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PubMedDate not supplied

Circulatory responses to acute asphyxia are not affected by the glutamate antagonist lubeluzole in fetal sheep near term.

OBJECTIVE: Asphyxia is one of the main causes of perinatal brain damage that can result in psychomotor deficits during later development. Recently lubeluzole, a new glutamate antagonist, was shown to improve clinical outcome considerably without any safety concerns in adults who had acute ischemic stroke. However, our preliminary experiments showed transient alterations in heart rate as well as arterial hypertension after intravenous application of this compound in fetal sheep. The aim of the present study was to examine in detail whether lubeluzole affects circulatory responses to acute asphyxia in fetal sheep near term. METHODS: Eleven fetal sheep were chronically instrumented at a mean gestational age of 133 +/- 2 days (term is at 147 days). The fetuses in the study group (n = 6) received three bolus injections of lubeluzole at 30-minute intervals (3 x 0.11 mg/kg estimated body weight), and five controls received solvent. Organ blood flows and physiologic variables were measured before, during, and after arrest of uterine blood flow for 2 minutes (ie, at 0, 1, 2, 3, 4, and 30 minutes). RESULTS: Before asphyxia, distribution of combined ventricular output and physiologic variables in fetuses from the control group were in the normal range for chronically prepared fetal sheep near term. During acute asphyxia there was a redistribution of cardiac output toward the central organs accompanied by pronounced bradycardia and progressive increase in arterial blood pressure. There were nearly no differences between groups in the time course of physiologic and cardiovascular variables measured before, during, and after acute intrauterine asphyxia. CONCLUSION: Lubeluzole did not affect circulatory responses to acute asphyxia in fetal sheep near term.

Animals↗
PubMed1975

Effects of asphyxia and potassium on canine and feline electrocardiograms.

The effects of asphyxia and potassium on the electrocardiogram (ECG), lead II, were recorded from dogs and cats anesthetized with sodium pentobarbital and halothane. Electrocardiographic recordings were made during control periods, during asphyxia (occluded endotracheal tube), during infusion of an isotonic KCl solution and during infusion of an isotonic NaCl solution. Arterial and venous blood gas partial pressures (PaCO2, PvCO2, PaO2 and and PvO2), plasma Na+ and K+ concentrations, heart rate and mean arterial blood pressure were measured during control periods, asphyxia and during the periods of infusion. The vagi were severed to assess the effect of vagal tone on the ECG changes. The characteristic ECG changes during asphyxia and the electrolyte imbalances resulting from infusion of isotonic KCl and NaCl were determined during sodium pentobarbital and halothane anesthesia in both dogs and cats. The combination of halothane and high PCO2 caused cardiac arrhythmias. Spontaneous recovery from ventricular fibrillation, as a result of hyperkalemia, was recorded from cats. Disappearance of the P waves, which is characteristic of hyperkalemia, was infrequent in this study and the U waves associated with hypokalemia were not found. Severing the vagi did not alter the ECG changes characteristic of asphyxia, hyperkalemia and hypokalemia. It was found that asphyxia and infusion of fluids high or low in potassium can produce ECG changes in both dogs and cats that can be correlated with blood gas partial pressure changes or plasma potassium concentrations.

Anesthesia, Inhalation↗
PubMed2002

Intrapartum-related birth asphyxia in South Africa--lessons from the first national perinatal care survey.

BACKGROUND: The recent amalgamation of data by users of the Perinatal Problem Identification Programme (PPIP) throughout South Africa has culminated in the publication of the Saving Babies report. OBJECTIVES: To determine the absolute rate of death from intrapartum-related birth asphyxia, and the contribution of intrapartum-related asphyxia to total perinatal mortality in South African hospitals, and to identify the primary obstetric causes and avoidable factors for these deaths. METHODS: The amalgamated PPIP data for the year 2000 were obtained from 27 state hospitals (6 metropolitan, 12 town and 9 rural) in South Africa. In PPIP-based audit, all perinatal deaths are assigned primary obstetric causes and avoidable factors, and these elements were obtained for all deaths resulting from intrapartum-related birth asphyxia. RESULTS: There were 123,508 births in the hospitals surveyed, with 4,142 perinatal deaths among infants > or = 1,000 g, giving a perinatal mortality rate of 33.5/1,000 births. The perinatal mortality rate from intrapartum-related birth asphyxia was 4.8/1,000 births. The most frequent avoidable factors were delay by mothers in seeking attention during labour (36.6%), signs of fetal distress interpreted incorrectly (24.9%), inadequate fetal monitoring (18.0%) and no response to poor progress in labour (7.0%). The perinatal mortality rates for metropolitan, town, and rural areas were 30.0, 39.4 and 30.9/1,000 births respectively. The contribution of intrapartum-related birth asphyxia to perinatal mortality in these areas was 10.8%, 16.7% and 26.4% respectively. CONCLUSION: The high rates of perinatal death from intrapartum-related birth asphyxia in South Africa are typical of those in underdeveloped countries, with the most serious deficiencies in rural areas. Most of these deaths are avoidable and the reduction of these rates presents an important challenge to providers of perinatal care in this country. Areas worthy of research and action include provision of mothers' waiting facilities in rural regions, improvements in fetal monitoring, partogram-based labour management, and the establishment of midwifery staffing norms for South African labour units.

Asphyxia Neonatorum↗
PubMedDate not supplied

[A descriptive study of perinatal asphyxia and its sequelae].

INTRODUCTION: Perinatal asphyxia is a potential cause of brain injury that can produce some alterations on the neurologic development of the newborn. On the last years most part of the investigation have been focused on the physiopathology of the perinatal asphyxia, but correlation between asphyxia and brain damage is not well defined. PATIENTS AND METHODS: A retrospective study was made of the patients with the diagnosis of perinatal asphyxia born at the General Hospital of Segovia during a period of ten years (1992-2001). We took data about gestation, birth, neonatal period and follow-up period from their clinical histories. RESULTS: Over this period of ten years 703 cases of perinatal asphyxia have been diagnosed, supposing this an incidence of 7,2 cases of each 100 newborns. 116 of these newborns present risk factors of brain damage and were followed at least two years. 53 of the 116 newborns (45%) present evidence of hypoxic-ischemic encephalopathy on neonatal period. During the period of two years, 42 of the asphyxiated infants follow up (36%) present neurologic sequelae, being psychomotor retardation the most common. CONCLUSION: For a correct interpretation of the relationship between perinatal asphyxia and neurologic sequelae we have to analyze all of the perinatal data and discard any other possible aetiology or pathogenic mechanism.

Apgar Score↗
PubMed1995

Contribution of asphyxia to the induction of hearing impairment in jaundiced Gunn rats.

OBJECTIVES: This study was designed to determine whether asphyxia contributes to the induction of hearing impairment during neonatal jaundice. METHODS: Asphyxia was induced in jaundiced and nonjaundiced Gunn rats on postnatal days 1 (low bilirubin levels) and 10 (elevated bilirubin levels). Auditory nerve-brainstem evoked response thresholds were assessed in 21- and 28-day and 3-month-old rats. RESULTS: Asphyxia by itself or jaundice by itself did not lead to any type of hearing impairment. However, the combination of both high plasma bilirubin levels and asphyxia in 10-day-old rats but not in 1-day-old rats was accompanied by a progressive hearing loss in these rats. CONCLUSIONS: The contributory effect of asphyxia on neonatal jaundice may have important clinical relevance if asphyxia, for example, respiratory distress, accompanies neonatal jaundice.

Animals↗
PubMed1997

Perinatal asphyxia: multivariate analysis of risk factors in hospital births.

OBJECTIVE: To determine risk factors for perinatal asphyxia. DESIGN: Cohort study. SETTING: Teaching hospital. METHODS: All consecutive hospital births were evaluated during the study period. Asphyxia was defined on intrapartum and neonatal resuscitation criteria. Maternal, intrapartum and neonatal variables were recorded in all births. Data was analyzed after stratifying for live and stillbirths by univariate and logistic regression analyses. RESULTS: Amongst 2371 births (55 fetal deaths and 2316 live births), there were 86 cases of perinatal asphyxia (35 fetal deaths and 51 live births), providing an asphyxia rate of 36.3/1000 births. On multivariate analysis, risk factors significantly associated with asphyxia included prolonged second stage labor (OR 9.4), vaginal breech delivery (OR 6.6), elective cesarean delivery (OR 4.6), pregnancy induced hypertension (PIH) (OR 2.7) and fetal growth retardation (SFD) (OR 2.4). Amongst stillborn, the significant univariate factors associated with asphyxia were prolonged second stage labor (RR 1.7) and cord prolapse (RR 1.7). CONCLUSIONS: There is a need to strengthen intrapartum management and early identification of mothers with PIH or intrauterine growth retardation to reduce asphyxial morbidity and mortality.

Asphyxia Neonatorum↗
PubMed1997

[Electrophysiological studies in the follow-up of children with perinatal asphyxia history].

OBJECTIVES: The objective of this study was to analyze the usefulness of electrophysiological studies [electroencephalogram (EEG) and auditory-evoked potential (AEP)] during the follow-up of children with perinatal asphyxia antecedents. PATIENTS AND METHODS: A prospective epidemiological study of perinatal asphyxia in term neonates born at the University Hospital San Juan (Alicante, Spain) between November 1991 and February 1995 was performed. Perinatal asphyxia was graded as non-severe (1 minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart patterns and/or meconium-stained amniotic fluid and the need for immediate neonatal resuscitation) and severe (1 minute Apgar score < or = 3 and umbilical artery pH < 7.10). The incidence of hypoxic-ischemic encephalopathy (classification of Levene and Sarnat & Sarnat) during the neonatal period and neurological sequelae (classification of Finer and Amiel-Tison) during the follow-up period were studied. Electrophysiological studies (EEG and AEP) were made mainly between 12 and 18 months of life. RESULTS: During the study period there were 156 cases of perinatal asphyxia in full-term live births (31 severe and 125 non-severe). Hypoxic-ischemic encephalopathy was present in 25.6% of asphyxiated newborn infants, being mild in 30 cases, moderate in 5 and severe in 5. The incidence of neurological sequelae in 115 asphyxiated newborns followed for 24 month was 16.5%. This included mainly motor disabilities. We did not find any case of epilepsy, but there were 4 children with febrile seizures and one case of benign myoclonic seizures. EEG was performed in 88 cases during follow-up, and only was abnormal in two infants without seizures. AEP was performed in 82 cases during follow-up and hearing loss was detected in 4 children with neurosensorial hypoacusia (3 unilateral and 1 bilateral). CONCLUSIONS: Rutinary EEG is not useful during follow-up of children with antecedents of perinatal asphyxia. However, AEP is a hearing screening procedure for infants at risk of deafness, such as in perinatal asphyxia, and the cases of neurosensorial hearing loss detected by AEP in our population were clinically unapparent.

Asphyxia Neonatorum↗
PubMed1995

Newborn complications after intrapartum asphyxia with metabolic acidosis in the preterm fetus.

OBJECTIVE: Our purpose was to determine the nature of the complications in preterm newborns after intrapartum fetal asphyxia with metabolic acidosis at delivery. STUDY DESIGN: Thirty-seven preterm fetuses with metabolic acidosis were matched with 37 preterm fetuses with normal blood gas measurements at delivery. A complication score expressed the magnitude of newborn complications during the 10 days after delivery. RESULTS: The mean complication score for the preterm newborns at 32 to 36 weeks in the asphyxia group, 9.6, was significantly greater than that for the control group, 3.1. Fetal asphyxia was associated with severe complications in all systems. The complication scores for the preterm newborns < 32 weeks in the asphyxia group were of the same order as the control group. This may be related in part to a short duration of the asphyxial insult. The Apgar score at 1 minute was a valuable predictor of newborn complications in both the asphyxia and control groups. CONCLUSIONS: Intrapartum fetal asphyxia with metabolic acidosis at delivery is an important factor in the occurrence of severe complications, particularly in the central nervous system, respiratory system, and kidney, of preterm newborns.

Acidosis↗
PubMed1999

Predictive value of electronic fetal monitoring for intrapartum fetal asphyxia with metabolic acidosis.

OBJECTIVE: To determine the predictive value of each fetal heart rate (FHR) variable and of patterns of FHR variables for fetal asphyxia during labor. METHODS: This matched case-control study included an asphyxia group of 71 term infants with umbilical artery base deficit greater than 16 mmol/L and a control group of 71 term infants with umbilical artery base deficit less than 8 mmol/L. Each FHR record available for the 4 hours before delivery was scored in 10-minute cycles for each FHR variable. Selected patterns of important FHR variables were examined during the last hour before delivery for their predictive value for fetal asphyxia. RESULTS: The FHR variables associated with fetal asphyxia included absent and minimal baseline variability and late and prolonged decelerations. Fetal heart rate patterns with absent baseline variability were the most specific but identified only 17% of the asphyxia group. The sensitivity of this test increased to 93% with the addition of less specific patterns. The estimated positive predictive value ranged from 18.1% to 2.6%, and the negative predictive value ranged from 98.3% to 99.5%. CONCLUSION: A narrow 1-hour window of FHR patterns including minimal baseline variability and late or prolonged decelerations will predict fetal asphyxial exposure before decompensation and newborn morbidity. Thus, with careful interpretation, predictive FHR patterns can be a useful screening test for fetal asphyxia. However, supplementary tests are required to confirm the diagnosis and to identify the large number of false-positive patterns to avoid unnecessary intervention.

Acidosis↗
PubMed1995

Asphyxia.

The prevention of fetal asphyxia or hypoxia starts with prepregnancy counseling and continues with careful antenatal care and intrapartum fetal surveillance. Further progress in eliminating antepartum and intrapartum deaths will only be made when it is accepted that, even with intense investigation by detailed autopsy, the cause of many deaths remains unknown. Many of these deaths may be ascribed to hypoxia. In the future, with more detailed non-invasive probing with CAT scanning and magnetic resonance imaging, other causes may be determined. The mother at risk of hypoxia requires specialized attention. Such mothers will include those with severe cardiac, pulmonary or circulatory problems. Others will be those with endocrine problems, such as diabetes or thyroid dysfunction. At present, failure of fetal growth is generally ascribed to hypoxia, but undoubtedly, in solution to such problems of possible hypoxia is elective delivery at the appropriate time. What Hensleig said in 1986 (Hensleig et al, 1986) is equally true today: 'Preventative programmes will remain unsuccessful until the causation of cerebral palsy is more understood. What we are presently lacking is an understanding of the underlying conditions responsible for brain injury when asphyxia occurs despite our best efforts. While we have learned much about the causation and prevention of perinatal mortality very little has been established about the causation and prevention of cerebral palsy'. Finally, Hall (1989), in a review of birth asphyxia and cerebral palsy, concludes the following five points. 1. The incidence of cerebral palsy is not falling despite improved obstetrics. 2. The cause of more than 90% of cases of cerebral palsy remains unknown. 3. Asphyxia is hard to define and measure and is rarely the cause of cerebral palsy. 4. Hypoxic ischaemic encephalopathy is the most reliable indicator of asphyxia. 5. Neither traditional clinical signs nor electronic monitoring allow reliable recognition of asphyxia.

Cerebral Palsy↗
PubMedDate not supplied

Admission test as predictor of intrauterine fetal asphyxia.

This study determined the accuracy of the admission test in predicting intrauterine fetal asphyxia. A total of 229 subjects were included. The admission test, a short continuous electronic fetal monitoring recording, was made immediately on admission, on all patients in labor, and was categorized as "reassuring", "equivocal", or "ominous". Intrauterine fetal asphyxia was considered to be present when the umbilical cord blood pH was 7.2 and/or the Apgar score was 7 at 1 minute; an "ominous" admission test has a high accuracy (LR = 8.54) in predicting intrauterine fetal asphyxia, while a "reassuring" admission test does not rule out the possibility of asphyxia (LR = 0.39). "Reassuring" tracing is associated with low risk (6.5%) for asphyxia as measured by Apgar score and umbilical cord pH, while "ominous" tracing is associated with high risk (50%) for asphyxia. In detecting an umbilical cord pH of 7.2, fetal heart rate variability is the most specific (98%), while absence of acceleration is the most sensitive (50%).

Asia↗
PubMed1990

Intrapartum asphyxia in pregnancies complicated by intra-amniotic infection.

Intra-amniotic infection has been reported to be associated with intrapartum asphyxia; however, the criteria used to define asphyxia have been imprecise. In the present study of 123 women with intra-amniotic infection and 6769 women without infection, the mean umbilical artery pH was 7.28 in both groups. The frequency of acidemia (umbilical artery pH less than 7.20) was not significantly different between the infection group and controls (15 versus 10%; P = .12). Likewise, there was no significant difference between the groups when a lower umbilical artery pH value (less than 7.15) was used to define acidemia. None of the infants from infected mothers had metabolic acidemia with a pH of less than 7.15 and none had a pH of less than 7.00. Significantly more (P less than .05) infants in the infected group did have low 1-minute (20 versus 5%) and 5-minute (3 versus 1%) Apgar scores of 6 or less, criteria often used to define asphyxia. However, none of the newborns from the infected group had recently proposed criteria for the diagnosis of birth asphyxia (ie, leading to neurologic impairment) such as metabolic acidemia, seizures in the immediate newborn period, and low Apgar scores (3 or less). Birth asphyxia is rarely associated with intra-amniotic infection, and in the absence of other signs of fetal jeopardy such as an ominous fetal heart rate pattern, an immediate cesarean to prevent asphyxia does not appear justified once the diagnosis of chorioamnionitis is made.

Acidosis↗
PubMed1987

Redistribution of fetal circulation during repeated asphyxia in sheep: effects on skin blood flow, transcutaneous PO2, and plasma catecholamines.

To improve the understanding of fetal responses to labour, we have ascertained whether reduced fetal skin blood flow after asphyxia reflects redistribution of the circulation, and if so, whether this can be detected by transcutaneous PO2 monitoring. We also studied the relation between plasma concentrations of catecholamines and organ blood flow. Eight experiments were conducted on 8 acutely-prepared fetal sheep in utero between 125 and 135 days of gestation. In each fetus 11 episodes of asphyxia were induced within 33 min by intermittent arrest of uterine blood flow for 90 s. The distribution of blood flow was measured before and after asphyxia (at 35.5 min) by the isotope-labelled microsphere method. Blood samples were drawn at 0, 33 (i.e. after 90 s recovery), and 40 min to determine blood gases, acid-base balance, and catecholamine concentrations. Fetal transcutaneous PO2, heart rate, arterial blood pressure, and arterial O2 saturation were recorded continuously. Repeated fetal asphyxia increased plasma catecholamine concentrations and caused a circulatory redistribution to the brain (181% change), adrenals (116% change), and lungs (105% change) at the expense of many peripheral organs, particularly of the skin (-61% change). The pattern of these changes was different from that observed by others in persistent hypoxia or asphyxia. The decrease in skin blood flow, which depressed transcutaneous PO2 and increased the arterial-transcutaneous PO2 difference, correlated with the decrease in blood flow to other peripheral organs and with an increase in blood flow to the brain stem. We conclude that reduced blood flow to the fetal skin after repeated episodes of asphyxia indicates circulatory redistribution, which can be detected by transcutaneous PO2 measurements. We suggest that monitoring of variables that depend on skin blood flow may improve fetal surveillance during complicated labour.

Animals↗
PubMed1986

Intrauterine asphyxia and long-term outcome in preterm fetuses.

The long-term outcome of 108 infants born before the 33rd week of gestation was evaluated and correlated to a fetal heart tracing from the last 24 hours before delivery. Infants with signs of asphyxia (N = 30) were born at the same gestational age as those without (N = 78), but had a significantly lower birth weight (P less than .001). Severe intraventricular hemorrhage occurred more often in infants with asphyxia (30%) than in those without (5%) (P less than .05). Fourteen of 30 asphyxia infants (47%) and 11 of 78 nonasphyxia infants (14%) died within the first two years (P less than .005). At two years of age, four (25%) asphyxia and eight (12%) nonasphyxia infants have developmental or neurologic abnormalities (not significant). Of the eight infants with asphyxia born before the 29th week of gestation in the present study, none was normal at two years of age. The authors conclude that signs of asphyxia, as determined from fetal heart rate pattern, were associated with poor fetal outcome, and especially in infants born before the 29th week of gestation. The clinical implications of these findings are discussed.

Birth Weight↗
PubMed1994

Cerebral blood flow and metabolism during repeated asphyxias in newborn piglets: influence of theophylline.

The effect of theophylline on cerebral blood flow (CBF), oxygen transport, and energy metabolism was investigated during and following brief episodes of asphyxia. CBF was determined by microspheres during control, asphyxia, and recovery with reventilation after a single asphyxia (recovery I) and after 7 repeated asphyxias (recovery II). In addition, cerebral energy metabolism by 31P NMR spectroscopy and cerebral oxygen consumption (CMRO2) in newborn piglets treated with 30 mg/kg theophylline (serum levels 22-25 micrograms/ml) were compared with nontreated piglets. Theophylline increased CMRO2 during recovery I (348 mumol O2/min/100 g vs. 144 for non-theophylline) but not during control, asphyxia, or recovery II. There was no significant difference between the theophylline and non-theophylline groups in depletion of phosphoenergetics as measured by 31P NMR.

Animals↗
PubMed2004

Naloxone for preventing morbidity and mortality in newborn infants of greater than 34 weeks' gestation with suspected perinatal asphyxia.

BACKGROUND: Studies in animal models have suggested that naloxone, a specific opiate antagonist, may improve outcomes for newborn infants with perinatal asphyxia. OBJECTIVES: In newborn infants of greater than 34 weeks' gestation with suspected perinatal asphyxia: to assess the effects of naloxone versus placebo or no drug, and of single versus multiple doses of naloxone, on mortality, long term neurological problems, severity of hypoxic-ischaemic encephalopathy, and frequency of neonatal seizures. SEARCH STRATEGY: We used the standard search strategy of the Cochrane Neonatal Review Group. This included searches of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 3, 2003), MEDLINE (1966 - August 2003), EMBASE (1980 - August 2003), conference proceedings, and previous reviews. SELECTION CRITERIA: Randomised or quasi-randomised controlled trials comparing naloxone versus placebo, or no drug, or another dose of naloxone, in newborn infants of greater than 34 weeks' gestation with suspected perinatal asphyxia. DATA COLLECTION AND ANALYSIS: We extracted data using the standard methods of the Cochrane Neonatal Review Group, with separate evaluation of trial quality and data extraction by two authors. The pre-specified outcomes for this review were: death before hospital discharge, severe neurodevelopmental disability, severity of hypoxic-ischaemic encephalopathy, and seizures in the neonatal period. MAIN RESULTS: We identified only one eligible randomised controlled trial. This study compared the use of naloxone with placebo in newborn infants with an Apgar score of six or less at one minute after birth. There were not any data on the pre-specified outcomes for this review. REVIEWER'S CONCLUSIONS: There are insufficient data available to evaluate the safety and effectiveness of the routine use of naloxone for newborn infants of greater than 34 weeks' gestation with suspected perinatal asphyxia. A further randomised controlled trial is needed to determine if naloxone benefits newborn infants with suspected perinatal asphyxia. Such a trial should assess clinically important outcomes such as mortality, and adverse short and long term neurological outcomes.

Asphyxia Neonatorum↗
PubMed2001

Reduced postnatal cerebral glucose metabolism measured by PET after asphyxia in near term fetal lambs.

The effects of fetal asphyxia on cerebral function and development, involve the transition from fetal to neonatal life. Changes in cerebral glucose metabolism may be an early postnatal indicator of fetal asphyxia. The objective is to develop an experimental lamb model involving the transition from fetal to neonatal life and to examine the effect of fetal asphyxia with cerebral hypoxic ischemia on early postnatal cerebral glucose metabolism. Fetal asphyxia was induced by total umbilical cord occlusion in eight near-term fetal lambs (134-138 days) with the ewe under isoflurane-opiate anesthesia. The mean occlusion time until cardiac arrest was 14.5 (4.2) min (SD). Lambs were immediately delivered and standardized resuscitation was instituted after 2 min asystole. At 4 hr postnatal age, [18-F]Fluoro-2-deoxy-glucose (18-FDG) was injected intravenously in eight asphyxiated lambs and in eight controls. Cerebral glucose metabolism was examined by positron emission tomography (PET). As a result the mean arterial blood pressure, acid-base values, blood glucose and serum lactate at 4 hr postnatal age did not differ significantly between lambs subjected to umbilical cord occlusion and controls. EEG was abnormal in all lambs subjected to cord occlusion and normal in the controls at 4 hr postnatal age. Global cerebral metabolic rate (CMRgl) as determined by PET was significantly lower in lambs subjected to cord occlusion mean/median (SD) 22.2/19.6 (8.4) micromol/min/100 g) than in controls mean/median (SD) 37.8/35.9 (6.1); P < 0.01). Global CMRgl is significantly reduced in newborn lambs 4 hr after fetal asphyxia induced by umbilical cord occlusion. A reduction in CMRgl is an early indicator of global hypoxic cerebral ischemia.

Acidosis↗
PubMed1976

The effects of asphyxia on afferent activity recorded from the cervical vagus in the duck.

Recordings were made of nervous activity from duck arterial chemoreceptors, arterial baroreceptors and pulmonary receptors during steady-state conditions (normoxic normocapnia, hypoxia, and hypercapnia) and apnoeic asphyxia. Arterial chemoreceptors were stimulated by hypoxia and intra-arterial KCN injection and showed an increasing discharge throughout asphyxia. During the first 2 min of asphyxia the time course of the development of asphyxic bradycardia paralleled that of the increase in arterial chemoreceptor discharge. Arterial baroreceptors discharged at a constant latency from the heart beat when mean arterial pressure was constant, while a drug-induced increase in mean arterial pressure was associated with a reduced latency and increased baroreceptor activity per heart-beat. During asphyxia mean arterial pressure often rose so that, despite the effect of bradycardia, baroreceptor activity per heart-beat and activity per unit time increased. Pulmonary receptors showed a linear relationship (negative slope) between discharge rate and % CO2 in inspired air and usually stopped firing in apnoeic asphyxia. The initiation and maintenance of diving bradycardia are discussed in terms of these results.

Animals↗