In several Fellowship Exam papers (but none since 2007) the exam candidates were asked to describe the changes to the foetal circulation which occur after birth, and the various pathological states which interfere with this normal process. However, ever since the establishment of an official CICM Primary Exam, this matter appears to have been exiled into the First Part Syllabus. To that effect, there is a rather detailed summary on the circulatory changes in the newborn in the First Part exam preparation section. Here, the time-poor exam candidate's time will not be wasted with any further digressions into physiology, considering especially the possibility that this topic will never appear in the Second Part again.

Previous SAQs on this topic included the following:

• Question 10 from the second paper of 2007 
• Question 11 from the first paper of 2005
• Question 6 from the first paper of 2001

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