simultaneous local measurements of ultrasound contrast agent (CA) densitometry. Experiments were performed with piglets (7 kg) under general anesthesia. The cerebral blood flow (CBF) and volume (CBV) were changed by inducing various degrees of hypercapnia. NIRS measurements were performed with a quasi-continuous wave system, using an optode distance of 3–6 cm. The concentration changes in oxygenated and deoxygenated hemoglobin and their sum and difference ( cO 2Hb, cHHb, ctHb, cHbD) were continuously calculated. Ultrasound contrast agent (SF 6) was administered as a short intra-venous bolus. Ultrasound equipment was used in pulse inversion second harmonic gray scale imaging mode at low transmit power setting. Three regions-of-interest (0.25 cm 2) were analyzed in each image. Wash-in curves were constructed as spatial mean gray level vs. time. The variables collected with both methods changed according to the induced changes in the physiological condition. Changes in the PaCO 2, pH and carotid flow induced highly correlated changes in cO 2Hb, cHHb, ctHb and cHbD, and in the variables derived from CA analyses. NIRS and CA methods measure regional, respectively, local changes in CBV and CBF. Moreover, NIRS can yield complementary information about the cerebral oxygenation.

Respiratory status of infants with esophageal atresia.

In infants with esophageal atresia (EA), lung opacities on a chest radiograph (CXR) are usually considered the cause of respiratory distress (RD). However, in some instances signs of RD and CXR changes show no correlation. The aim of this study was to investigate the pathogenesis of RD in EA patients with a normal CXR. In 41 infants with EA, CXR findings were correlated with clinical manifestations and blood-gas analysis data. The degree of abnormal gas exchange was quantitated by the arterial/alveolar oxygen tension ratio (a-ARO2). Of the 41 infants, 39(95%) presented with RD. No lung opacities were found in 130 of 294 CXRs examined (44%). An a-ARO2 below 0.75 (lower limit of normal) was calculated in 215 of 247 arterial blood samples analyzed (87%). When a temporal correlation was established, RD with a clear CXR was characterized by signs of extra- and intrathoracic airway obstruction, often associated with an a-ARO2 below 0.75. The degree of hypoxemia was greater than the degree of hypercapnia. We conclude that in infants with EA, RD with a clear CXR is related to both tracheomalacia and upper-airway obstruction that may cause miliary atelectasis not detected by conventional CXR with intrapulmonary shunting and hypoxemia.

Lung and chest wall mechanics in ventilated patients with end stage idiopathic pulmonary fibrosis

BACKGROUNDIdiopathic pulmonary fibrosis is an inflammatory disease which leads to chronic ventilatory insufficiency and is characterised by a reduction in pulmonary static and dynamic volumes. It has been suggested that...

Relationship between resting hypercapnia and physiologic parameters before and after lung volume reduction surgery in severe chronic obstructive pulmonary disease.

Patients with severe chronic obstructive pulmonary disease (COPD) have varying degrees of hypercapnia. Recent studies have demonstrated inconsistent effects of lung volume reduction surgery (LVRS) on PaCO2; however, most series have excluded patients with moderate to severe hypercapnia. In addition, no study has examined the mechanisms responsible for the reduction in PaCO2 post-LVRS. We obtained spirometry, body plethysmography, diffusion capacity, respiratory muscle strength, 6-min walk test, and incremental symptom-limited maximal exercise data in 33 consecutive patients pre- and 3 to 6 mo post-LVRS, and explored the relationship between changes in PaCO2 and changes in the measured physiologic variables. All patients underwent bilateral LVRS via median sternotomy and stapling resection by the same cardiothoracic surgeon. Patients were 57 +/- 8 yr of age with severe COPD, hyperinflation, and air trapping (FEV1, 0.73 +/- 0.2 L; TLC, 7.3 +/- 1.6 L; residual volume [RV], 4.8 +/- 1.4 L), and moderate resting hypercapnia (PaCO2, 44 +/- 7 mm Hg; range, 32 to 56 mm Hg). Post-LVRS, PaCO2 decreased by 4% (PaCO2 pre 44 +/- 7 mm Hg, PaCO2 post 42 +/- 5 mm Hg; p = 0.003). Patients with higher baseline values of PaCO2 had the greatest reduction in PaCO2 post-LVRS (r = -0.61, p < 0.001). Significant correlations existed between reduction in PaCO2 and changes in FEV1 (r = -0.56; p = 0.0007), maximal inspiratory pressure (PImax) (r = -0.46; p = 0.009), diffusing capacity of the lungs for carbon monoxide (DLCO) (r = -0.47; p = 0.008), and RV/TLC (r = 0.41; p = 0. 02). Correlation existed also between reduction in PaCO2 and breathing pattern at maximal exercise: maximal minute ventilation (V Emax) (r = -0.47; p = 0.009), and tidal volume (VT) (r = -0.40; p = 0.02). The changes in PaCO2 post-LVRS showed marked intersubject variability. We conclude that LVRS, by reducing hyperinflation, air trapping, and improving respiratory muscle function, enables the lung and chest wall to act more effectively as a pump, thereby increasing alveolar ventilation and reducing baseline resting PaCO2. In addition, patients with higher baseline levels of PaCO2 demonstrate the greatest reduction in PaCO2 post-LVRS, and should not be excluded from receiving LVRS.

AN EVIDENCE-BASED APPROACH TO PRESSURE-AND VOLUME-LIMITED VENTILATION STRATEGIES

In summary, based on the evidence reviewed, clinicians should continue to adopt a pressure-limited ventilation strategy for patients with acute lung injury, but combine this strategy with relatively liberal use of PEEP. Critical care clinicians can look forward to more information about the degree of hypercapnia that can be safely permitted in the full reports of the RCTs reviewed and in related critical care literature.

Carbon dioxide and the cerebral circulation.

Carbon dioxide and the cerebral circulation.

Cardiopulmonary effects of sevoflurane in cats: comparison with isoflurane, halothane, and enflurane

The cardiopulmonary effects of sevoflurane (mean, 2·6, 3·8–3·9 and 5·2 per cent) were compared with those of halothane (1·2, 1·8 and 2·4 per cent), enflurane (2·4, 3·6 and 4·8 per cent) and isoflurane (1·6, 2·4 and 3·2–3·3 per cent) at end-tidal concentrations equivalent to 1, 1·5 and 2 minimal alveolar concentrations ( macs) during spontaneous or controlled ventilation ( sv or cv) in 57 cats. Cats were assigned to four groups of nine animals each in sv trial and four groups of five or six animals each in cv trial. During sv, respiration rate was decreased by sevoflurane and isoflurane at 2 mac and by enflurane at each mac multiple when compared with control values, whereas halothane increased respiration rate at 2 mac. The degree of hypercapnia and acidosis induced by sevoflurane was not different from that induced by isoflurane and was less than that induced by halothane at 1 to 1·5 mac or enflurane at 2 mac. During sv and cv, four anaesthetics decreased heart rate at 2 mac when compared with control values, but there was no significant difference between anaesthetics. Sevoflurane, like halothane and isoflurane, induced hypotension at 2 mac when compared with 1 mac.

Halothane anaesthesia in the rabbit: a comparison of the effects of medetomidine, acepromazine and midazolam on breath-holding during induction

SUMMARY The effects of induction of anaesthesia with halothane were studied in rabbits which received either no pre-anaesthetic medication, acepromazine (0.5 and l mg/kg bwt im), medetomidine (0.25 and 0.5 mg/kg bwt im) or midazolam (1 and 2 mgkg bwt im). All rabbits had periods of apnoea (> 1 min) during induction, resulting in moderate hypercapnia and acidosis. The degree of hypercapnia was not influenced by pre-anaesthetic treatment. All animals showed a significant reduction in heart rate ( P P

Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates.

The authors sought to develop a model for assessing in vivo regulation of cerebral vasoregulation by nitric oxide (NO), originally described as endothelial-derived relaxing factor, and to use this model to establish the role of NO in the regulation of cerebral blood flow (CBF) in primates. By using regional intraarterial perfusion, the function of NO in cerebral vasoregulation was examined without producing confounding systemic physiological effects. Issues examined were: whether resting vasomotor tone requires NO; whether NO mediates vasodilation during chemoregulation and autoregulation of CBF; and whether there is a relationship between the degree of hypercapnia and hypotension and NO production. Twelve anesthetized (0.5% isoflurane) cynomolgus monkeys were monitored continuously for cortical CBF, PaCO2, and mean arterial pressure (MAP), which were systematically altered to provide control and experimental curves of chemoregulation (CBF vs. PaCO2) and autoregulation (CBF vs. MAP) during continuous intracarotid infusion of 1) saline and 2) an NO synthase inhibitor (NOSI), either L-n-monomethyl arginine or nitro L-arginine. During basal conditions (PaCO2 of 38-42 mm Hg) NOSI infusion of internal carotid artery (ICA) reduced cortical CBF from 62 (saline) to 53 ml/100 g/per minute (p<0.01), although there was no effect on MAP. Increased CBF in response to hypercapnia was completely blocked by ICA NOSI. The difference in regional (r)CBF between ICA saline and NOSI infusion increased linearly with PaCO2 when PaCO2 was greater than 40 mm Hg, indicating a graded relationship of NO production, increasing PaCO2, and increasing CBF. Diminution of CBF with NOSI infusion was reversed by simultaneous ICA infusion of L-arginine, indicating a direct role of NO synthesis in the chemoregulation of CBF. Hypotension and hypertension were induced with trimethaphan camsylate (Arfonad) and phenylephrine at constant PaCO2 (40 +/- 1 mm Hg). Autoregulation in response to changes in MAP from 50 to 140 mm Hg was unaffected by ICA infusion of NOSI. In primates, cerebral vascular tone is modulated in vivo by NO; continuous release of NO is necessary to maintain homeostatic cerebral vasodilation; vasodilation during chemoregulation of CBF is mediated directly by NO production; autoregulatory vasodilation with hypertension is not mediated by NO; and increasing PaCO2 induces increased NO production.

Metabolic, hemodynamic, and ventilatory responses to respiratory load in sedated neonatal piglets

Some neonatal species fail to develop the expected degree of hypercapnia during hypoventilation with mechanical loads. We studied 13 spontaneously breathing, sedated piglets (1-9 days old), grouped by age as young (< or = 3 day old) or old (> 3 day old). Baseline measurements of minute ventilation, arterial blood pressure (BP), cardiac output, and O2 consumption were repeated after continuous (inspiratory and expiratory) flow-resistive loading of 330 cmH2O.l-1 x s for 10 min. Older animals [n = 6, age 6.6 +/- 1.9 (SD) days, wt 1.99 +/- 0.5 kg] increased metabolic rate (9.8 +/- 1.4 to 10.5 +/- 1.3 ml.min-1 x kg-1, P < 0.01), whereas younger animals (n = 7, 2.6 +/- 0.6 days, 1.37 +2- 0.3 kg) invariably decreased metabolic rate with loading (9.7 +/- 1.6 to 7.9 +/- 2.6 ml.min-1 x kg-1); changes were different between groups (P < 0.02). Although ventilation decreased with loading in both groups (P < 0.01), younger animals showed a relatively greater fall from baseline values (38 vs. 27%). Despite differences in the degree of hypoventilation, arterial CO2 tension increased similarly in both groups (21%). BP increased (P < 0.01) with loading in older but not younger animals. We conclude that the decreased metabolic rate and limited hemodynamic response in younger piglets reflect an accomodative response to hypoventilation in contrast to that of older animals, which display an adult pattern of increased metabolic rate and BP with loaded breathing.

Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission

Prior to the start of supportive therapy at the site of the accident, arterial blood samples from 47 patients with acute head injury were taken for blood gas analysis. At the same time, the degree of unconsciousness was assessed using the Glasgow-Coma-Scale. After transport to the hospital, arterial blood gases and the level of unconsciousness were again determined. A very close correlation was found between the initial depth of unconsciousness and the degree of hypercapnia (R = -0.90). Patients with head injury and other multiple injuries did not differ in this report (R = -0.95) from those with isolated head injury. The correlation between PaO2 and the degree of unconsciousness was less well defined, and the results showed a greater degree of scatter (R = 0.54). The acidosis observed resulted mainly from the rise in PaCO2. The absence of any correlation between the base excess and the Glasgow-Coma-Scale levels (R = -0.27) makes a common metabolic derangement unlikely. As a result of intubation and controlled ventilation, the hypercapnia of the comatose patients had been corrected, and a correlation could no longer be found between the Glasgow-Coma-Scale level and the PaCO2. In order to avoid hypoventilation, which carries with it the danger of a rise in intracranial pressure, all patients with severe head injury should be intubated and ventilated as soon as possible after the accident.

Blood gases, pH, and lactate in appropriate- and small-for-gestational-age fetuses

The pH, P O2, P CO2, and lactate concentration were measured in umbilical blood samples obtained by cordocentesis from 208 appropriate-for-gestational-age and. 196 small-for-gestational-age fetuses at 18 to 38 weeks' gestation. In the appropriate-for-gestational-age fetuses umbilical venous ( n = 173) and arterial ( n = 35) P O2 and pH decreased, and umbilical venous and arterial P CO2 increased with advancing gestation. Blood lactate concentration did not change. Compared with the appropriate-for-gestational-age fetuses, the small-for-gestational-age fetuses were hypoxemic, hypercapnic, hyperlacticemic, and acidotic. There was mixed respiratory and metabolic acidosis, and the decrease in pH was significantly correlated with both hypercapnia and hyperlacticemia. In the umbilical artery ( n = 53) there was a significant linear correlation between the degree of hypoxemia and the degrees of hypercapnia or acidosis. In the umbilical vein ( n = 143) the correlations between the degree of hypoxemia and the degrees of hypercapnia, hyperlacticemia, or acidosis were exponential.