Mechanisms of late decelerations of the fetal heart rate during hypoxia

Harris, Joseph L.; Krueger, Terry R.; Parer, Julian T.

doi:10.1016/0002-9378(82)90215-0

Cited by 63 publications

(21 citation statements)

References 9 publications

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“…The precise mechanism for increased parasympathetic activity is unknown. Speculatively, it could, at least in part, represent dysfunction of parasympathetic nuclei as neurons recover from hypoxic inhibition, leading to oscillations in vagal tone (Harris et al 1982;Westgate et al 2001b). Although potentially increased inter-occlusion FHRV could represent pacemaker dysfunction, as seen at the end of a period of 30 min of umbilical cord occlusion in preterm fetal sheep (George et al 2004), in the present study there were no significant periods of asystole or other abnormal rhythms on the electrocardiogram.…”

Section: Fetal Heart Rate Variability During the Occlusion Seriesmentioning

confidence: 45%

Sympathetic neural activation does not mediate heart rate variability during repeated brief umbilical cord occlusions in near‐term fetal sheep

Lear

Galinsky

Wassink

et al. 2015

The Journal of Physiology

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Key pointsr Fetal heart rate variability and changes in the ST segment of the electrocardiogram are used clinically during labour to identify fetuses at risk of severe metabolic acidosis or death.r Sympathetic nervous system activity contributes to heart rate variability in healthy normoxic fetuses, and is critical for the rapid haemodynamic adaptations to repeated episodes of asphyxia induced by brief complete umbilical cord occlusions at rates consistent with active labour.r We now show that chemical sympathectomy did not alter fetal heart rate variability between episodes of brief repeated asphyxia or elevation of the ST segment during asphyxia.r The lack of influence of the sympathetic system on fetal heart rate variability between episodes of brief asphyxia suggests that measures of fetal heart rate variability are unlikely to help monitor changes in sympathetic nervous system activity during active labour.Abstract Changes in fetal heart rate variability (FHRV) and ST segment elevation (measured as the T/QRS ratio) are used to evaluate fetal adaptation to labour. The sympathetic nervous system (SNS) is an important contributor to FHRV under healthy normoxic conditions, and is critical for rapid support of blood pressure during brief labour-like asphyxia. However, although it has been assumed that SNS activity contributes to FHRV during labour; this has never been tested, and it is unclear whether the SNS contributes to the rapid increase in T/QRS ratio during brief asphyxia. Thirteen chronically instrumented fetal sheep at 0.85 of gestation received either chemical sympathectomy with 6-hydroxydopamine (6-OHDA; n = 6) or sham treatment (control; n = 7), followed 4-5 days later by 2 min episodes of complete umbilical cord occlusion repeated every 5 min for up to 4 h, or until mean arterial blood pressure fell to <20 mmHg for two successive occlusions. FHRV was decreased before occlusions in the 6-OHDA group (P < 0.05) and 2-4.5 h during recovery after occlusions (P < 0.05) compared to the control group. During each occlusion there was a rapid increase in T/QRS ratio. Between successive occlusions the T/QRS ratio rapidly returned to baseline, and FHRV increased above baseline in both groups (P < 0.05), with no significant effect of sympathectomy on FHRV or T/QRS ratio. In conclusion, these data show that SNS activity does not mediate the increase in FHRV between repeated episodes of brief umbilical cord occlusion or the transient increase in T/QRS ratio during occlusions. Abbreviations 6-OHDA, 6-hydroxydopamine; FHR, fetal heart rate; FHRV, fetal heart rate variability; MAP, mean arterial pressure; RMSSD, root mean square of successive RR intervals; SDNN, standard deviation of RR intervals; SNS, sympathetic nervous system; STV, short-term variation.

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Section: Fetal Heart Rate Variability During the Occlusion Seriesmentioning

confidence: 45%

Sympathetic neural activation does not mediate heart rate variability during repeated brief umbilical cord occlusions in near‐term fetal sheep

Lear

Galinsky

Wassink

et al. 2015

The Journal of Physiology

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“…Bradycardia may be mediated by inhibition of oxygen-sensitive L-type Ca 2ϩ channels (29). In fetuses with a mature autonomic nervous system, such as near-term sheep, hypoxia-induced bradycardia also has a parasympathetic component (15).…”

Section: Tyrosine Hydroxylase Deficiency Resembles Fetal Hypoxiamentioning

confidence: 99%

High oxygen prevents fetal lethality due to lack of catecholamines

Ream

Chandra²,

Peavey³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This acute FHR during hypoxia represents a key fetal adaptation, believed to help reduce myocardial work and oxygen requirements (11). This initial bradycardia, which is mediated by chemoreflex vagal pathways (5,17,23), occurs before the increase in blood pressure and is an indication of the severity of the hypoxic insult (5). Recently, it was reported that the slope of the initial bradycardia increases during short repeated cord occlusions associated with severe acidosis, indicating an increase in chemoreflex responses with fetal metabolic deterioration (3).…”

mentioning

confidence: 99%

Mild chronic hypoxemia modifies expression of brain stem angiotensin peptide receptors and reflex responses in fetal sheep

Pulgar¹,

Hong²,

Jessup³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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The effects of chronic mild hypoxemia on the binding of angiotensin receptors in selected brain stem nuclei and reflex responses were studied in fetal sheep. Fetal and maternal catheters were placed at 120 days' gestation, and animals received intratracheal maternal administration of nitrogen (n ϭ 16) or compressed air in controls (n ϭ 19). Nitrogen infusion was adjusted to reduce fetal brachial artery PO2 by 25% during 5 days. Spontaneous baroreflex sensitivity and spectral analysis of the pulse interval were analyzed during the 5 days hypoxemia period using 90 min of daily recording. Brains of control and hypoxemic animals were collected, and brain stem angiotensin receptor binding was studied by in vitro autoradiography at 130 days of gestation. After 5 days of hypoxemia, some animals in each group were submitted to one complete umbilical cord occlusion during 5 min. [125 I]sarthran binding showed that chronic mild hypoxemia significantly increases angiotensin type 1 receptor, angiotensin type 2 receptor, and ANG-(1-7) angiotensin receptor binding sites in the nucleus tractus solitarius and dorsal motor nucleus of the vagus (P Ͻ 0.05). Hypoxemia induced lower baroreflex sensitivity and a higher low frequency-to-high frequency ratio in the fetus, consistent with a shift from vagal to sympathetic autonomic cardiac regulation. Cord occlusion to elicit a chemoreflex response induced a greater bradycardic response in hypoxemic fetuses (slope of the initial fall in heart rate; 11.3 Ϯ 1.9 vs. 6.4 Ϯ 1.2 beats ⅐ min Ϫ1 ⅐ s Ϫ1 , P Ͻ 0.05). In summary, chronic mild hypoxemia increased binding of angiotensin receptors in brain stem nuclei, decreased spontaneous baroreflex gain, and increased chemoreflex responses to asphyxia in the fetus. These results suggest hypoxemia-induced alterations in brain stem mechanisms for cardiovascular control.fetus; hypoxemia; baroreflex OXYGEN DEPRIVATION IMPOSES diverse challenges to fetal development, with changes in the autonomic cardiovascular control via baroreflex and chemoreflex pathways playing a major role as a survival strategy (16). In fetal sheep, acute episodes of hypoxemia induce a redistribution of cardiac output to maintain blood flow and oxygen delivery to the heart and brain (14). This response is initiated by stimulation of peripheral chemoreceptors and maintained by endocrine mechanisms involving secretion of hormones such as catecholamines, neuropeptide Y, arginine vasopressin, and cortisol (11). During acute severe hypoxia, i.e., complete occlusion of the umbilical cord, fetuses respond with a fall in heart rate (FHR) and an increase in blood pressure. This acute FHR during hypoxia represents a key fetal adaptation, believed to help reduce myocardial work and oxygen requirements (11). This initial bradycardia, which is mediated by chemoreflex vagal pathways (5, 17, 23), occurs before the increase in blood pressure and is an indication of the severity of the hypoxic insult (5). Recently, it was reported that the slope of the initial bradycardia increases during short ...

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Mechanisms of late decelerations of the fetal heart rate during hypoxia

Cited by 63 publications

References 9 publications

Sympathetic neural activation does not mediate heart rate variability during repeated brief umbilical cord occlusions in near‐term fetal sheep

Sympathetic neural activation does not mediate heart rate variability during repeated brief umbilical cord occlusions in near‐term fetal sheep

High oxygen prevents fetal lethality due to lack of catecholamines

Mild chronic hypoxemia modifies expression of brain stem angiotensin peptide receptors and reflex responses in fetal sheep

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