Umbilical cord blood analysis

The pH, base excess and pCO2, or acid base status of arterial blood flowing through the umbilical cord provides valuable objective evidence of the metabolic condition of neonates at the moment of birth.

The purpose of cord blood gas analysis is to determine the acid-base status of the neonate at the moment of delivery. 

Umbilical cord blood gas analysis has a role in hospital delivery suites in cases of suspected fetal distress/asphyxia. 

The fetus depends for oxygen and nutrients on maternal blood supply. 

The fetal and maternal circulation is proximate at the placenta where gas/nutrient exchange between maternal and fetal circulation occurs. 

Oxygen and nutrients diffuse across the placental membrane from maternal arterial blood and is transported to the fetus via a single large umbilical vein. 

The fetal blood returns to the placenta via two small umbilical arteries. 

The fetal deoxygenated blood contains the waste products of fetal metabolism, including carbon dioxide (pCO2), for elimination from maternal circulation via lungs and kidneys. 

The  umbilical cord contains three blood vessels: one large vein carrying oxygenated blood to the fetus and two much smaller arteries carrying deoxygenated blood that is relatively rich in carbon dioxide and other metabolic waste products from the fetus.

Thus venous cord blood reflects the combined effect of maternal acid-base status and placental function.

The arterial cord blood reflects neonatal acid-base status.

The acid-base parameters of pH, base excess and lactate must be derived from arterial rather than venous cord blood when assessing the neonatal condition. 

Umbilical venous blood gas values more closely resemble those of adult arterial blood than do those of umbilical arterial blood: the umbilical vein that carries oxygenated blood rather than the umbilical artery. 

After separation from maternal circulation, and throughout life, oxygenated blood is carried in arteries from lungs to the tissues and deoxygenated blood is carried from tissues back to the lungs in veins.

Cord blood gas analysis’value lies in its ability to provide objective evidence of asphyxia at the moment of birth.

Cord blood gas analysis is more reliable in this regard than routine clinical assessment at birth using the Apgar scoring system.

Asphyxia reduces tissue oxygen of sufficient severity and duration to cause metabolic acidosis impairing aerobic metabolism of glucose, and cells must depend for their function and survival on less effective anaerobic pathways that result in reduced ATP energy production and accumulation of metabolic acids; principally lactic acid.

Such an acid influx overwhelms the Normal buffering mechanisms, and pH falls below normal limits. 

Cord-blood metabolic acidosis is characterized by reduced blood pH and decreased base excess implying  that sometime during labor, oxygenation of fetal tissues was severely compromised. 

Cord-blood respiratory acidosis is a relatively common transitory state that resolves soon after birth when the baby starts to breathe.

Cord-blood respiratory acidosis is of little clinical significance.

Maternal factors for hypoxemia:

respiratory disease





Excessive uterine activity-hyper stimulation by drugs

prolonged spontaneous labor

placental abruption

Umbilical cord compression


cord prolapse or entanglement


Maternal reduced oxygen-carrying capability due to:


carboxy- hemoglobinemia

 Utero-placental dysfunction

placental abruption

placental infarction/dysfunction marked by intrauterine growth restriction, 

oligohydramnios or abnormal Doppler studies



Decreased fetal oxygen-carrying capability

significant anemia due to isoimmunization, maternal fetal bleed or vasa previa

carboxy- hemoglobinemia due to smoking

Decreased uterine blood flow due to:

hypotension (shock, sepsis)

regional anesthesia

maternal positioning


Chronic maternal conditions:


chronic hypertension


antiphospholipid syndrome

Significant metabolic acidosis, defined as cord arterial blood pH <7.0 and base excess <–12.0 mmol/L (base deficit >12.0 mmol/L), occurs in around 0.5-1 % of deliveries.

The severe intrapartum hypoxia is associated with increased risk of hypoxic brain-cell injury and associated hypoxic-ischemic encephalopathy.

Hypoxic-ischemic encephalopathy

dysfunction is caused by perinatal asphyxia. 

Symptoms of hypoxic ischemic encephalopathy among affected neonates include hypotonia, poor feeding, respiratory difficulties, seizures and reduced level of consciousness. 

Patients with mild hypoxic ischemic encephalopathy survive with little or no long-term consequences, but most of those with moderate/severe disease either die during the neonatal period or survive with severe and permanent neuro/psychological deficit.

Cerebral palsy is an outcome for some with hypoxic ischemic encephalopathy.

Hypoxic ischemic encephalopathy is thus a significant cause of perinatal death and birth-related permanent disability.

Around 75 % of babies with significant metabolic acidosis (pH <7.0, base excess <–12.0 mmol/L) do not suffer any signs of neurological illness or other adverse effects,

The diagnosis of hypoxic ischemic encephalopathy depends in part on demonstrating significant cord-blood metabolic acidosis, and a normal arterial cord-blood pH and base excess result usually excludes the possibility of perinatal asphyxia. 

Significant cord metabolic acidosis (pH <7.0 and base excess <–12 mmol/L) is necessary, but not sufficient to confirm that an acute intrapartum hypoxic event was the cause of encephalophy/cerebral palsy.

The only effective treatment for hypoxic 

ischemic encephalopathy is controlled cooling of the baby to a rectal temperature of 34 ± 0.5 °C for 48-72 hours. 

Sampling cord blood for gas and acid-base analysis comprises three steps:

clamping a segment of the cord

removing the clamped cord segment

needle aspiration of two blood samples (one venous, one arterial) from the excised clamped cord segment into preheparinized syringes.  

Immediately after birth, ideally before the baby’s first breath, an approximate 20-cm segment of cord must be isolated between two sets of two clamps. 

Delay in clamping by as little as 45 seconds after birth results in significant change in acid-base parameters: the longer the delay, the greater is the change.

Once isolated from maternal/neonatal circulation, the acid-base parameters of clamped cord blood are stable at room temperature for 60 minutes.

Arterial blood specimens should be analyzed within 30 minutes of sampling

The umbilical arteries are much smaller and less visible than umbilical veins, so it is recommended that blood from both artery and vein are sampled and analyzed, so that arterial blood results can be validated as truly arterial. 

It is standard practice to clamp the umbilical cord within seconds of birth, however delaying cord clamping by 2-3 minutes after birth is beneficial to the baby because of the placental blood transfusion it permits. 

The benefits to the baby associated with delayed clamping include higher birthweight, increased hemoglobin concentration and iron reserves, but there is small increased risk of jaundice.

Sampling blood within seconds of birth directly from the still pulsating unclamped umbilical cord, rather than from a separated clamped cord segment, is advocated by some.

Cord blood analysis is recommended:

Cesarean delivery for fetal compromise

Low 5-minute Apgar score

Severe intrauterine growth restriction

Abnormal fetal heart rate tracing

Maternal thyroid disease

Intrapartum fever

Multifetal gestations

Some authorities recommend that cord blood gas analysis be performed at all births.

Advantages of routine cord blood gas testing: establishing the prevalence of metabolic acidosis at an obstetric unit, can only be determined by performing cord-blood testing at all births,.

This is a safety audit measure, that results in improved perinatal outcomes.

Lactic acid is the principal metabolic acid responsible for the fall in cord-blood pH and base excess associated with cord-blood metabolic acidosis and birth asphyxia.

It follows, theoretically at least, that arterial cord-blood lactate concentration should be as reliable an indicator of birth asphyxia and risk of HIE as the more established tests, arterial cord-blood pH and base excess. 

Cord-blood lactate concentration is a good predictor of cord-blood pH and base excess, and that it is at least as good as pH and base excess in predicting outcome.

There is no consensus on the cut-off lactate value that should be used to define significant cord metabolic acidosis, as there is for pH and base excess (pH <7.0, base excess <–12.0 mmol/L).  

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