SYMPOSIUM: NEONATOLOGY
An acid (HA) is a substance that donates Hþ ions (e.g. carbonic
Understanding blood gases/
acidebase balance
Nitin Goel
Jennifer Calvert
Abstract
Acidebase balance is regulated by intracellular & extracellular buffers and
by the renal and respiratory systems. Normal pH is necessary for the
optimal function of cellular enzymes and metabolism. Disorders of acide
base balance can interfere with these physiological mechanisms leading
to acidosis or alkalosis and can be potentially life threatening. Blood
gas analysis is a routine procedure performed in the neonatal unit and
combined with non-invasive monitoring, aids in the assessment and
management of ventilation and oxygenation and provides an insight
into the metabolic status of the patient. The following discussion details
the basic terminology and pathophysiology of acidebase balance and the
main disorders. It aims to provide a logical and systematic approach to
the understanding and interpretation of blood gases in the newborn
period. The application of these concepts, together with relevant history
and examination, will help the clinician assess the medical condition,
make therapeutic decisions and evaluate the effectiveness of any inter-
vention provided.
Keywords acidebase balance; acidosis; alkalosis; anion gap; base
deficit; blood gas analysis; pH
Introduction & terminology
Acidebase balance is the complex physiological process, which
acts to maintain a stable extracellular pH within the body. It is
regulated by intracellular & extracellular buffers and by the renal
and respiratory systems. Any derangement in this balance can
interfere with physiological processes and can be potentially life
threatening. An understanding of acidebase balance is required
for the interpretation of blood gases, to assess both the respira-
tory and metabolic status of patients and thereby enable their
effective clinical management.
Normal pH is maintained between 7.35 and 7.45, which
creates an optimal environment for cellular metabolism. The pH
is inversely related to the concentration of Hþ ions.
pH a 1=Hþ
Nitin Goel MBBS MD MRCPCH is a Neonatal Registrar at the Neonatal
Intensive Care Unit in the University Hospital of Wales, Cardiff, UK.
Conflict of interest: none.
Jennifer Calvert BA BM BCh MRCP(UK) MRCPCH is a Consultant Neonatologist
at the Neonatal Intensive Care Unit, University Hospital of Wales,
Cardiff, UK. Conflict of interest: none.
PAEDIATRICS AND CHILD HEALTH 22:4
acid). In contrast, a base (A) accepts Hþ ions, (e.g. hydroxyl
ions, ammonia) and in solution combines with the acid to
neutralize it. An acid can dissociate into Hþ and a conjugate
base.
HA4Hþ þ A
Equilibrium is maintained based on the above equation.
Thus addition of acid (HA) increases Hþ and A and shifts the
equation towards the right. During normal metabolism, Hþ ions
are constantly being produced and neutralized to maintain pH
homeostasis. Neonates produce higher levels of Hþ due to their
rapid growth and metabolism and therefore maintaining balance
can be challenging in newborn period.
Normal acidebase regulation
The process of maintaining pH balance during normal metabo-
lism involves buffer systems and compensatory mechanisms in
the respiratory and renal systems.
Buffer systems
Buffers are substances that attenuate the change in pH when
acid/base levels increase. On addition of acid, they bind to
any extra Hþ ions and prevent decline in pH. Similarly when
base is added, the buffers prevent a rise in pH by releasing Hþ
ions. The best buffers are weak acids and bases and work best
when they are 50% dissociated. The pH at which this happens
is called pK and is close to 7.40 for some buffers. The
HendersoneHasselbalch equation expresses the relationship
between pH, pK and concentrations of an acid and its conju-
gate base.
pH ¼ pK þ log½A =½HA
Extracellular buffers: the bicarbonate system is the principal
buffer in the extracellular fluid (ECF) and is based on the rela-
tionship between carbon dioxide (CO2) and bicarbonate
(HCO3), where the former combined with water acts as an acid
(carbonic acid H2CO3) and the latter as base.
Hþ þ HCO
3 4H2 CO3 4CO2 þ H2 O
The pK for this buffer is 6.1. For bicarbonate buffer, the
HendersoneHasselbalch equation is:
pH ¼ 6:1 þ log½HCO
3 =½CO2 
Mathematical manipulation of the above equation produces the
following relationship,
½Hþ  ¼ 24  pCO2 =½HCO
3
which emphasizes that Hþ ion concentration and hence pH is
determined by the ratio of pCO2 and HCO3 concentration, and
not their absolute values.
When Hþ ions are added to the system, the equation shifts to
right and pH is maintained at the expense of HCO3 ions, referred
142 Ó 2011 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: NEONATOLOGY
to as ‘Base Deficit’. There is also an increase in dissolved CO2
levels (as H2CO3), which can be clinically estimated by measuring
the partial pressure of CO2 (pCO2). Thus with addition of Hþ ions,
the pH decreases with a decrease in base and an increase in CO2
levels. The lungs then excrete the excess CO2. With addition of
base, there is a decrease in CO2 and the lungs then reduce CO2
excretion. In this way the bicarbonate buffer system works as an
open system and plays an important role in pH homeostasis.
Intracellular buffers: these are non-bicarbonate buffers and
include various proteins and organic phosphates. The proteins
consist of acid histidine, with a side chain, which accepts Hþ ions
in exchange for intracellular potassium (Kþ) and sodium (Naþ)
ions. In acute metabolic acidosis, hyperkalaemia can develop due
to the exchange of Kþ for Hþ.
Phosphate can bind up to three Hþ ions and in its mono- and
di-hydrogen forms acts as an effective buffer in the urine.
þ
4 4H þ HPO4
H2 PO1 2
Bone is also an important buffer and releases base on dissolution,
so can buffer an acid load, but at the expense of bone density.
During bone formation, it also consumes base thus buffering any
excess.
Compensatory mechanisms
Although buffers represent the first line of defence against pH
changes, they cannot maintain acidebase balance in disease
states for prolonged periods of time or with sudden significant
alterations of Hþ ion production. Instead, compensatory physi-
ological changes by the renal and respiratory systems are
employed. In a primary metabolic disorder, the respiratory
system provides the compensation, whereas in a primary respi-
ratory disorder, the regulation is by the renal system. Respiratory
responses occur more rapidly (minutesehours) than renal
mechanisms, which take about 3e4 days, with renal base
excretion more rapid than acid excretion. These compensatory
mechanisms must be followed by corrective measures to
normalize the acidebase balance, by treating the primary cause
of the imbalance.
Respiratory compensation: the respiratory system modifies pH
by balancing the production of Hþ with excretion of CO2.
During normal metabolism CO2 is generated, which is a weak
acid. Any increase in physical activity leads to an increase in
metabolism and thus an increase in pCO2. The lungs respond
by increasing ventilation and excreting excess CO2, thus
maintaining a normal pCO2 (4.5e6 kPa). Conversely, hypo-
ventilation causes CO2 retention and thus an increase in pCO2.
The resulting increase in Hþ ions directly stimulates chemore-
ceptors in the brain causing an increase in respiratory rate.
Thus changes in alveolar ventilation can alter pH and vice
versa.
Renal compensation: the kidneys prevent loss of HCO3 in the
urine and maintain plasma levels by excreting acid and gener-
ating new bicarbonate. They can thus respond to acidebase
imbalance by acidifying or alkalinizing the urine. This is
accomplished by:
PAEDIATRICS AND CHILD HEALTH 22:4
(1) Reabsorption of filtered HCO3, which takes place in the
proximal tubules (85%) and in the thick ascending loop of
Henle (15%).
Normally large amounts of bicarbonate enter the proximal
tubules (PT) daily and if this bicarbonate is not reclaimed by the
nephrons, severe acidosis can result. In the proximal tubular
cells, CO2 derived from cell metabolism or diffusion through the
tubular lumen, combines with water to form carbonic acid. This
dissociates into Hþ ions and bicarbonate via carbonic anhydrase.
The bicarbonate is transported back to the circulation, while the
Hþ ions are secreted into the tubular lumen, where they combine
with the filtered bicarbonate to form H2O and CO2. The CO2
diffuses back in the PT cells to repeat the cycle. The net effect is
that for each Hþ ion secreted, one HCO3 is retained, so that
bicarbonate reserves are continuously regenerated.
Factors causing an increase in Hþ ion secretion and thus
increased bicarbonate reabsorption include increased filtered
bicarbonate, volume depletion due to any cause and resulting
activation of renineangiotensin system, increased plasma pCO2
and hypokalaemia. Conversely Hþ ions secretion and thus
bicarbonate reabsorption is decreased in conditions with reduced
filtered bicarbonate, expansion of ECF volume and decreased
plasma pCO2. Hyperparathyroidism and disease states such as
proximal renal tubular acidosis (RTA), cystinosis, or neph-
rotoxins can also affect proximal tubules and limit bicarbonate
reabsorption.
Newborn infants and in particular preterm babies have
a lower glomerular filtration rate, immature tubular function and
limited capacity to retain bicarbonate and are therefore predis-
posed to metabolic acidosis.
(2) Excretion of Hþ ions which takes place at the distal tubules
and the collecting duct, thus acidifying the urine. The prin-
cipal buffers at these sites are phosphate and ammonia.
In normal conditions large amounts of phosphate ions are
present in the tubular fluid, which combine with Hþ ions,
forming titratable acid, thus reducing urinary pH. However,
phosphate buffering capacity is limited as there is no mechanism
for increasing urinary phosphate excretion in response to acide
base status.
Ammonia is generated in the cells of the proximal tubules,
diffuses into the tubular fluid and combines with the intra-
luminal Hþ ions to form ammonium ion, which cannot diffuse
back into the tubular cells, thus making ammonia an effective
buffer.
These two processes reduce free Hþ in the tubular fluid,
thereby increasing Hþ excretion into the urine and allowing the
generation of new bicarbonate in the cells, which can then
enter the plasma to replenish depleted levels. The major
regulator of Hþ secretion in the distal tubule is aldosterone with
other influencing factors being pCO2 and the sodium concen-
tration delivered to these segments. Sodium is reabsorbed in
exchange for either potassium or Hþ ions, under the influence
of aldosterone. These mechanisms may be impaired by intrinsic
defects in the tubules causing primary distal renal tubular
acidosis (RTA), or by various insults including nephrocalci-
nosis, vitamin D intoxication or Amphotericin B administra-
tion, which produce secondary distal RTA. Patients with distal
RTA cannot acidify their urine and have a urine pH more than
5.5, despite acidosis.
143 Ó 2011 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: NEONATOLOGY
Disturbances of acidebase balance
þ the rate of breathing is increased and CO2 is excreted. The
Abnormalities in blood pH, due to an increase in H ions above
normal, is called ‘acidaemia’ (pH less than 7.35), and due to
a decrease is termed ‘alkalaemia’ (pH more than 7.45). The
clinical process, which causes the acid or alkali to accumulate, is
called ‘acidosis or alkalosis’, respectively.
As shown in Figure 1, acidosis is caused by conditions
resulting in either a reduction in HCO3 or an increase in pCO2,
leading to an increase in Hþ ions and decreased pH. Alkalosis is
caused when the primary disturbance causes either an increase
in HCO3 or a decrease in pCO2, leading to a decrease in Hþ ions
and an increased pH.
Metabolic acidosis
This results from an alteration in the balance between production
and excretion of acid; by increased exogenous intake or endoge-
nous production of Hþ ions, inadequate excretion, or by excessive
loss of bicarbonate in urine or stools (Table 1). Premature infants
less than 32 weeks gestation, frequently manifest a proximal or
distal RTA. In proximal RTA, there is limited secretion of Hþ ions
and incomplete bicarbonate reabsorption. Urine pH remains less
than 5, but becomes alkaline after a bicarbonate infusion, even
without normal serum bicarbonate levels. In distal RTA, the distal
tubules cannot secrete Hþ ions and thus the urine pH remains
alkaline (more than 7), rarely falling below 5.5.
Carbohydrate, fat and protein metabolism in the body
generate about 2e3 mEq/kg/day Hþ ions. Normally the CO2,
resulting from complete oxidation of carbohydrates and fats is
removed by the lungs. However anaerobic metabolism, as in
tissue hypoxia, produces lactic acid from glucose metabolism
and ketoacids from triglycerides, leading to acidosis.
↑PCO
Respiratory acidosis
Hyperventilation
↓PCO
CO + H O ↔ H CO ↔ H+ + HCO
Hypoventilation
↑PCO
Respiratory alkalosis
↓PCO
Respiratory compensation
Figure 1 Acidebase regulation: interplay of bicarbonate buffer, respiratory and renal systems.
PAEDIATRICS AND CHILD HEALTH 22:4
Systemic acidosis stimulates the respiratory centre directly,
acidosis also stimulates the kidneys to increase Hþ ion excre-
tion, accompanied by bicarbonate reabsorption. In renal insuf-
ficiency, the ability of kidneys to generate ammonia and secrete
Hþ ions is limited, leading to acidosis. In unstable neonates,
respiratory compensation is limited and because of tubular
immaturity, the acidosis worsens rapidly if the underlying cause
is not treated.
Anion gap: an important tool in evaluating the cause of meta-
bolic acidosis is the ‘anion gap’, the difference in the measure-
ment of the most abundant serum cation (Naþ) and the sum of
two most abundant serum anions (HCO3 and chloride, Cl).
½Naþ   ð½Cl  þ ½HCO
3 Þ
This gap also represents the difference between unmeasured
anions (phosphate, sulphate, proteins, acids e.g. lactate, ketoa-
cids) and unmeasured cations (potassium, magnesium, calcium).
It should not be interpreted in isolation but in conjunction with
other laboratory abnormalities and the clinical history. The
normal anion gap for neonates is 5e15 mEq/litre.
An elevated anion gap represents an increase in unmeasured
anions (Figure 2) and can result from overproduction or under
excretion of acids. Normal anion gap acidosis results from the net
loss of bicarbonate. In these cases Cl reabsorption is increased
and it becomes the major anion accompanying Naþ and so the
sum of anions in plasma remains normal. Thus, normal anion
gap acidosis is also referred to as hyperchloraemic metabolic
acidosis.
pH < 7.35 ↓HCO –
Metabolic acidosis
↑Bicarbonate
reabsorption
↑HCO –
–
↓Bicarbonate
reabsorption
↓HCO –
Metabolic alkalosis
pH > 7.45 ↑HCO –
Metabolic compensation
144 Ó 2011 Elsevier Ltd. All rights reserved.
 PAEDIATRICS AND CHILD HEALTH 22:4

Acidebase disorders, blood gas findings and common causes in neonates

Disorder Blood gas analysis (normal range) Causes
pH pCO2 HCO3L BE
(7.30e7.45) (4.5e6 kPa) (19e24 mmol/l) (L3 to D3)

Metabolic acidosis
Uncompensated Y Normal Y Y Increased anion gap (more than 16 mEq/l)
Compensated Low Y Y Y Hypoxaemia/lactic acidosis: sepsis, shock, respiratory or cardiac disorders, anaemia, intraventricular haemorrhage,
Normal perinatal asphyxia, necrotizing enterocolitis
Renal failure
Inborn errors of metabolism
Total parenteral nutrition

Normal anion gap (8e16 mEq/l)

Prematurity: hyperchloraemic acidosis
Renal tubular acidosis: proximal/distal
Gastrointestinal bicarbonate losses: ileostomy, diarrhoea

SYMPOSIUM: NEONATOLOGY
Metabolic alkalosis
Uncompensated [ Normal [ [ Decreased urinary chloride (<10 mEq/l)
Compensated High [ [ [ Gastric losses: vomiting, pyloric stenosis, excess naso-gastric aspirates
145

Normal Diuretics
Chloride losing diarrhoea
Hypokalaemia

Increased urinary chloride (>20 mEq/l)

Hyperaldosteronism
Adrenal hyperplasia
Excess alkali administration
Respiratory acidosis
Uncompensated Y [ Normal Normal Respiratory abnormalities: respiratory distress syndrome, chronic lung disease, pneumothorax, meconium aspi-
Compensated Low [ [ [ ration, transient tachypnoea of newborn, pneumonia, pulmonary hypoplasia, congenital lung malformations
Normal Central nervous system depression: hypoxic ischaemic encephalopathy, excess opioids, raised intracranial pres-
sure, central hypoventilation, meningitis, malformations
Neuro-muscular disorders: congenital myopathies, neuropathies, spinal and neuro-muscular junction disorders
Ó 2011 Elsevier Ltd. All rights reserved.

Upper airway obstruction: Pierre-Robin sequence, choanal atresia, laryngeal oedema/spasm/mass etc.
Iatrogenic: inadequate ventilator settings in mechanically ventilated patient
Respiratory alkalosis
Uncompensated [ Y Normal Normal Increased sensitivity of respiratory centre: hypoxia due to any cause
Compensated High Y Y Y Medications: Caffeine
Normal Extra pulmonary CO2 losses: ECMO, dialysis
Iatrogenic: over-ventilation of mechanically ventilated patient

Table 1
 SYMPOSIUM: NEONATOLOGY
Normal Acidosis Acidosis
plasma (no gap) (increased gap)
UC UC UC
UA UA
UA
HCO
HCO
Na Na Na
HCO
Cl Cl
Cl
The anion gap
UC, unmeasured cations; UA, unmeasured anions.
Figure 2 Anion gap.
Metabolic alkalosis
This results from increased bicarbonate and/or excessive loss of
Hþ ions. It is uncommon in the neonatal period. Causes are
related to increased renal reabsorption of HCO3, loss of Hþ ions
or increase addition of bicarbonate (Table 1).
The buffers try to minimize the changes, but bicarbonate and
pH rise, respiration is depressed, and there is an increase in
pCO2. Respiratory compensation is limited by increasing
hypoxia, so cannot normalize the pH. The kidneys respond
to this by increasing base excretion, with urine pH increasing to
8.5e9.0. The alkalosis can worsen if there is co-existing ECF
contraction and hypokalaemia, as it conversely increases bicar-
bonate reabsorption. This can only be corrected by treating the
underlying disorder.
Hypochloraemia and hypokalaemia are usually present, due
to increased urinary losses. Measurement of urinary chloride can
help differentiate the causes of metabolic alkalosis (Table 1). If
urine chloride levels are less than10 mEq/litre, the underlying
cause is generally volume depletion from extra-renal losses, with
loss of Naþ, Kþ and chloride. These cases are responsive to
sodium chloride. The use of diuretics in neonates can lead to
increased fluid and Naþ losses in the kidneys, stimulating Naþ
reabsorption in exchange for Hþ ions, thus leading to bicarbonate
reabsorption and metabolic alkalosis. If metabolic alkalosis is
secondary to excessive mineralocorticoid activity or potassium
depletion, the urine chloride is more than20 mEq/litre, and is
resistant to sodium chloride treatment.
Respiratory acidosis
This occurs due to inadequate pulmonary excretion of
CO2 leading to increases in pCO2 and H2CO3, with a resulting
rise in Hþ ions. This occurs both acutely and in a chronic
form, in conditions affecting the respiratory or neurological
systems (Table 1). The rise in pCO2 is initially buffered by
PAEDIATRICS AND CHILD HEALTH 22:4
non-bicarbonate buffers, protein & phosphate. If the rise is
sustained, as in preterm babies with chronic lung disease, the
kidneys are stimulated to excrete Hþ ions and to generate &
reabsorb bicarbonate. This causes plasma bicarbonate levels to
increase above normal and the pH returns to normal. This is
the compensated phase of respiratory acidosis and occurs over
days.
Respiratory alkalosis
This occurs with excessive pulmonary losses of CO2 and result-
ing fall in pCO2. This occurs with hyperventilation due to any
cause (Table 1). It is often iatrogenic, related to mechanical
ventilation. A rapid decrease in pCO2 has been associated with
periventricular leukomalacia and intraventricular haemorrhage,
so timely intervention is critical.
With decreased pCO2, pH rises and a rapid buffering occurs
with release of Hþ ions to decrease the plasma bicarbonate.
There is also increased renal excretion of HCO3. This results
in a decrease in plasma bicarbonate and pH normalizes. Final
correction is achieved by treatment of the underlying
disorder.
Mixed disorders
In certain conditions, more than one disturbance can co-exist.
This should be suspected if the compensatory response falls
outside the expected range. For example, in respiratory
distress syndrome or pneumonia with sepsis, respiratory
acidosis (due to ventilatory failure) and metabolic acidosis
(due to lactic acidosis) often co-exist. The respiratory disease
prevents the compensatory fall of pCO2 and the metabolic
component prevents compensatory rise of plasma bicar-
bonate, resulting in a greater fall in pH. Similarly in chronic
lung disease with the use of loop diuretics, respiratory
acidosis and metabolic alkalosis can result. Thus the plasma
bicarbonate and pH are higher than expected. Patients with
hepatic failure can have metabolic acidosis and respiratory
alkalosis, with a greater than usual drop in plasma bicar-
bonate & pCO2 and little change in pH.
Implications of acidebase disorders
The effects of pH changes at a cellular level are poorly
understood. A low pH can reduce myocardial contractility and
impair catecholamine action, increasing the risk of
arrhythmia. The metabolic activity of proteins is pH depen-
dent and any changes may adversely affect enzyme activity.
An increase in Hþ ions can also cause disturbances in ion
transport within the kidneys. With acidosis, a decrease in
carbohydrate tolerance is observed and with alkalosis, an
increase in neuro-muscular irritability can occur, either in
a latent form or manifesting as tetany.
Invasive & non-invasive blood gas analysis in the neonatal unit
Blood gas analysis is routinely performed in the neonatal unit.
In conjunction with non-invasive monitoring, it enables
clinicians to appropriately assess & monitor the respiratory
status and modify ventilation strategy accordingly. It can also
provide information on metabolic status, acidebase
146 Ó 2011 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: NEONATOLOGY

imbalance and whether any respiratory or renal compensation

is taking place. Guide for blood gas values in neonates
Blood gas values vary depending on the site of the sample,
Analyte Normal reference ranges
i.e., arterial, capillary or venous; arterial samples are the most
(arterial sample)
informative. The technique of sampling is equally important; the
sample site should be warm if capillary, the sample itself should
pH 7.30e7.45
be free flowing, un-diluted with no air bubbles and processed in
PaCO2 (kPa) 4.5e6.0
a timely manner (less than 15 min). Arterial gases provide
PaO2 (kPa) 6.0e8.0
information about pulmonary gas exchange, while central
HCO3 (mmol/l) 19e24
venous samples give information regarding the acidebase status
BE (mmol/l) 3 to þ3
of tissues in conditions of severe hypoperfusion. If the sample is
taken from an arterial line running heparinized saline solution, Table 2
there is a risk of dilution with erroneously low pCO2 and bicar-
bonate values. Central venous pH is lower than arterial pH by
approximately 0.03 units and venous pCO2 is higher by 0.8 kPa.
any specific medical condition can vary with clinical practice, for
These differences increase in hypoventilation and circulatory
example with approaches such as “permissive hypercarbia” or
failure, with a pH difference up to 0.1 units and pCO2 difference
“gentle ventilation”. Understanding that pH is maintained by the
of up to 3.2 kPa.
ratio of HCO3/pCO2, a patients’ acidebase status can be readily
Capillary blood samples are commonly used in the neonatal
ascertained from a blood gas.
unit for blood gas estimation. The capillary values for pH and
The following steps can be used as a guide for blood gas
pCO2 are usually within 1 kPa of the corresponding arterial
interpretation (see Table 1):
values. However, they have their limitations and are less reli-
1. Is there acidaemia or alkalaemia, i.e., pH less than 7.30 or pH
able for babies with hypotension, poor perfusion or cold
more than 7.45?
peripheries. Capillary blood samples also cannot reliably
2. Is it primarily metabolic, i.e., HCO3 less than 19 or more
monitor oxygenation status or predict the degree of hypo-
than 24 mmol/litre & BE less than 3 or more than þ3? OR
xaemia. In these settings, an arterial blood gas is more useful,
Is it primarily respiratory, i.e., pCO2 less than 4.5 or more
although invasive.
than 6 kPa?
Non-invasive monitoring using pulse oximetry to monitor
3. Is there any compensation?
oxygen saturation in blood (SpO2) and transcutaneous moni-
4. Is there a mixed disorder present, i.e., values outside the
toring are useful adjuncts to blood gas measurements. Pulse
normal compensation?
oximeters work on the principle that oxygenated and deoxy-
Blood gases should always be interpreted in conjunction with
genated haemoglobin absorb different wavelengths of light. The
information from a detailed history and thorough clinical
oximeter provides a measure of the oxygen saturation of pulsatile
examination, the type of sample and non-invasive monitoring.
arterial blood compared with that from non-pulsatile venous
The prudent use of blood gas analysis in conjunction with
blood. It can be unreliable in hypoperfusion or with movement
continuous monitoring allows optimal assessment of the patient
artefacts. Transcutaneous electrodes measure oxygen (TcPO2)
and prompt intervention when required, the response to which
and CO2 pressures (TcPCO2). They rely on diffusion from vaso-
can then be monitored and the blood gas repeated after an
dilated vessels in heated skin, so are particularly useful in the
appropriate time period to ensure clinical improvement.
newborn period when the skin is thin, but can be unreliable in
Management should always be directed at the underlying cause
hypoperfusion. Transcutaneous levels usually match arterial
and an understanding of the processes involved in acidebase
blood levels closely, thus careful application can be used to
monitor trends and may allow the frequency of blood gas
balance aids this interpretation. A
sampling to be reduced. Continuous end tidal CO2 monitors can
also be useful for monitoring CO2 levels in infants with stable
ventilation. FURTHER READING
1 Greenbaum Larry A. Chapter 52.7. Acidebase balance. In:
Kleigman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson text-
Clinical interpretation of blood gases
book of paediatrics. 18th Edn. WB Saunders, 2007.
Blood gas analyzers measure pH, pCO2, PO2 and HCO3 (Table 2 Quigley R, Baum M. Neonatal acid base balance and disturbances.
2). They measure ‘actual’ HCO3 in the blood sample from Semin Perinatol 2004 Apr; 28: 97e102.
which they calculate ‘actual’ BE. Normally all the bicarbonate in 3 Adelman RD, Solhaug MJ. Chapter 52. Hydrogen ion. In: Behrman RE,
blood is produced by the ‘metabolic’ system, i.e., liver and Kleigman RM, Jenson HB, eds. Nelson textbook of paediatrics. 16th
kidneys. However hypercapnia increases H2CO3 dissociation into Edn. WB Saunders, 2000.
bicarbonate. ‘Standardised’ figures therefore calculate bicar- 4 Modi N. Chapter 39. In: Rennie JM, Roberton NRC, eds. Textbook of
bonate derived from CO2 and subtract this from the actual neonatology. 3rd Edn. Churchill Livingstone, 1999.
measurements to reflect metabolic function. Thus in patients 5 Cloherty JP, Eichen EC, Stark AR, eds. Manual of neonatal care.
with respiratory problems, it is advisable to use the ‘standard- 6th Edn. Lippincott Williams & Wilkins, 2008.
ized’ HCO3 and BE. Normal ranges vary slightly with gestation 6 Woodrow P. Essential principles: blood gas analysis. Nurs Crit Care
& postnatal age and the desired values of these parameters for 2010 MayeJun; 15: 152e6.

PAEDIATRICS AND CHILD HEALTH 22:4 147 Ó 2011 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: NEONATOLOGY
7 Lorenz JM, Kleinman LI, Markarian K, Oliver M, Fernandez J.
Serum anion gap in the differential diagnosis of metabolic
acidosis in critically ill newborns. J Pediatr 1999 Dec; 135:
751e5.
8 Brouilette RT, Waxman DH. Evaluation of the newborn’s blood gas
status. Clin Chem 1997 Jan; 43: 215e21.
9 Edwards SL. Pathophysiology of acid base balance: the theory practice
relationship. Intensive Crit Care Nurs 2008; 24: 28e40.
10 Williams AJ. ABC of oxygen: assessing and interpreting
arterial blood gases and acidebase balance. BMJ 1998 Oct 31;
317: 1213e6.
11 Foxall F. Arterial blood gas analysis: an easy learning guide. 1st Edn.
London: M&K Update Ltd, 2008.
12 Hennessey IAM, Japp AG. Arterial blood gases made easy. 1st Edn.
Edinburgh: Churchill Livingstone, 2007.
PAEDIATRICS AND CHILD HEALTH 22:4
Practice points
C A stable pH is essential for optimal cellular metabolism and
can be challenging in the newborn period
C Acidebase balance is regulated by buffers, the respiratory &
renal systems
C When the compensatory response falls outside the expected
value, a mixed acidebase disorder is likely
C Blood gases can be used to monitor acidebase balance
C Blood gases should always be interpreted in conjunction with
information from the clinical history & examination and non-
invasive monitoring
148 Ó 2011 Elsevier Ltd. All rights reserved.