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The degree of metabolic acidosis at birth has been calculated in cord artery and vein samples from 21 term fetuses with cord artery pH less than 7.20. The aim of the study was to compare base deficit values calculated from either Siggaard-Andersen alignment nomogram (BD blood) or the Acid-Base chart (BD extra cellular fluid, BDecf). BDblood was found to be consistently higher in the cord artery as compared with BDecf, 13.2 +/- 3.5 and 9.9 +/- 2.9 mmol/l (Mean +/- SD), respectively. A significant correlation was found between cord artery PCO2 and BDblood whereas BDecf appeared unaffected by PCO2. In cases with cord entanglement BDecf a-v differences were increased to 3.4 +/- 2.3 mmol/l as compared with the small a-v difference noted in acidotic cases without cord entanglement, 1.1 +/- 1.25 mmol/l. It is speculated that with acutely emerging, intermittent asphyxia due to cord compression, a cord artery and vein difference in metabolic acidosis may exist and where the vein captures the basal level and the artery the acute changes. It is concluded that BDecf in both cord artery and vein add valuable information on the mechanisms behind metabolic acidosis.

Electrocardiogram waveform, short term heart rate variability and catecholamine concentrations were studied with maternally-induced anesthesia in eleven growth-retarded guinea-pig fetuses and their normal-sized littermates at 63 days of gestation. Intrauterine growth retardation was induced by unilateral uterine artery ligation performed between day 32 and 35. In the growth-retarded group fetal weight was reduced by 45%. Blood gases, acid-base status and oxygen content were similar in the two groups. The growth-retarded guinea-pig fetuses were hypoglycemic and demonstrated a rise in hemoglobin concentration. The T/QRS ratio (T wave amplitude/QRS amplitude) was similar in both groups. The short-term heart rate variability was significantly reduced in the growth-retarded group. Plasma catecholamine concentrations were increased in growth-retarded fetuses but differed only significantly for noradrenaline compared to controls. We suggest that similar T/QRS ratio in both groups of fetuses indicates that aerobic myocardial metabolism is maintained among growth-retarded fetuses. The mechanism behind the reduced variability is unclear.

Fetal heart rate (FHR) and fetal electrocardiogram (ECG) recordings were obtained from a scalp electrode with maternal thigh as reference and used for ST waveform analysis in 201 patients in labour. Nearly 45% had suspicious or abnormal FHR traces whilst only 27% had T/QRS ratio greater than 0.25 (mean +/- 2 SD). A normal T/QRS ratio identified 99.3% of fetuses with normal buffering capacity in cord artery blood. Of 13 infants with a cord artery blood pH less than 7.15, standard bicarbonate was less than 15.0 mmol/l in five who had an average T/QRS ratio less than 0.25 throughout labour. Of the eight with respiratory acidosis, five had an increase in T/QRS ratio greater than 0.25 for longer than 20 minutes prior to delivery, in two the ratio increased during the last few minutes and one had no change (pH 7.14). Persistent elevation of T/QRS in the first stage of labour identified those with decrease in buffer capacity in cord arterial blood (sensitivity of 94.1%). Acute hypoxia was recognized by the rapid rise in T/QRS. The specificity of T/QRS to identify fetuses at risk increased by combining the ST waveform analysis with FHR changes.

The effects of acute beta 1-blockade on fetal cardiovascular reactions during asphyxia were evaluated in 11 exteriorized sheep fetuses. Gestational age was 110-142 days. Asphyxia was induced either by ventilating the mother with low oxygen gas mixture or by mechanical reduction of placental blood flow. During asphyxia all fetuses reacted to metoprolol injection with a decrease in heart rate, myocardial contractility, cardiac output and arterial blood pressure. Five experiments resulted in irreversible fetal cardiovascular collapse. Isoprenaline was given to the fetuses during hypoxia to test the ability to further increase heart rate and activate myocardial beta-adrenoceptors. In those experiments with fetal cardiovascular demise after metoprolol, the isoprenaline injection did not result in a significant tachycardia. The surviving fetuses could increase their heart rate as a sign of a capacity to further increase the sympatho-adrenergic drive.

The metabolic response to different degrees of hypoxia was studied in 14 lamb fetuses. We have previously found a substantial rise in the fetal arterial plasma hypoxanthine (HX) level, in parallel with alterations of other hypoxia indices during induced asphyxia. Measurements of the arterio-venous (A-V) difference in the HX level across the CNS demonstrated a late efflux of this substance from the fetal brain, with a high resistance to asphyxia. In this study, the effluxes of HX, lactate, and in some cases glucose, from the myocardium, liver, hindleg (skeletal muscle) and placenta were investigated in acutely exteriorised sheep fetuses with graded asphyxia. The main findings were as follows: (a) myocardium: a release of HX early during asphyxia, the magnitude of which paralelled the amount of mechanical work performed by the heart; a significant lactate influx into the heart during normoxia and recovery period; (b) liver: hepatic HX release even during normoxia, increasing to substantial amounts in connection with increasing asphyxia; (c) hindleg: release of HX only during the recovery period; lactate efflux during all periods apart from severe asphyxia, when an influx was seen for both substances; (d) placenta: production of lactate during normoxia, and an efficient clearance of both lactate and HX from the fetal plasma in combination with their concentration increasing during asphyxia. It is concluded that the myocardium and liver are the main contributors to the elevated HX level during fetal asphyxia among the fetal organs investigated, while skeletal muscle releases HX mostly during the period of reoxygenation.

To evaluate the effect of chronic beta 1-adrenoceptor blockade on physiological adaptation to asphyxia a study was done on exteriorized sheep fetuses of 127-142 days gestational age. Eleven pregnant ewes were infused with metoprolol for 5 days prior to experiment. Another 10 ewes were infused with saline and served as controls. Asphyxia was induced by intermittent complete obstruction of maternal placental blood flow. Fetal electro-cardiogram, heart rate, cardiac output, myocardial contractility and cerebral blood flow were measured together with blood pH, lactate and hypoxanthine. Neurophysiological responses were evaluated by changes in somatosensory evoked electroencephalogram. The beta 1-blocked fetuses showed less responsiveness in myocardial contractility and heart rate during reoxygenation. This curtailed reaction resulted in accelerated lactic acidosis, increased break-down of intracellular energy rich substances and impaired cerebral function. Nine of the ten controls survived the experiment and 8 of them regained their somatosensory evoked EEG potentials, whereas 7 of the 11 beta-blocked fetuses survived and only 3 regained original somatosensory evoked EEG potentials. It is concluded that beta 1-adrenoceptor blockade impairs the adaptive responses to asphyxia in the ovine fetus and decreases its ability to survive severe asphyxia.

Previous studies from this laboratory have shown that changes in the ST waveform in the fetal electrocardiogram are a sign of fetal asphyxia. In the present study, seven chronically instrumented fetal lambs between 117 and 143 days' gestation were studied during 16 one-hour periods of maternally induced hypoxia. The aim was to test the hypothesis of a relationship between the concentration of circulating catecholamines and T-wave amplitude. The response to hypoxia was aged-dependent. Fetuses below 126 days of gestation did not react with electrocardiographic changes and output of epinephrine unless acidosis occurred. In more mature fetuses, hypoxia per se would induce a surge of epinephrine and changes in the ST waveform. Overall there was a strong correlation between the T/QRS ratio and the level of circulating epinephrine. During normoxia, epinephrine was undetectable (less than 0.1 nmol/L) in most fetuses; norepinephrine showed an increase at term. The analysis showed one fetus with chronic changes in the ST waveform (T/QRS ratio greater than 0.30) related to a marked increase in the plasma level of epinephrine in spite of normal blood gas values. These findings complement previous results in the acute and chronically instrumented fetal lamb and suggest that changes in the ST waveform expressed as T/QRS ratio identify a change to anaerobic myocardial metabolism mediated by beta-adrenergic stimulation.

Waveform changes in the fetal electrocardiogram (ECG) are under reassessment as a means of fetal surveillance. The purpose of the study was to identify ST waveform changes from the fetal scalp lead during labour and to compare any change with conventional signs of fetal distress. Two scalp electrodes provided a sufficiently stable signal from which ST waveform changes could be identified and measured as the T/QRS ratio. No infant was clinically hypoxic. Only 26% of the 46 patients studied had a continuously normal CTG whereas 67% had no ST waveform abnormalities. A relation was found between the two variables as the mean T/QRS ratio increased from 0.20 (SD 0.11) during epochs of normal CTG to 0.27 (SD 0.17) with CTG changes. A linear correlation (r = 0.58, P less than 0.01) was found between the T/QRS ratio before birth and the cord plasma lactate values.

Progressive changes in the S-T interval of the fetal electrocardiogram (FECG) were studied in 14 lamb fetuses, acutely exteriorized and subjected to graded hypoxia. The aims of the study were to investigate whether beta-adrenoceptor stimulation and hypoxia exerted additive or potentiating effects on the FECG and several cardiovascular parameters and whether the hypoxic changes of the FECG could be blocked by beta-adrenoceptor blocking agents. The FECG changes were studied in order to correlate them with cardiovascular function, as measured by heart rate, mean arterial pressure, end diastolic pressure, maximum dP/dt and combined cardiac output, estimated by the thermodilution method, as well as with blood gases, acid base status, blood lactate and glucose. Injections of small doses (0.02 to 0.4 microg kg-1 min-1) of isoprenaline induced the same pattern of changes in the FECG as we have previously recorded during hypoxia. By increasing the isoprenaline dose an increase in the duration of the FECG changes and amplitude of the T-wave changes was obtained. Propranolol was found to completely abolish the FECG changes induced by isoprenaline, as well as by mild hypoxia. During severe hypoxia the FECG changes could not be abolished by propranolol. Our previous findings indicated that the hypoxic changes could be regarded as a sign of myocardial glycolysis. Thus, the present finding that even small doses of isoprenaline given to the fetus, initiates the same pattern of FECG changes corroborate this hypothesis.

The aim of the present study was to investigate the changes in electrocardiographic waveform and the release of catecholamines in the fetal lamb during nonacidemic fetal hypoxia. Chronically instrumented fetal lambs were subjected to reproducible hypoxia by reduction of the maternal placental blood flow. This was achieved by complete obstruction of the maternal aorta for 60 seconds. The fetuses were divided into an immature (119 to 126 days, n = 10) and a mature group (129 to 141 days, n = 6). Both groups of fetuses had a marked fall in oxygen tension (from 2.43 +/- 0.12 to 1.46 +/- 0.12 and 2.22 +/- 0.15 to 1.11 +/- 0.17 kilopascals [kPa] in the immature and mature groups, respectively) and in oxygen saturation (from 48% +/- 3% to 17% +/- 2% and 49% +/- 3% to 15% +/- 3%, respectively), but only modest changes occurred in pH and carbon dioxide tension. Basal fetal catecholamine concentrations did not differ between the groups but increased more significantly in the mature group with acute hypoxia. An increase in the T wave amplitude of the fetal electrocardiogram occurred in both groups during the latter part of occlusion with peak values shortly after removal of the occlusion. A linear correlation was found between the plasma epinephrine concentration and the T/QRS ratio in the mature group. Fetuses in both groups showed a marked bradycardia of similar magnitude during the occlusion but differed during the early phase of heart rate recovery by a slower acceleration of heart rate in the mature group. In connection with this marked bradycardia, the mature group showed a significant rise in mean arterial blood pressure at end of the occlusion. We suggest that fetal maturity has a significant influence no only on the release of catecholamines during nonacidemic hypoxia but also on the cardiovascular reaction pattern and changes in the ST waveform.

Electrocardiograms (ECG) were made immediately after delivery in 28 infants with normal cardiotocographic patterns in labour and in 29 with abnormal patterns. Changes in the S-T segment and T-wave were quantified in a scoring system. High and peaked T-waves (high T/QRS-ratios) were significantly more common in the group with abnormal cardiotocographic patterns. The infants with ECG-changes also had significantly lower Apgar scores and more neonatal complications. The immediate postpartum ECG seems to be a useful indication of the accumulated hypoxic stress to which the child has been subjected in labour.

Recording the fetal ECG as a means of fetal monitoring during labour has been investigated by many researchers. Different signal processing methods have been used, making comparisons difficult so that agreement on several topics has not been reached. We suggest the basis of a standard method of recording and processing the signal which we believe will be acceptable to the research and clinical communities.

Changes in the ST waveform of the fetal ECG have been detected in 47 term deliveries with vertex presentations using a specially developed microprocessor-based system for on-line recording of T wave amplitude. The T wave was quantified by the T/QRS ratio. The recording included one scalp electrode for exploration and a maternal skin electrode as reference. Signal quality allowed optimal ST waveform assessment in 89% of the cases. The degree of perinatal asphyxia was judged from cord artery acid-base status and the neonatal outcome. In completely normal fetuses at term the mean T/QRS ratio was 0.148 with a standard deviation of 0.048. With this basic information we can proceed in the investigation of the T/QRS ratio as a means for fetal surveillance.

An increase in T wave amplitude of the fetal ECG (FECG) has experimentally been correlated to elevated catecholamine levels and myocardial glycogenolysis. The FECG changes have also been described during human delivery. The present aim was to investigate whether these ECG changes could be reproduced in an easily handled real time microprocessor system, and to correlate them to biochemical and clinical data. During 40 deliveries the FECG signal was transferred to a microcomputer system for real time averaging of the FECG. There was a high capacity of the system to reproduce the ST waveform changes though the averaging procedure reduced the QRS magnitude by 10%. With a normal umbilical artery pH (greater than or equal to 7.25) the highest T/QRS ratios recorded during each delivery was 0.26 +/- 0.19 (mean +/- S.D.). With lowered pH (less than 7.25) the T/QRS increased to 0.33 +/- 0.10 (P less than 0.02). A similar difference between the two groups was seen when the T/QRS ratios from the last hour before birth were compared; 0.13 +/- 0.08 and 0.18 +/- 0.05, respectively (P less than 0.01). Changes in the ST waveform with T/QRS greater than or equal to 0.30, ST segment alterations, or negative T waves appeared during 40% of the deliveries, however, 30% were short standing changes (less than 30 min). Intermediate CTG changes during at least 30 min occurred in 41% and the pattern was classified as abnormal in 18%. Using the scalp electrode as signal source, the ECG analysis could add further information to the routine CTG recording on the fetal condition during delivery.

The effect of intra-uterine hypoxia on the hypoxanthine and lactate concentration in fetal sheep with catheters chronically implanted was investigated. Experiments were conducted on five fetuses. Sixty-four blood samples from nine hypoxic and recovery periods were analysed. A significant increase of hypoxanthine and lactate occurred in parallel with the fall of arterial oxygen saturation (SaO2) and arterial oxygen pressure (PaO2) during the first 20 min of hypoxia. The elevations in plasma hypoxanthine and lactate were significantly greater during more severe hypoxia than mild hypoxia, as judged from the amount of low oxygen gas mixture given to the ewe (7 or 9%). There were no difference in PaO2 and only minor difference in SaO2 between the two groups. The increase in lactate over 20 min was the same throughout the one-hour period of hypoxia, while the increase of hypoxanthine was less pronounced at the end of the period. This might be due to the fact that hypoxanthine was cleared from fetal plasma at a fairly rapid rate, half of the excess concentration being eliminated after 25 +/- 21 min compared to 85 +/- 47 min for lactate in six experiments post hypoxia. Linear regression analysis revealed a highly significant correlation between hypoxanthine and SaO2, pH and lactate (P less than 0.001). These three variables explained 77% of the variance of hypoxanthine, when calculated by multiple regression analysis.

Waveform analysis of the fetal ECG for fetal surveillance is regaining widespread interest. This paper presents our present knowledge on ST waveform analysis during human labour. A unipolar scalp lead with the maternal thigh as reference makes it possible to identify the T wave and at the same time decrease signal noise. The development of an ECG analyser (STAN) has enabled us to collect 201 ECG recordings during labour on which ST analysis could be undertaken. The data indicate that waveform analysis of the fetal ECG improves fetal surveillance during labour.