This chapter is relevant to Section G1(v)  of the 2017 CICM Primary Syllabus, which asks the exam candidate to "describe the circulatory and respiratory changes that occur at birth". This has never been the subject of any First part questions, but appears extensively in the old pre-2007 Fellowship papers (Question 10 from the second paper of 2007, Question 11 from the first paper of 2005, Question 6 from the first paper of 2001). "The transfer from the fetal to the neonatal state is complex", says the college model answer helpfully, though it is not clear how making this statement in one's written answer would have contributed to one's marks. Fortunately,  the circulatory events at birth can be summarised by saying that the normal extrauterine pattern of circulation results in the pressure-driven closure of the foramen ovale and ductus arteriosum.

In brief summary:

At birth,

  • Lungs are aerated with the first breaths (which purges liquid and creates and FRC) and with crying (which maintains the FRC)
  • This decreased pulmonary vascular resistance
  • At the same time, systemic vascular resistance is increased by clamping the umbilical cord
  • Right ventricular output is thereby channeled into the pulmonary circulation instead of the systemic
  • Increased pulmonary blood flow and increased systemic vascular resistance results in increased left atrial pressure, reversing the flow across the foramen ovale (which therefore closes immediately)
  • Increased aortic pressure reverses flow across the ductus arteriosus, which closes over around 24 hours (at least functionally - anatomic closure takes several days)
  • Closure of these structures leads to the separation of the pulmonary and systemic circulations, which concludes the transition to the adult pattern of circulation.

Causes of a persistent foetal circulation:

  • Low lung volume states (e.g. hyaline membrane disease and perinatal asphyxia)
  • Pulmonary hypoplasia (e.g. diaphragmatic hernia and Potter’s syndrome)
  • Meconium aspiration
  • Chronic placental insufficiency
  • Sepsis 
  • Hyperviscosity syndrome
  • Perinatal hypoxia, hypothermia and acidosis from any cause
  • Pulmonary thromboemobolism

Causes of reversion to foetal circulation:

  • Medical or surgical (eg. infusion of prostaglandin E2 to maintain an open ductus arteriosus in cases of duct-dependent congential heart disease, eg.  transposition of the great arteries)
  • Hypoxia, hypothermia and acidosis from any cause - occurring in the critical period before permanent closure of the ductus arteriosus and foramen ovale

Probably the single best resource for this is Chris Nickson's entry in LITFL, which is exactly all you need to know and nothing more. Oh's Manual dedicates haf a page to the topic, at the beginning of Shelley D. Riphagen's chapter (Ch.103, p. 1071: "The Critically Ill Child"). A short but highly examinable list of reasons for postnatal reversion to foetal circulation is also available there, and is reproduced below with little modification. If for whatever reason your situation calls for a more detailed knowledge of the topic, there is an excellent article by van Vonderen et al (2014) which explores not only the physiological changes at birth but the methods we have used to investigate them, and the historical changes in this branch of human biology. Wherever no other specific reference is mentioned, this article was the main source for the content offered here.

Circulatory and respiratory changes at birth

These diagrams are from van Vonderen et al (2014):

CIRCULATORY CHANGES AT BIRTH from van Vonderen

In textual long form, which defeats the point of point form:

  • Foetal lungs are cleared of fluid and aerated. 
    • With the first breaths, the lungs are aerated, creating an FRC. The foetus is capable of generating negative pressures in excess of 30 cm H2O, and these are triggered by light, warm temperature and handling.
    • Transpulmonary pressures generated by the first breaths probably play the dominant role. The pressure generated by the first breaths causes the interstitial space pressure to become subatmospheric, attracting the fluid into that space.
    • Adrenaline released during birth stimulated the lung endothelium to activate sodium channels which then reabsorb sodium out of lung water. This causes an osmotic shift of fluid out of the lung.
    • There is also the theory that passing through the vagina somehow squeezes water out of the foetal lung. Direct measurements have found that this squeeze equates to around 70 cm H2O. However, the foetal chest does not get much of that pressure - most of it is squandered on deforming the foetal skull. 
  • FRC is created and maintained
    • First breaths create and maintain the FRC by being expiration-limited, like a sort of intentional gas trapping. The infant ends up finishing the prolonged expiration on a closed glottis with abdominal muscles still forcefully contracting. 
    • Crying, grunting etc - all these manoeuvres serve this principle
    • The effect of this is that the alveoli are splinted
    • Surfactant also serves to reduce lung recoil, maintaining open alveoli
  • Aeration of lungs leads to decreased pulmonary arterial resistance
    • ​The sudden drop in the pulmonary vascular resistance makes the lungs a path of least resistance for right ventricular blood.
    • Right ventricular output is therefore directed into the pulmonary circulation, increasing left ventricular preload.
    • Some of the pulmonary blood flow also consists of oxygenated blood rom the ductus arteriosus.
    • Aeration is not the only factor contributing to changes in pulmonary vascular resistance: Oh's Manual also mentions gradual postnanatal regression of smooth muscle in the pulmonary vessel walls.
  • Foramen ovale shunt is reversed.
    • Pre-birth, much of LV preload consist of venous return through the foramen ovale.
    • There is an inverse relationship between pulmonary blood flow and flow though the foramen ovale.
    • As pulmonary blood flow contributes more and more of LV venous return, so the foramen ovale is forced closed.
  • Ductus arteriosus shunt is reversed. 
    • Ductus arteriosus is a large shunt from the pulmonary arteries to the aorta, and its diameter is approximately the same as that of the descending aorta.
    • It shunts right ventricular blood into the systemic circulation, bypassing the lungs. About 10% of the RV output still goes into the pulmonary circulation.
    • With decreased pulmonary vascular resistance, this shunt is reversed. Then, about 50% of the pulmonary blood flow ends up being oxygenated blood from the aorta, shunting back into the pulmonary circulation via the ductus arterisus
  • Ductus venosus will remain patent for days, but will eventually close.
    • ​Ductus venosus sends some of the left umbilical vein blood flow directly to the inferior vena cava. About 50% of the blood in the IVC passes through the liver and the rest bypasses the liver via the ductus venosus.
    • Functional closure occurs very shortly after birth, but this ductus ends up being anatomically patent for some number of days. If it fails to close, it turns into an intrahepatic portosystemic shunt. If it closes politely, it becomes the ligamenum venosum.
  • Systemic vascular resistance is increased by clamping of the umbilical cord
    • The umbilical/placental circulation is a high-flow, low-resistance system. 
    • Before birth the left ventricular preload is mostly dependent on umbilical venous blood flow, i.e. blood returning from the placenta.
    • After the cord is clamped, LV preload depends mainly on venous return via pulmonary blood flow.
    • Clamping the cord ends up increasing systemic vascular resiastance and improving venous return to the heart by 30-50%.

Causes of a persistent foetal pattern of circulation

An excellent resource for this is D'cunha et al (2001). In short, a persistently foetal pattern of circulation is mainly caused by anything which keeps pulmonary vascular resistance high. That could be a whole host of causes. The linked article organises them into acute or chronic:

Chronically increased PVR in a structurally normal heart

  • Primary persistent foetal circulation (due to hypermuscularisation of the pulmonary vessels from prolonged hypoxia or ischaemia in utero)
    • Placental insufficiency
    • Hyperviscosity, eg. high haematocrit due to late umbilical clamping
    • Prepartum ingestion of COX inhibitors which could prematurely close the ductus arteriosus

Acutely increased PVR due to physiological pulmonary vasoconstriction

  • Hypoxia
  • Hypercapnea
  • Acidosis
  • Hypothermia

Causes of perinatal hypoxia, acidosis and hypothermia

  • Sepsis
  • Diaphragmatic hernia
  • Hyaline membrane disease
  • Pulmonary thromboembolism

References

Murphy, Peter John. "The fetal circulation." Continuing Education in Anaesthesia, Critical Care & Pain 5.4 (2005): 107-112.

Kiserud, Torvid. "Physiology of the fetal circulation." Seminars in Fetal and Neonatal Medicine. Vol. 10. No. 6. WB Saunders, 2005.

Kiserud, Torvid, and Ganesh Acharya. "The fetal circulation." Prenatal Diagnosis: Published in Affiliation With the International Society for Prenatal Diagnosis 24.13 (2004): 1049-1059.

Fishman, Alfred P., and Dickinson W. Richards. "Physiological changes in the circulation after birth." Circulation of the Blood. Springer New York, 1982. 743-816.

van Vonderen, Jeroen J., et al. "Measuring physiological changes during the transition to life after birth." Neonatology 105.3 (2014): 230-242.

Koos, Brian J., and Arezoo Rajaee. "Fetal breathing movements and changes at birth." Advances in Fetal and Neonatal Physiology. Springer New York, 2014. 89-101.

Hooper, Stuart B., et al. "Cardiovascular transition at birth: a physiological sequence." Pediatric research (2015).

D’cunha, Chrysal, and Koravangattu Sankaran. "Persistent fetal circulation." Paediatrics & child health 6.10 (2001): 744.