Postnatal Placental Respiration

Dunn (1966) wrote:

    "The transfer of respiratory function from the
    placenta to the lungs at birth stands out as the
    most dramatic, complex and important event in
    our lives.  How does this transfer take place?
    We know that there is often a delay after
    delivery before breathing commences and that
    a further interval must pass before pulmonary
    respiration meets the requirements of the
    newborn infant [2].  What of the placenta during
    this time?  Does its respiratory function cease at
    the moment of delivery, or is it maintained until
    the lungs have assumed their new
    responsibility?" [1, p607]

Much of the information in the Czech language
reference cited by Dunn [2] may be found in
Štembera et al. (1965) [3].  Štembera et al. showed
that umbilical blood flow during the first two minutes
after birth continues at the prenatal rate.  Dunn cited
other research indicating that oxygen delivery
continues for 2 to 4 minutes after birth, and that
even if a baby breathed within 30 seconds of birth, 5
minutes might pass before oxygen levels in the
infant's major arteries rose to levels at or above
those continuing to be received via the umbilical
cord [4].

Dunn pointed out that ideas at that time about
respiratory adaptation at birth were based on
research that involved ligation of the umbilical cord
[5-7].  That an infant, if assisted by ventilation with
air or oxygen, can begin breathing after the cord is
cut remains an ongoing fault of more recent
research.  Thus factors continue to be sought to
determine why some infants lapse into "respiratory
depression" at birth [8, 9].

Dunn was one of a dwindling few by the 1960s who
seemed to understand the obvious, that oxygen
transport from the placenta following delivery
continues and remains sufficient to meet the infant's
respiratory needs:

    "Postnatal placental respiration has most to
    offer to the infant that is slow to breathe at
    birth.  Blood flowing down the umbilical vein is
    directed through the foetal pathways to the
    coronary and cerebral circulations [10].  In
    addition, it seems likely that this arterialised
    blood is directed into the pulmonary circulation
    when respiration starts [11].  If so, it may
    perform a most important service in helping to
    overcome the intense pulmonary
    vasoconstriction that accompanies asphyxial
    changes in the blood [12] and hence, by
    improving pulmonary perfusion, enhances the
    effectiveness of ventilation.

    It is not possible fully to appreciate the
    significance of postnatal placental respiration
    without also taking into account the unique and
    fascinating characteristics of the umbilical
    circulation during the second and third stages
    of labour [13, 14, 15].  Immediately after
    delivery the placenta seems capable of both
    combating acidosis in the infant and providing it
    with oxygen, glucose [3] and a blood
    transfusion.  Recent recommendations for
    neonatal resuscitation [16, 17] hardly ask for
    more.  Perhaps CHARLES WHITE of
    Manchester [18] was justified after all when he
    wrote in 1773:

    'The common method of tying and cutting the
    navel string in the instant the child is born, is
    likewise one of those errors in practice that has
    nothing to plead in its favour but custom.' " [1,
    pp607-8]

Some of the citations in this brief and lucid
annotation are disturbing to read.  The paper by
James et al. (1958) of which Apgar was a co-author,
discusses the umbilical artery (singular) as the
vessel that transports blood from the placenta to the
fetus.  

    "The recent work of Dawes and associates [19],
    on the fetal circulation, indicates that the
    umbilical artery blood represents the blood
    going to the fetal tissues and not fetal venous
    blood." [5, p380]

In fact the paper by Dawes et al. clearly shows the
umbilical vein as the conduit of blood from the
placenta, 80 percent saturated with oxygen [19,
p565, and pp574-5],

The tables in the paper by James et al. comparing
pH, oxygen, and carbon dioxide in the umbilical
artery and vein are difficult to interpret, and not
clarified by the explanation:

    "Blood samples were obtained from the artery
    and vein in a clamped segment of the umbilical
    cord at the moment of delivery." [5, p379]

None of the infants in this study were allowed the
benefit of postnatal placental respiration.  

    "To determine the biochemical status of the
    depressed group, samples from either the
    umbilical artery, the portal vein area in the liver,
    or from the right or left atria have been used.
    This has been considered justifiable for several
    reasons. In many of these infants the heart rate
    is slow and the pulse feeble." [5, p381]

Can we trust they knew from where they were
actually getting their samples?  Then in describing
oxygen levels in umbilical artery and vein blood:

    "There is a wide range in the oxygen levels in
    both the umbilical artery and vein blood and in
    the A-V difference.  All the infants exhibited
    sone degree of asphyxia with a low oxygen
    saturation and a high CO2 tension. Of the 63
    umbilical artery samples, 26 had an oxygen
    saturation below 10 per cent and 7 had no
    measurable oxygen. Fourteen of these severely
    anoxic infants were not depressed (score 8 and
    9) and cried spontaneously within seconds of
    delivery" [5, p381]

In conclusion, the suggestion is made that asphyxia
occurs during all births:

    "These studies have revealed the varying
    degrees of asphyxia which occur during all
    forms of delivery.  Contrary to earlier reports, ~,
    4, ~ an infant may make the initial respiratory
    gasps with no measurable oxygen in his arterial
    blood. In this sense, anoxia, as measured by
    the oxygen saturation of the umbilical artery's
    blood, correlates poorly with postnatal vigor." [5,
    p385]

Respiratory depression was noted to occur in babies
born alive in apparently very good condition (with
placental function completely intact up to the time of
birth):

    "These are the infants who appear vigorous,
    with good tone and heart rate, yet fail to
    breathe immediately." [5,p391]

James et al. blamed anesthesia, and suggested
regional anesthesia as preferable:

    "Since inhalation anesthesia administered to the
    mother will always augment the metabolic
    depression, regional anesthesia would seem
    more desirable for delivery of an infant with
    fetal distress." [5, p392]

Why are the research data of Ranck and Windle
(1959) and Faro and Windle (1969) neglected and
forgotten [20, 21], while clamping the umbilical cord
at birth, and assigning an Apgar score remain
current?  Placental respiration continues after birth,
and every newborn child deserves to have this
important continuing support from the mother
protected.


(in progress)
References
  1. Dunn PM (1966) Postnatal
    placental respiration.
  2. Štembera ZK, Hodr J (1962)
    Hladiny kysliku v cevach
    pupecnikovych po prvnim
    vdechu plodu po porodu.
  3. Štembera ZK et al. (1965)
    Umbilical blood flow in
    healthy newborn infants
    during the first minutes after
    birth.
  4. Engström L et al. (1966) The
    onset of respiration. A study
    of respiration and changes
    in blood gases and acid-
    base balance.
  5. James LS, et al. (1958) The
    acid-base status of human
    infants in relation to birth
    asphyxia and the onset of
    respiration.
  6. Oliver TK Jr et al. (1961)
    Serial blood-gas tensions
    and acid-base balance
    during the first hour of life in
    human infants.
  7. Prod'hom LS et al. (1964)
    Adjustment of ventilation,
    intrapulmonary gas
    exchange, and acid-base
    balance during the first day
    of life.
  8. Baskett TF et al. (2006)
    Predictors of respiratory
    depression at birth in the
    term infant.
  9. Milsom I et al. (2002)
    Influence of maternal,
    obstetric and fetal risk
    factors on the prevalence of
    birth asphyxia at term in a
    Swedish urban population.
  10. Born GV et al. (1954)
    Changes in the heart and
    lungs at birth.
  11. Redmond A et al. (1965)
    Relation of onset of
    respiration to placental
    transfusion.
  12. Dawes GS (1966)
    Pulmonary circulation in the
    foetus and new-born.
  13. Dunn PM. The placental
    venous pressure during and
    after the third stage of labour
    following early cord ligation.
  14. Gunther M. The transfer of
    blood between baby and
    placenta in the minutes after
    birth.
  15. Lind J. Physiological
    adaptation to the placental
    transfusion.
  16. Adamsons K Jr, et al.
    Resuscitation by positive
    pressure ventilation and tris-
    hydroxymethylamino-
    methane of rhesus monkeys
    asphyxiated at birth.
  17. Westin B et al. (1962)
    Hypothermia and
    transfusion with oxygenated
    blood in the treatment of
    asphyxia neonatorum.
  18. White C (1773) A Treatise on
    the Management of Pregnant
    and Lying-In Women.
  19. Dawes GS et al. (1954)  The
    Fetal Circulation in the Lamb.
  20. Ranck JB, Windle WF (1959)
    Brain damage in the
    monkey, Macaca mulatta, by
    asphyxia neonatorum.
  21. Faro MD, Windle WF  (1969)
    Transneuronal degeneration
    in brains of monkeys
    asphyxiated at birth.
Full References
  1. Dunn PM. Postnatal placental respiration. Dev Med Child Neurol. 1966 Oct;
    8(5): 607-8.
  2. Štembera ZK, Hodr J. Hladiny kysliku v cevach pupecnikovych po prvnim
    vdechu plodu po porodu. Čs Fysiol 1962; 11:482.
  3. Štembera ZK, Hodr J, Janda J. Umbilical blood flow in healthy newborn
    infants during the first minutes after birth. Am J Obstet Gynecol. 1965 Feb
    15;91:568-74.
  4. Engström L, Karlberg P, Rooth G, Tunell R. The onset of respiration. A
    study of respiration and changes in blood gases and acid-base balance.
    New York : Aid for Cripple children, 1966. (Harvard depository HC2GNM).
  5. James LS, Weisbrot IM, Prince CE, Holaday DA, Apgar V. The acid-base
    status of human infants in relation to birth asphyxia and the onset of
    respiration. J Pediatr. 1958 Apr;52(4):379-94.
  6. Oliver TK Jr, Demis JA, Bates GD. Serial blood-gas tensions and acid-base
    balance during the first hour of life in human infants. Acta Paediatr. 1961
    Jul;50:346-60.
  7. Prod'hom LS, Levison H, Cherry RB, Drorbaugh JE, Hubbell JP Jr., Smith
    CA. Adjustment of ventilation, intrapulmonary gas exchange, and acid-
    base balance during the first day of life. Pediatrics 1964 May;33(5);682-
    693.
  8. Baskett TF, Allen VM, O'Connell CM, Allen AC. Predictors of respiratory
    depression at birth in the term infant. BJOG. 2006 Jul;113(7):769-74.
  9. Milsom I, Ladfors L, Thiringer K, Niklasson A, Odeback A, Thornberg E.
    Influence of maternal, obstetric and fetal risk factors on the prevalence of
    birth asphyxia at term in a Swedish urban population. Acta Obstet Gynecol
    Scand. 2002 Oct;81(10):909-17.
  10. Born GV, Dawes GS, Mott JC, Widdicombe JG. Changes in the heart and
    lungs at birth. Cold Spring Harbor Symposia on Quantitative Biology 1954;
    19:102-8.
  11. Redmond A, Isana S, Ingall D. Relation of onset of respiration to placental
    transfusion. Lancet. 1965 Feb 6;1:283-5.
  12. Dawes GS. Pulmonary circulation in the foetus and new-born. Br Med Bull.
    1966 Jan;22(1):61-5.
  13. Dunn PM. The placental venous pressure during and after the third stage
    of labour following early cord ligation. J Obstet Gynaecol Br Commonw.
    1966 Oct;73(5):747-56.
  14. Gunther M. The transfer of blood between baby and placenta in the
    minutes after birth. Lancet. 1957 Jun 22;272(6982):1277-80.
  15. Adamsons K Jr, Behrman R, Dawes GS, James LS, Koford C.
    Resuscitation by positive pressure ventilation and tris-
    hydroxymethylaminomethane of rhesus monkeys asphyxiated at birth. J
    Pediatr. 1964 Dec;65:807-18.
  16. Westin B, Nyberg R, Miller JA Jr, Wedenberg E. Hypothermia and
    transfusion with oxygenated blood in the treatment of asphyxia neonatorum.
    Acta Paediatr Suppl. 1962;139:1-80.
  17. Lind J. Physiological adaptation to the placental transfusion: the eleventh
    blackader lecture. Can Med Assoc J. 1965 Nov 20;93(21):1091-100.
  18. White C. A Treatise on the Management of Pregnant and Lying-In Women
    (1773). Canton, MA: Science History Publications, 1987, chap 5.  Available
    from http://www.shpusa.com/bkindex.html
  19. Dawes GS, Mott JC, Widdicombe JG. The Fetal Circulation in the Lamb. J.
    Physiol. 126: 563-87, 1954.
  20. Ranck JB, Windle WF. Brain damage in the monkey, Macaca mulatta, by
    asphyxia neonatorum. Exp Neurol. 1959 Jun;1(2):130-54.
  21. Faro MD, Windle WF. Transneuronal degeneration in brains of monkeys
    asphyxiated at birth. Exp Neurol. 1969 May;24(1):38-53.
top