Blood Gas interpretation in Paediatrics

This guide is written in Paediatric and Neonatal context, so the focus is somewhat different to adult diseases. Most blood gases in newborn babies and children are done by a ‘capillary’ sample; or sometimes venous while inserting a cannula and rarely arterial.

Before interpreting a blood gas, ask yourself:

– Do you know the clinical diagnosis and background information?

– Know the situation why blood gas was done

– Is the patient deteriorating or improving clinically?

– What intervention or change has happened; and what is expected on blood gas?

– How much O2 is given? Is patient’s SaO2 maintained?

– Is there a previous blood gas to compare the trend?

– Do you need to intervene / discuss this with senior doctors?

Normal ranges:

  pH 7.35 – 7.45

  pCO2 4.7-6.0 kPa (35 – 45 mmHg)

  HCO3 22-26 mEq/L

  Base deficit -2 to +2 mmol/L

Remember

We focus less on pO2 in neonates or children, as samples are commonly capillary or venous

Newborn babies often tolerate mild acidosis and target pH may be 7.25 or 7.3 in certain clinical situations

Steps to blood gas interpretation:

1) What is pH: Is there acidosis or alkalosis (or pH is normal)?

  Changes to pH alters body’s metabolic and other physiological functions and can cause deterioration in the patient.

2) What is pCO2 (respiratory component): Is there respiratory contribution to acidosis (or sometimes alkalosis)?

  Rising pCO2 indicates respiratory insufficiency and impending failure; requiring immediate interventions to improve gas exchange.

  If pCO2 isn’t the cause of acidosis or alkalosis, the disorder is likely to be metabolic!

3) What is HCO3 and Base deficit (metabolic components):

  Is there a significant metabolic contribution to acidosis or alkalosis?

  Hypotension, sepsis or volume loss causes poor circulation with low HCO3 and base; prompting interventions to improve circulation.

Compensatory changes take time and are best left for senior doctor’s interpretation. Respiratory acidosis is compensated by renal excretion of H⁺and retention of filtered HCO3; Respiratory alkalosis by renal excretion of HCO3. Metabolic acidosis is compensated by lungs expelling pCO2 & vice versa.

Renal compensation of HCO3 can take hours or days but CO2 compensation by lungs can happen within minutes.

Useful Mnemonic= ROME

Respiratory component Opposite (pCO2 is in opposite direction to pH)

Metabolic component Equal (HCO3 & pCO2 is in same direction as pH)

(but it doesn’t work for mixed disorders)

Respiratory Acidosis, common causes:           

– Obstruction of airways e.g. Croup, Foreign body, Asthma

– Inadequate alveolar ventilation e.g. RDS, Bronchiolitis, Pneumonia

– Hypoventilation e.g. Neuromuscular diseases, excess opiates, severe scoliosis

– Ventilation/perfusion imbalance e.g. Collapse, Pneumothorax

Manage with CPAP, High-Flow O2, Ventilation etc

Metabolic Acidosis, common causes:

– Poor circulation causing lactic acidosis Hypotension, Sepsis, Shock, Anaphylaxis

– Excessive loss of HCO3 in the urine or gute.g. Renal Tubular Acidosis, chronic diarrhoea, Spironolactone

– Other acids in blood – DKA, Inborn error of metabolism, Ethanol, Methanol poisoning, renal failure

Manage with establishing adequate circulatory volume with fluid boluses, colloid, inotropes if necessary

Respiratory Alkalosis, common causes:

– Hyperventilation e.g. Panic attack, High altitude, Anaemia, Pulmonary oedema

– Excessive mechanical ventilation

– Drugs: Catecholamines, salicylates, doxapram, nicotine

– Hyperthermia, hepatic encephalopathy

Manage by treating the cause; e.g. for Panic attack with rebreathing in to paper bag; etc

Metabolic Alkalosis, common causes:

– Loss of acid with excessive vomiting e.g. Pyloric stenosis, Bulemia, Nasogastric free drainage

– Volume contraction with loop or thiazide diuretics,

– Congenital Adrenal Hyperplasia, Primary Aldosteronism, Renin secreting tumor, Bartter and Gitelman syndromes

Treat the cause