Blood Gas Interpretation

Introduction
pH
Acid (H+)
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
The Base Excess
Acid-Base Disorders
The Blood Gas Machine
Areas of Uncertainty in Clinical Practice

Introduction

Blood gases are helpful in determining the adequacy of respiratory function of the baby (oxygenation and ventilation) as well as the baby's acid/base balance. Blood gases can be performed from arterial (either a stab or via an arterial line), venous (through an intravenous cannula) or capillary (heel prick) specimens. Repeated arterial stabs are strongly discouraged, as they are painful and do not represent oxygenation as well as pulse oximetry. Arterial stabs may be taken from the radial artery (provided there is also a palpable ulnar pulse) or from the brachial artery, although this is in close proximity to the median nerve. All three specimens will give a good assessment of acid/base status and pCO₂, whereas arterial specimens are required to assess pO₂. It is always important to note the FiO₂ (percentage inspired oxygen) when interpreting blood gases. Each unit should have their own reference ranges.

pH

The pH is a negative logarithm of hydrogen ion concentration [H⁺], that is a decrease in pH from 7.0 to 6.0 represents a ten-fold increase in [H⁺]. Although each unit will define neonatal pH a little differently, if, say a normal neonatal pH is defined as 7.30 to 7.40, then

pH > 7.4 is an alkalosis
pH < 7.3 is an acidosis

The pH is proportional to HCO₃ (or base excess), therefore

an abnormal increase in HCO₃ (or base excess) increases the pH (metabolic alkalosis)
an abnormal fall in HCO₃ (or base excess) decreases the pH (metabolic acidosis)

The pH is inversely proportional to pCO₂, therefore

an abnormal increase in pCO₂ decreases the pH (respiratory acidosis)
an abnormal decrease in pCO₂ increases the pH (respiratory alkalosis)

Acid (H+)

Many organic acids are produced during normal metabolism. Sometimes they can accumulate in the blood (e.g. lactic acid). The hydrogen ion (H+) may be 'mopped up' by buffers including bicarbonate (HCO₃). Bicarbonate is unique because it can be converted to CO₂, which can be blown off by the lungs (provided the baby is not in respiratory failure). The following bi-directional equation demonstrates this

Respiratory Acidosis (eg pCO₂ >= 50 mmHg, pH < 7.30)

This occurs when the pCO₂ is abnormally high and is due to inadequate alveolar ventilation. Causes include depression of the breathing centre in the brain, upper airway obstruction, stiffness of the chest wall or significant ventilation/perfusion imbalance. If the respiratory acidosis is chronic, the body will respond by trying to excrete acid and retain bicarbonate in the urine resulting in a compensatory rise in serum bicarbonate (metabolic alkalosis). The treatment of a respiratory acidosis is to treat the underlying cause and to consider the need for commencing or increasing mechanical ventilation. The latter is achieved by either increasing the tidal volume (increasing PIP or decreasing PEEP) or by increasing the respiratory rate.

Respiratory Alkalosis (eg pCO₂ < 35 mmHg, pH > 7.40)

This occurs when the pCO₂ is abnormally low and is usually due to excessive mechanical ventilation or to abnormal control of ventilation (e.g. during hypoxic-ischaemic encephalopathy). The baby may also be trying to compensate for a primary (intracellular or extracellular) metabolic acidosis, although the pH will never become alkalotic (as the baby will never over-compensate). The treatment of a respiratory alkalosis is to wean the mechanical ventilation by reducing PIP or tidal volume, then respiratory rate.

Metabolic Acidosis (eg HCO₃< 17 mmol/L or B.E. < minus 6.0 mEq/L, pH < 7.30)

This may occur where there is a rise in free H⁺ ions that cannot be totally buffered. In this case the anion gap is increased. Causes include lactic acidosis secondary to tissue hypoxia (e.g. hypotension, sepsis and PDA) or the inability to excrete/buffer accumulated organic acids (e.g. protein loading and renal immaturity). Another common cause of metabolic acidosis, particularly in the extremely premature infant is excessive loss of HCO₃ in the urine or gut. In this case the anion gap is normal. Metabolic acidosis is rarely due to an inborn error of metabolism. The treatment of a metabolic acidosis is to treat the underlying cause, consider volume expansion (e.g. 10 mls/kg of normal saline) if the baby is thought to be hypovolaemic or to administer NaHCO₃ if the metabolic acidosis is severe (controversial) or refractory (e.g. bicarbonate wasting). Bicarbonate should not be given if the pCO₂ is elevated as the pH will not change (according to the above formula, a metabolic acidosis is merely being replaced by a respiratory acidosis).

Metabolic Alkalosis (eg HCO₃ > 28 mmol/L or B.E. > plus 4.0 mEq/L, pH > 7.40)

This occurs where the plasma HCO₃ or base excess is abnormally high. Causes include hypochloraemia (the level of bicarbonate and chloride in plasma are reciprocally related), which may be due to diuretic therapy or upper gastrointestinal obstruction (e.g. pyloric stenosis). The baby may also be trying to compensate for a respiratory acidosis, although the pH will never become alkalotic (as the baby will never over-compensate). The treatment of a metabolic alkalosis is to treat the underlying cause (e.g. chloride replacement) or the underlying cause of the respiratory acidosis.

Base Excess

This is one way of looking at the metabolic component. It refers to the 'amount of base that would have to be added to one litre of the baby's blood at 40 mmHg pCO₂ to return the pH to normal. It is a calculated value and will be erroneous if the pCO₂ is not normal. In these circumstances, the 'metabolic' component of the blood gas should be assessed using the plasma HCO₃ level.

Acid-Base Disorders

Any one of the above four scenarios can occur in isolation, with or without compensation. These are classified as simple acid-base disorders. When a combination of simple acid-base disturbances occurs, the baby has a mixed acid-base disorder. When there is a mixed disorder, it is sometimes difficult to know which is the primary and which is the compensatory component. In such circumstances a helpful principle is that normal physiological processes never over-compensate. The pH can be relatively normal in the following situations

respiratory acidosis with metabolic compensation
metabolic acidosis with respiratory compensation
metabolic alkalosis with respiratory compensation
respiratory alkalosis with metabolic compensation

The fourth is extremely unusual in neonates.

The Blood Gas Machine

This measures pH, pCO₂ and pO₂ and may measure glucose and lactate. It calculates HCO₃, base excess and oxygen saturation. Measurements that are inaccurate, including Hb and oxygen saturation, should not be used to decide therapy (although newer machines contain co-oximetry and are very accurate).

Areas of Uncertainty in Clinical Practice

The main controversy relates to the use of bicarbonate (HCO₃) for the treatment of a metabolic acidosis

There is no evidence that the correction of an acute metabolic acidosis improves survival or long term neurodevelopmental outcome.
The extra pCO₂ produced (in the above equation) can cross cell membranes and paradoxically worsen the intracellular acidosis (as it combines with intracellular water, and with the equation in reverse, produces excess H+, which can't cross back out).
Sodium bicarbonate is hyper-osmolar and if given rapidly, particularly to premature babies, may cause intraventricular haemorrhage.
The exact reference ranges for pH, pCO₂, HCO₃ and base excess will vary from unit to unit. The above ranges are given for practical demonstration only.

References

Ganong WF. Review of Medical Physiology, 19th Ed. 1999, p. 697-704. Appleton & Lange, Stanford, Connecticut

Taeusch HW, Ballard RA (Eds). Avery's Diseases of the Newborn 7th Ed. W.B. Saunders Company, Philadelphia. 1998