EFFECTS OF HYPOXEMIA ON FETAL HEART-RATE, VARIABILITY AND CARDIAC-RHYTHM

1. Experiments were carried out in 30 chronically catheterized foetal sheep (128-144 days; term 150 days) and in seven of these foetuses bef ore, during and after acute hypoxaemia. The extent to which changes in sympathoadrenal activity and cardiac vagal activity affected the foet al cardiac response to hypoxaemia was measured. Three measurements wer e used: foetal heart rate (FHR), heart rate variability (HRV; measured as the coefficient of variation in pulse interval) and power spectral density (PSD; measured over the frequency ranges of 0.04-1.3 Hz). Car diac vagal activity was blocked by atropine, beta-adrenoceptor activit y was blocked by propranolol. 2. Under normoxaemic conditions, cardiac vagal blockade caused a rise in mean arterial pressure (MAP; P<0.001) , an increase in FHR (P<0.001), a decrease in HRV (P<0.001) and a decr ease in PSD (P<0.001). beta-Adrenoceptor blockade caused a rise in MAP (P<0.001), a fall in FHR (P<0.01), a decrease in HRV (P<0.001) but no change in PSD. 3. During mild hypoxaemia (Po-2 = 12-14.5 mmHg) and mo derate hypoxaemia (Po-2 = 10-11.9 mmHg), foetal MAP (P<0.001, P<0.001) , HRV (P<0,01, P<0.001) and PSD in the frequency range 0.04-0.45 Hz in creased (P<0.05-P<0.001). Foetal heart rate decreased when foetuses be came moderately hypoxaemic (P<0.001). 4.After cardiac vagal blockade, hypoxaemia was associated with an increase in FHR compared with non-bl ocked hypoxaemic foetuses (P<0.01, P<0.001). The increase in HRV was a bolished (P<0.001, P<0.001) as was the increase in PSD (P<0.01-P<0.001 ). 5, After beta-adrenoceptor blockade, the bradycardia that occurred during hypoxaemia was enhanced (P<0.01, P<0.05), the increase in HRV w as not affected and neither was the increase in PSD. 6. As FHR and HRV of normoxaemic foetal sheep were affected both by atropine and propra nolol, it would seem that both cardiac vagal and sympathoadrenal activ ity modulate the foetal heart under resting conditions. The lack of an y effect of beta-adrenoceptor blockade on PSD under these conditions s uggests that power spectral analysis (PSA) is not as sensitive as the other two methods in detecting sympathetically mediated modulation of the heart. 7. Because the hypoxaemia induced bradycardia and increase in HRV and in PSD were abolished by atropine (P<0.01-P<0.001), it is c oncluded that during hypoxaemia foetal HRV is mainly modulated by chan ges in cardiac vagal tone. Propranolol had no effect on foetal HRV, al though it reduced it under normoxaemic conditions; therefore, it is co ncluded that cardiac sympathetic neural activity was not increased in acute hypoxaemia uncomplicated by acidosis. However, there was strong evidence of increased sympathoadrenal tone on the foetal heart in hypo xaemia, that is, there was a rise in FHR in hypoxaemic atropinized foe tuses and a greater fall in FHR in beta-adrenoceptor blocked hypoxaemi c foetuses, Therefore, this increased sympathetic influence on the foe tal heart during hypoxaemia must be predominantly the result of increa sed adrenomedullary secretion of catecholamines. 8. Maintenance of foe tal cardiac output depends on the chronotropic and ionotropic effects of catecholamines. Therefore, this adrenomedullary influence on the fo etal heart during hypoxaemia is important to offset the opposing effec ts of increased cardiac vagal tone.