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Previous studies from this laboratory have demonstrated early and progressive alterations in the ST-T period of the fetal and neonatal electrocardiogram in relation to asphyxia. The aims of the present study were to investigate the metabolic background of these hypoxic ECG changes by means of serial myocardial biopsies in fetal lambs, relating these changes to the hypoxic depletion of glycogen, ATP and creatine phosphate stores in the heart and to the altered myocardial performance as measured by heart rate, mean arterial blood pressure, combined cardiac output and max. dP/dt. The experiments were performed on 21 fetal lambs, acutely exteriorized and subjected to graded hypoxia. During hypoxia there was a significant relationship between the degree of changes in the ST-T period according to a scoring system and the depletion of myocardial glycogen and ATP, a highly significant correlation between the rate of myocardial glycogenolysis and the rate of increase in T wave amplitude, and a parallelism between the amount of glycogen available and fetal cardiovascular function. The myocardium was capable of regenerating its glycogen stores under conditions of adequate oxygenation and in the absence of acidosis and hypoglycaemia.

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.

No abstract

Progressive changes in the S-T interval of the fetal ECG were studied in 22 lamb fetuses, acutely exteriorized and submitted to graded hypoxia. The ECG changes were studied in order to correlate them with cardiovascular function, as measured by heart rate, mean arterial pressure, end diastolic pressure and combined cardiac output, estimated by the thermodilution method, as well as with blood gases and acid-base status. Close correlations were obtained between PaO2, pH and base deficit and the severity of ECG changes, graded according to a scoring system. Alterations in the ECG pattern consistently preceeded signs of failing cardiovascular function. Our previous findings indicated that the hypoxic ECG changes could be regarded as a sign of myocardial glycolysis. Accordingly, similar progressive ECG changes could be induced by isoprenaline injections. It is concluded that progressive changes of the S-T interval of the fetal ECG contains information about fetal hypoxic stress before signs of failing cardiovascular function are seen.