Hypoxia with acidosis in extremely preterm born infants was not associated with an increased risk of death or impaired neurodevelopmental outcome at 6.5 years.

AIM: It is not clear whether perinatal acidosis can predict poor outcomes in extremely preterm infants and we investigated associations between intrapartum hypoxia and mortality and neurodevelopmental outcomes. METHODS: We used nationwide data on 705 infants from the Extremely Preterm Infants in Sweden Study, delivered at 22-26 weeks of gestation during 2004-2007. Comprehensive neurodevelopmental assessments were performed on survivors at 2.5 (n = 456) and 6.5 (n = 441) years of corrected age. Gestational age-related changes in umbilical cord arterial pH were compared with reference values for term newborn infants, and base excess was also calculated. Associations between low blood gas values (<10th percentile) and mortality and neurodevelopmental outcome were estimated. RESULTS: Cord blood determination was more common in surviving infants (P < .001), with pH determined in 322/705 (46%) and base excess in 311/705 (44%). Extremely preterm infants had higher pH values than term infants (P < .0001), with no change from 22 to 26 weeks of gestation (P = .61, r2  = .001). Multiple logistic regression showed no association between low blood gas values and risk of death or neurodevelopmental impairment at 6.5 years (P ≥ .17). CONCLUSION: Hypoxia with acidosis at birth was not associated with an increased risk of death or impaired neurodevelopmental in extremely preterm born children at 6.5 years.

Extrarenal Signs of Proximal Renal Tubular Acidosis Persist in Nonacidemic Nbce1b/c-Null Mice.

BACKGROUND: The SLC4A4 gene encodes electrogenic sodium bicarbonate cotransporter 1 (NBCe1). Inheritance of recessive mutations in SLC4A4 causes proximal renal tubular acidosis (pRTA), a disease characterized by metabolic acidosis, growth retardation, ocular abnormalities, and often dental abnormalities. Mouse models of pRTA exhibit acidemia, corneal edema, weak dental enamel, impacted colons, nutritional defects, and a general failure to thrive, rarely surviving beyond weaning. Alkali therapy remains the preferred treatment for pRTA, but it is unclear which nonrenal signs are secondary to acidemia and which are a direct consequence of NBCe1 loss from nonrenal sites (such as the eye and enamel organ) and therefore require separate therapy. SLC4A4 encodes three major NBCe1 variants: NBCe1-A, NBCe1-B, and NBCe1-C. NBCe1-A is expressed in proximal tubule epithelia; its dysfunction causes the plasma bicarbonate insufficiency that underlies acidemia. NBCe1-B and NBCe1-C exhibit a broad extra-proximal-tubular distribution. METHODS: To explore the consequences of Nbce1b/c loss in the absence of acidemia, we engineered a novel strain of Nbce1b/c-null mice and assessed them for signs of pRTA. RESULTS: Nbce1b/c-null mice have normal blood pH, but exhibit increased mortality, growth retardation, corneal edema, and tooth enamel defects. CONCLUSIONS: The correction of pRTA-related acidemia should not be considered a panacea for all signs of pRTA. The phenotype of Nbce1b/c-null mice highlights the physiologic importance of NBCe1 variants expressed beyond the proximal tubular epithelia and potential limitations of pH correction by alkali therapy in pRTA. It also suggests a novel genetic locus for corneal dystrophy and enamel hypomineralization without acidemia.

Effects of Hypercapnia and Hypercapnic Acidosis on Hospital Mortality in Mechanically Ventilated Patients.

OBJECTIVES: Lung-protective ventilation is used to prevent further lung injury in patients on invasive mechanical ventilation. However, lung-protective ventilation can cause hypercapnia and hypercapnic acidosis. There are no large clinical studies evaluating the effects of hypercapnia and hypercapnic acidosis in patients requiring mechanical ventilation. DESIGN: Multicenter, binational, retrospective study aimed to assess the impact of compensated hypercapnia and hypercapnic acidosis in patients receiving mechanical ventilation. SETTINGS: Data were extracted from the Australian and New Zealand Intensive Care Society Centre for Outcome and Resource Evaluation Adult Patient Database over a 14-year period where 171 ICUs contributed deidentified data. PATIENTS: Patients were classified into three groups based on a combination of pH and carbon dioxide levels (normocapnia and normal pH, compensated hypercapnia [normal pH with elevated carbon dioxide], and hypercapnic acidosis) during the first 24 hours of ICU stay. Logistic regression analysis was used to identify the independent association of hypercapnia and hypercapnic acidosis with hospital mortality. INTERVENTIONS: Nil. MEASUREMENTS AND MAIN RESULTS: A total of 252,812 patients (normocapnia and normal pH, 110,104; compensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245) were included in analysis. Patients with compensated hypercapnia and hypercapnic acidosis had higher Acute Physiology and Chronic Health Evaluation III scores (49.2 vs 53.2 vs 68.6; p < 0.01). The mortality was higher in hypercapnic acidosis patients when compared with other groups, with the lowest mortality in patients with normocapnia and normal pH. After adjusting for severity of illness, the adjusted odds ratio for hospital mortality was higher in hypercapnic acidosis patients (odds ratio, 1.74; 95% CI, 1.62-1.88) and compensated hypercapnia (odds ratio, 1.18; 95% CI, 1.10-1.26) when compared with patients with normocapnia and normal pH (p < 0.001). In patients with hypercapnic acidosis, the mortality increased with increasing PCO2 until 65 mm Hg after which the mortality plateaued. CONCLUSIONS: Hypercapnic acidosis during the first 24 hours of intensive care admission is more strongly associated with increased hospital mortality than compensated hypercapnia or normocapnia.

Prognosis of patients presenting extreme acidosis (pH <7) on admission to intensive care unit.

PURPOSE: The purpose was to determine prognosis of patients presenting extreme acidosis (pH <7) on admission to the intensive care unit (ICU) and to identify mortality risk factors. MATERIALS AND METHODS: We retrospectively analyzed all patients who presented with extreme acidosis within 24 hours of admission to a polyvalent ICU in a university hospital between January 2011 and July 2013. Multivariate analysis and survival analysis were used. RESULTS: Among the 2156 patients admitted, 77 patients (3.6%) presented extreme acidosis. Thirty (39%) patients suffered cardiac arrest before admission. Although the mortality rate predicted by severity score was 93.6%, death occurred in 52 cases (67.5%) in a median delay of 13 (5-27) hours. Mortality rate depended on reason for admission, varying between 22% for cases linked to diabetes mellitus and 100% for cases of mesenteric infarction (P = .002), cardiac arrest before admission (P < .001), type of lactic acidosis (P = .007), high Simplified Acute Physiology Score II (P = .008), and low serum creatinine (P = .012). CONCLUSIONS: Patients with extreme acidosis on admission to ICU have a less severe than expected prognosis. Whereas mortality is almost 100% in cases of cardiac arrest before admission, mortality is much lower in the absence of cardiac arrest before admission, which justifies aggressive ICU therapies.

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB-dependent mechanism.

OBJECTIVES: Hypercapnic acidosis protects against ventilation-induced lung injury. We wished to determine whether the beneficial effects of hypercapnic acidosis in reducing stretch-induced injury were mediated via inhibition of nuclear factor-κB, a key transcriptional regulator in inflammation, injury, and repair. DESIGN: Prospective randomized animal study. SETTING: University research laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: In separate experimental series, the potential for hypercapnic acidosis to attenuate moderate and severe ventilation-induced lung injury was determined. In each series, following induction of anesthesia and tracheostomy, Sprague-Dawley rats were randomized to (normocapnia; FICO2 0.00) or (hypercapnic acidosis; FICO2 0.05), subjected to high stretch ventilation, and the severity of lung injury and indices of activation of the nuclear factor-κB pathway were assessed. Subsequent in vitro experiments examined the potential for hypercapnic acidosis to reduce pulmonary epithelial inflammation and injury induced by cyclic mechanical stretch. The role of the nuclear factor-κB pathway in hypercapnic acidosis-mediated protection from stretch injury was then determined. MEASUREMENTS AND MAIN RESULTS: Hypercapnic acidosis attenuated moderate and severe ventilation-induced lung injury, as evidenced by improved oxygenation, compliance, and reduced histologic injury compared to normocapnic conditions. Hypercapnic acidosis reduced indices of inflammation such as interleukin-6 and bronchoalveolar lavage neutrophil infiltration. Hypercapnic acidosis reduced the decrement of the nuclear factor-κB inhibitor IκBα and reduced the generation of cytokine-induced neutrophil chemoattractant-1. Hypercapnic acidosis reduced cyclic mechanical stretch-induced nuclear factor-κB activation, reduced interleukin-8 production, and decreased epithelial injury and cell death compared to normocapnia. CONCLUSIONS: Hypercapnic acidosis attenuated ventilation-induced lung injury independent of injury severity and decreased mechanical stretch-induced epithelial injury and death, via a nuclear factor-κB-dependent mechanism.

[Noninvasive ventilation and acute respiratory failure]. / Noninvasiivinen ventilaatio ja äkillinen hengitysvajaus.

Noninvasive ventilation is effective in acute respiratory failure, in which drug therapy and administration of supplemental oxygen do not suffice and attempts are made to prevent the patient from ending up in invasive respirator therapy. The treatment is suited for acute respiratory failure for instance in cases of exacerbation of chronic obstructive pulmonary disease, in which a disturbance of pulmonary ventilation leads to the accumulation of carbon dioxide and to respiratory acidosis. Disadvantages associated with artificial airways are avoided, number of complications are reduced, hospitalization periods become shorter, mortality decreases and costs are saved.

Acidosis, non-invasive ventilation and mortality in hospitalised COPD exacerbations.

BACKGROUND: Reports of non-invasive ventilation (NIV) use in clinical practice reveal higher mortality rates than in corresponding randomised clinical trials. AIM: To explore factors related to chronic obstructive pulmonary disease (COPD) admissions and NIV use that may explain some of the previously reported high mortality rates. METHODS: National UK audit of clinical care of consecutive COPD admissions from March to May 2008. Retrospective case note audit with prospective case ascertainment. Participating units completed a web-based audit proforma of process and outcomes of clinical care. RESULTS: 232 hospital units collected data on 9716 patients, mean age 73, 50% male. 1678 (20%) of those with gases recorded on admission were acidotic and another 6% became acidotic later. 1077 patients received NIV, 55% had a pH<7.26 and 49% (305/618) had or were still receiving high flow oxygen. 30% (136/453) patients with persisting respiratory acidosis did not receive NIV while 11% (15/131) of acidotic admissions had a pure metabolic acidosis and did. Hospital mortality was 25% (270/1077) for patients receiving NIV but 39% (86/219) for those with late onset acidosis and was higher in all acidotic groups receiving NIV than those treated without. Only 4% of patients receiving NIV who died had invasive mechanical ventilation. CONCLUSIONS: COPD admissions treated with NIV in usual clinical practice were severely ill, many with mixed metabolic acidosis. Some eligible patients failed to receive NIV, others received it inappropriately. NIV appears to be often used as a ceiling of treatment including patient groups in whom efficacy of NIV is uncertain. The audit raises concerns that challenge the respiratory community to lead appropriate clinical improvements across the acute sector.

Bronchopulmonary dysplasia in very low birth weight infants.

OBJECTIVE: The developments in newborn care have enabled many more very low birth weight premature infants to live. The aim of our study was to determine the risk factors for bronchopulmonary dysplasia (BPD) development by evaluating mild and moderate/severe BPD in extramural neonates with a birth weight <1501 g. METHODS: A case-control study was conducted between January 1, 2004- December 31, 2006 at the Dr. Sami Ulus Children's Hospital Neonatal Intensive Care Unit. Patients with BPD and without BPD were compared. Bronchopulmonary dysplasia was diagnosed and classified according to the Bancalari criteria. One-hundred and six (106) extramural premature infants with a birth weight <1501 g and admitted to the Neonatal Unit in the first three days of life and survived for more than 28 postnatal days were included. Patients with multiple congenital anomalies and complex cardiac pathologies were excluded. The maternal and neonatal risk factors, clinical features, mechanical ventilation treatment were compared. The principal risk factors for BPD development were analyzed and followed by logistic regression test. RESULTS: The diagnosis was mild BPD in 27 of the 106 patients and moderate/severe BPD in 29. The incidence of BPD was 52.8%. Fifty of 106 patients had no BPD. Analysis of risk factors revealed that gestational age < or =28 weeks (p=0.019), birth weight < or =1000 g (p=0.007), hypothermia (p=0.003), acidosis (p=0.003) and hypotension (p=0.005) at admission, respiratory distress syndrome (RDS) ( p<0.001), mechanical ventilation therapy (p<0.001), surfactant therapy (p=0.005), higher amount of mean fluid therapy on 7(th) days (p=0.008), nosocomial infection (p<0.001), higher amount of mean packed red cell transfusions (p<0.001) and more than two packed red cell transfusions (p=0.033) were risk factors associated with the development of BPD. Multivariant logistic regression analysis showed acidosis at admission (OR 5.12, 95%CI 1.17-22.27, p=0.029), surfactant treatment (OR 7.53, 95%CI 2.14-26.45, p=0.002), nosocomial infections (OR 4.66, 95%CI 1.27-17.12, p=0.02) and PDA (OR 9.60, 95%CI 2.23-41.22, p=0.002) were risk factors increasing the severity of BPD. CONCLUSION: The most important risk factors for BPD development in our study were RDS and nosocomial infections while the presence of acidosis at admission, surfactant administration, nosocomial infections and the presence of PDA were the most important risk factors regarding BPD severity. Presence of acidosis at admission as a risk factor emphasized the importance of suitable transport conditions for premature infants.

Acid-base interpretation can be the predictor of outcome among patients with acute organophosphate poisoning before hospitalization.

OBJECTIVES: Acute organophosphate (OP) poisoning causing alteration in acid-base equilibrium was reported before. Hence, different acid-base statuses may present in patients with acute poisoning due to OP exposure. This study aims to determine the impact of acid-base interpretation in patients with acute OP poisoning before hospitalization in medical care units and to describe the pattern of mortality with different acid-base statuses. DESIGN AND PATIENTS: Over a 9-year retrospective study, from July 1996 to August 2005, a total of 82 consecutive patients with acute OP poisoning were admitted to the China Medical University Hospital (Taichung, Taiwan) within 24 hours after exposure to OP and were enrolled into this study. RESULTS: Patients with acute OP poisoning were divided into 4 groups: without acidosis, metabolic acidosis, respiratory acidosis, and mixed acidosis. Overall survival (Kaplan-Meier curves) among groups was statistically significant (P < .0001). The mortality rate of acute OP poisoned patients with metabolic acidosis was 25%, and 75% of those patients died of cardiovascular failure. The mortality rate of acute OP poisoning with respiratory acidosis was 50%, and 50% of those patients died of respiratory failure. CONCLUSIONS: Acid-base interpretation can be effective in quick diagnosis and prediction of the outcome of patients with acute OP poisoning (without acidosis < metabolic acidosis < respiratory acidosis < mixed acidosis) before hospitalization. Major causes of death are different between the respiratory acidosis and metabolic acidosis groups of patients with acute OP poisoning.

The use of noninvasive mechanical ventilation in COPD with severe hypercapnic acidosis.

STUDY OBJECTIVES: To compare the effect of noninvasive mechanical ventilation (NIV) in severely acidotic with mildly acidotic patients with acute hypercapnic chronic obstructive lung disease (COPD). DESIGN: Comparison of NIV in consecutively enrolled patients with acute hypercapnic COPD with mild (pH 7.25-7.35) or severe (pH<7.25) acidosis on time to normalise pH and improve PaCO(2), duration of NIV treatment, length of stay in hospital and survival. Results (meadian (IQR)): Twenty-nine patients had 36 episodes of acute hypercapnic respiratory failure: Seventeen with pH<7.25 and 19 with pH 7.25-7.34. Compared with the mildly acidotic group, the severely acidotic group took a similar length of time for pH to normalise and PaCO(2) improve (12 (6-34) vs 12 (4-28)h, respectively, P=0.42), with similar duration of NIV treatment (60 (35-96) vs 68 (36-48)h, respectively, P=0.25) and hospital length of stay (8 (7-18) vs 9 (5-17) days, respectively, P=0.61). Overall survival was 89%, with 95% in the mild and 82% in the severely acidotic groups. CONCLUSIONS: Noninvasive ventilation is effective in the treatment of patients with severe acidosis due to acute hypercapnic COPD.

Hypercapnic acidosis and mortality in acute lung injury.

OBJECTIVE: We tested the hypothesis that hypercapnic acidosis is associated with reduced mortality rate in patients with acute lung injury independent of changes in mechanical ventilation. DESIGN: Secondary analysis of randomized clinical trial data using hypothesis-driven multivariate logistic regression. SETTING: Randomized, multiple-center trial (n = 861) comparing 12 mL/kg to 6 mL/kg predicted body weight tidal volumes previously published by the National Institutes of Health Acute Respiratory Distress Syndrome (ARDS) Network. PATIENTS: Acute lung injury patients enrolled in a randomized, multiple-center trial (n = 861). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The adjusted odds ratio and 95% confidence intervals (CI) for 28-day mortality rate associated with hypercapnic acidosis defined as day 1 pH <7.35 and Pa(CO2) >45 mm Hg were 0.14 (95% CI 0.03-0.70, p = .016) in the 12 mL/kg predicted body weight tidal volume group and 1.18 (95% CI 0.59-2.35, p = .639) in the 6 mL/kg predicted body weight tidal volume group. Other definitions of hypercapnic acidosis spanning a range of magnitudes suggest a dose-response association between hypercapnic acidosis and 28-day mortality in the 12 mL/kg predicted body weight tidal volume group. None of our definitions of hypercapnic acidosis were associated with reduction in 28-day mortality in the 6 mL/kg predicted body weight tidal volume group. CONCLUSIONS: Hypercapnic acidosis was associated with reduced 28-day mortality in the 12 mL/kg predicted body weight tidal volume group after controlling for comorbidities and severity of lung injury. These results are consistent with a protective effect of hypercapnic acidosis against ventilator-associated lung injury that was not found when the further ongoing injury was reduced by 6 mL/kg predicted body weight tidal volumes.

The use of oxygen in acute exacerbations of chronic obstructive pulmonary disease: a prospective audit of pre-hospital and hospital emergency management.

Treatment with high-flow oxygen in acute exacerbations of chronic obstructive pulmonary disease (AECOPD) can cause or aggravate acute hypercapnic respiratory failure and adversely affect prognosis. National guidelines for the management of COPD recommend an initial fractional inspired oxygen concentration (FiO2) of no more than 0.28. However, a prospective audit of 101 consecutive episodes of AECOPD demonstrated that oxygen therapy with an FiO2 in excess of 0.28 is common, potentially deleterious and predominantly initiated in the ambulance. Patient awareness, aids to disease identification and ambulance protocols are likely to hold the key to improvement in the acute care of these patients.

[Can subpartal fetal acidosis be avoided? Investigations on the complex causes of intrauterine asphyxia]. / In welchem Umfang ist die subpartale fetale Azidose vermeidbar? - Untersuchungen zum Ursachengefüge der intrauterinen Asphyxie.

OBJECTIVE: The extent to which faulty medical treatment and defective apparatus are concomitant causes for the development of subpartal acidosis was investigated in a retrospective study. At the same time, the incidence of acidosis in the Lippe-Detmold Hospital, Department of Gynaecology and Obstetrics, its morbidity and mortality were analysed. METHODS: Data from all case histories of neonates with acidosis (pH in the umbilical artery < 7.100) who were born between 1 st January 1992 and 31 st December 1998 at the Department of Gynecology and Obstetrics at the Lippe-Detmold Hospital were evaluated electronically. Analytical measurements of blood gases (pH, pCO 2 and pO 2 ) in umbilical artery and venous blood were available from all cases. The base excess was corrected by computations according to Siggaard-Andersen and R. Zander for the actual oxygen saturation. The delivery cardiotocograms (CTG) were appraised qualitatively. Equipment defects, mistakes on the part of doctors and/or midwives (including the head of the department) were recorded after critical analysis of each individual case and documented in accordance with a key. The neonatal data were taken from the files of the paediatric division of the hospital (head of the department Dr. K. Wesseler). RESULTS: In seven years under report, 9.876 babies were born, 156 (1.58 %) of whom showed a pH of less than 7.100 in the umbilical arterial blood. The mean actual pH value was 7.047 +/- 0.058, and the oxygen-corrected base excess was - 16.3 +/- 3.2 mmol/l. Correction of the base excess resulted in a numerical lowering by about 2.0 mmol/l. The rate of premature births was 17.4 %. One newborn baby died of hypoxic shock (0.67 %). 94 % of these neonates could be discharged in a healthy condition. 4.6 % still showed symptoms on discharge. Disorders of respiratory adaptation were the most prominent feature in morbidity from acidosis (about 18 %). Only two babies showed neonatal convulsions. Renal, cardiac and haemostaseological complications were rarely observed. Only 5 (3.9 %) of the 128 neonates with available recordings did not show any pathological changes in the CTG. 26.4 % of all acidoses had to be designated as "pure fate". In a further 35 % medical mistakes could not be discerned. Consequently, 61.4 % of the acidoses had to be designated as "unavoidable". In the remaining roughly 40 %, inadequate cardiotocographical knowledge, inattentiveness, defective equipment etc. clearly played a causal role. In the severe cases (pH in the umbilical artery < 7.000), medical mistakes were much more frequent (50 %). CONCLUSIONS: Three-fifths of all subpartal acidoses in this study have a fateful nature, i.e. they cannot be prevented even by optimal professional management in good time. About two-fifths are avoidable if appropriate equipment and trained staff are available around the clock. Use of cardiotocography alone enables the threat of asphyxia to be detected in 97 % of the cases. The short-term prognosis of subpartal acidosis is good provided very low pH values (< 6.900) can be avoided. In perinatological studies, the base excess value should be corrected by computation. "Quality control" worthy of the name should include critical single-case analysis at least in severe acidosis.

Effect of alkalinization and fluids on survival in acute, non-hypoxic respiratory acidosis.

Effects of intravenous normal saline, sodium bicarbonate, hypertonic saline, and Tromethamine were studied in 21 pigs and 60 rats subjected to acute, severe respiratory acidosis. Transient multiphasic alterations of systemic arterial pressures were seen with boluses of each agent-especially sodium bicarbonate and hypertonic saline-but any improvements in hemodynamic variables were transient. At the dose given, sodium bicarbonate significantly increased PaCO2 while decreasing hydrogen ion (H+) accumulation, whereas tromethamine buffered pH without significantly increasing PaCO2. However, no change of either arterial or venous H+ or PCO2 could be identified which rapidly produced death. Survival times were statistically equivalent among all groups. Therefore, intravenous treatment of respiratory acidosis with fluids or alkalinizing agents appears neither helpful nor harmful.

Benzyl alcohol toxicity in a neonatal intensive care unit. Incidence, symptomatology, and mortality.

We unknowingly "screened" all NICU infants for elevated levels of serum benzyl alcohol (Bz-OH) over a three-month period. The fortuitous "screening" procedure resulted from the interference by Bz-OH with a routine blood CO2 assay used for all infants; validity was proved by (1) replication of the interference pattern with Bz-OH or benzoic acid; (2) confirmation of elevated benzoic acid levels in serum in two of the four screening positive infants tested but not in control infants, and (3) disappearance of the interference patterns when Bz-OH solutions were discontinued in affected infants. Screened Bz-OH-positive infants were compared to screened negative control infants, matched for weight (less than 1000 g), severity of RDS (on respirators), exposure to Bz-OH, and survival for longer than 48 hours. Intraventricular hemorrhage (IVH), metabolic acidosis appearing prior to IVH, and mortality were increased in Bz-OH-positive infants (P less than .05 in each case); hyperbilirubinemia and thrombocytopenia were not. Gasping respirations were not a major symptom. It is concluded that Bz-OH poisoning was a major cause of morbidity and mortality in NICU infants weighing less than 1000 g at birth during the three-month screening period. A retrospective review of patient records covering a 16-month period showed significant improvement in the survival rate of infants weighing less than 1000 g following the discontinuation of Bz-OH solutions.

Evolution of the acid-base status in cardiac arrest.

In a study of the evolution of acid-base status in 26 patients who had cardiopulmonary arrest in the operating room, it appeared that:The determination of acid-base status within the first hour post-cardiac arrest is useful in differentiating final survivors from non-survivors. Respiratory or combined acidosis carries a poor prognosis not evidenced for metabolic acidosis. Late respiratory complications are more frequent in patients with initial combined acidosis. Treatment should be instituted on the basis of frequent determinations of acidbase status, since accurate diagnosis of degree and type of acidosis cannot be done on clinical grounds only. Recovery of consciousness is influenced by the type and severity of acidosis, less so by duration of arrest; and that high pCO(2) is associated frequently with unconsciousness after recovery of circulatory function.