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• Oxygenation is not the only factor regulating heart rates at birth.
  S.B. Hooper
  Published on: 5 February 2015
• Early cord clamping and stability of the circulatory transition during preterm birth
  Joseph J. Smolich
  Published on: 4 February 2015

• Published on: 5 February 2015

  Oxygenation is not the only factor regulating heart rates at birth.

  • S.B. Hooper, Professor
  • Other Contributors:
    • G.R. Polglase and A.B. te Pas

  The alternative explanation for the cardiovascular differences between immediate and delayed cord clamping at birth suggested in this commentary is not new and has been acknowledged for over 50 years. The basic premise is that asphyxia is the underlying cause of birth-related bradycardias and that avoiding asphyxia will avoid the bradycardia and associated cardiac instability. However, neonatologists have known for almo...

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  The alternative explanation for the cardiovascular differences between immediate and delayed cord clamping at birth suggested in this commentary is not new and has been acknowledged for over 50 years. The basic premise is that asphyxia is the underlying cause of birth-related bradycardias and that avoiding asphyxia will avoid the bradycardia and associated cardiac instability. However, neonatologists have known for almost as long that lung aeration is the primary consideration when resuscitating bradycardic infants at birth. While it was thought that the beneficial effects are due to increased oxygenation, the Bhatt (1) study showed that increasing pulmonary blood flow and restoring venous return lost due to cord clamping, was also a major contributing factor. This is supported by studies in asphyxic, bradycardic lambs (2). Although the association between severe asphyxia and bradycardia is well- established, most birth related bradycardias are unlikely to be caused by asphyxia. Indeed, the birth-related cardiovascular changes are often unrelated to changes in oxygenation, which is shown in the heart rate normograms published by Dawson (3) et al. In normal healthy term infants, over 50% had a heart rate below 100 bpm at 1 min after birth and in some infants, the heart rates increased while oxygenation remained unchanged or decreased. The Bhatt et al (1) study was designed to replicate a relatively common clinical scenario, whereby the elapsed time between delivery, cord clamping and effective ventilation onset is ~2min. As preterm infants are commonly given an opportunity to transition unassisted at birth, a 2 min time window between birth and the onset of effective respiratory support is not uncommon. To put this into context, lambs at this age do not initiate gasping until 4-5 min after cord clamping, can easily be resuscitated after 10 min and take 12-13 min before becoming asystolic (4). In the Bhatt (1) study, lambs did not gasp and heart rates did not decrease below 100 bpm and so they were only mildly asphyxic at worst. As the fetal heart rate (in utero) responses to cord clamping markedly differ from the heart response to cord clamping ex utero (4), making conclusions about neonatal cardiac responses based on fetal data is problematic. Similar problems arise if the newborn's face is surrounded by liquid (4). We note that in the study cited by the author, a saline-filled bag was placed over the lamb's head and the lambs were ventilated via a tracheostomy. Nevertheless, the alternative interpretation of their findings is that reducing the timing between cord clamping and ventilation onset leads to a more labile transition not because of oxygenation differences, but because it reduces the time that venous return and cardiac output are reduced. This is consistent with the conclusion of Bhatt et al (1). We disagree with the author's suggestion that avoiding asphyxia will by itself improve cardiovascular stability at birth. This is not only because of the reasons cited above, but because this simple view of the physiology surrounding transition will encourage clinicians to intervene and attempt to assist infants earlier than is perhaps necessary.

  1. Bhatt S, Alison B, Wallace EM, et al. Delaying cord clamping until ventilation onset improves cardiovascular function at birth in preterm lambs. J Physiol. 2013;591:2113-26.

  2. Klingenberg C, Sobotka KS, Ong T, et al. Effect of sustained inflation duration; resuscitation of near-term asphyxiated lambs. Arch Dis Child Fetal Neonatal Ed. 2013;98:F222-7.

  3. Dawson JA, Kamlin CO, Wong C, et al. Changes in heart rate in the first minutes after birth. Arch Dis Child Fetal Neonatal Ed. 2010;95:F177- 81.

  4. Sobotka KS, Morley C, Ong T, et al. Circulatory Responses to Asphyxia Differ if the Asphyxia Occurs In Utero or Ex Utero in Near-Term Lambs. PLoS One. 2014;9:e112264.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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• Published on: 4 February 2015

  Early cord clamping and stability of the circulatory transition during preterm birth

  • Joseph J. Smolich, Principal Research Fellow

  The review by Hooper et al1 is timely and mounts a compelling case for a stable circulatory transition during preterm birth. However, advocacy of early ventilation with delayed cord clamping as the primary way forward to ensure such a transition is open to question, as the main supportive evidence for this paradigm comes from an experimental study by the same group,2 for which an alternative interpretation of observed f...

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  The review by Hooper et al1 is timely and mounts a compelling case for a stable circulatory transition during preterm birth. However, advocacy of early ventilation with delayed cord clamping as the primary way forward to ensure such a transition is open to question, as the main supportive evidence for this paradigm comes from an experimental study by the same group,2 for which an alternative interpretation of observed findings has recently come to light. Thus, in preterm lambs, Bhatt et al2 reported relatively minor perinatal changes in heart rate, blood pressure and right ventricular output with early ventilation and delayed cord clamping. By contrast, early cord clamping followed by ventilation 2 minutes later was associated with 1) bradycardia, arterial blood pressure swings and large reductions in right ventricular output before ventilation, and 2) substantial rises in heart rate, blood pressure and right ventricular output after ventilation. The 2 minute interval employed by Bhatt et al2 between early cord clamping and the onset of ventilation is potentially problematic, however, as prior studies in fetal lambs have shown that asphyxia can develop within 2 minutes after complete occlusion of uterine arteries or the umbilical cord.3 4 Indeed, a preterm lamb birth study employing a lesser cord clamp- to-ventilation interval (1.5 minutes) has now shown that an asphyxial state rapidly develops by 45 seconds after cord clamping on aortic blood gas analysis, with a haemoglobin O2 saturation of <10% and O2 tension of <10 mmHg, associated with a fall in pH and rise in CO2 tension.5 Furthermore, similar to the onset and offset phases of brief in utero asphyxia,3 4 this asphyxial state was accompanied by 1) bradycardia, marked falls in ventricular outputs/central blood flows and redistribution of systemic flow towards the brain before ventilation, and 2) tachycardia with blood pressure and flow surges after ventilation.5 These data therefore suggest that the findings of Bhatt et al2 primarily reflected the haemodynamic effects of asphyxia occurring with an extended cord clamping-to-ventilation interval, rather than beneficial effects per se of early ventilation with delayed cord clamping. Consistent with the foregoing proposition, reducing the cord clamping-to- ventilation interval from 1.5 to 0.5 minutes (to avoid development of an established asphyxial state) markedly blunted perinatal haemodynamic fluctuations.5 This finding thus implies that circulatory stability during the preterm birth transition hinges on avoidance of asphyxia. Such avoidance can be achieved not only with the advocated paradigm of early ventilation and delayed cord clamping,1 but also with early cord clamping, if this is followed by a short interval before the onset of ventilation.5 References 1. Hooper SB, Polglase GR, te Pas AB. A physiological approach to the timing of umbilical cord clamping at birth. Arch Dis Child Fetal Neonatal Ed 2014; DOI: 10.1136/archdischild-2013-305703. 2. Bhatt S, Alison BJ, Wallace EM, et al. Delaying cord clamping until ventilation onset improves cardiovascular function at birth in preterm lambs. J Physiol 2013;591:2113-26. 3. Jensen A, Garnier Y, Berger R. Dynamics of fetal circulatory responses to hypoxia and asphyxia. Eur J Obstet Gynecol Reprod Biol 1999;84:155-72. 4. Hunter CJ, Blood AB, Power GG. Cerebral metabolism during cord occlusion and hypoxia in the fetal sheep: a novel method of continuous measurement based on heat production. J Physiol 2003;552:241-51. 5. Smolich JJ, Kenna KR, Cheung MM. Onset of asphyxial state in non- respiring interval between cord clamping and ventilation increases hemodynamic lability of birth transition in preterm lambs. J Appl Physiol 2015; DOI: 10.1152/japplphysiol.01147.2014.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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