understanding blood gases/acid–base balance

SYMPOSIUM: NEONATOLOGY

Understanding blood gases/acidebase balanceNitin Goel

Jennifer Calvert

AbstractAcidebase 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 22:4 142

An acid (HA) is a substance that donates Hþ ions (e.g. carbonic

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 þA�

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.

pH¼ pKþ 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 þHCO�3 4H2CO34CO2 þH2O

The pK for this buffer is 6.1. For bicarbonate buffer, the

HendersoneHasselbalch equation is:

pH¼ 6:1þ 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

� 2011 Elsevier Ltd. All rights reserved.

http://dx.doi.org/10.1016/j.paed.2011.09.005


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.

H2PO1�4 4Hþ þHPO2�

4

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:


(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.




Disturbances of acidebase balance

Abnormalities in blood pH, due to an increase in Hþ 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.

pH < 7.

pH > 7.

CO + H O ↔ H CO

↑PCO

↓PCO

Respiratory acidosis

Respiratory compensation

Hyperventilation

↓PCO

Hypoventilation

↑PCO

Respiratory alkalosis

Figure 1 Acidebase regulation: interplay of bicarbon


Systemic acidosis stimulates the respiratory centre directly,

the rate of breathing is increased and CO2 is excreted. The

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.

35

45

↔ H+ + HCO –

↓HCO –

↑HCO –

Metabolic compensation

↑Bicarbonate

reabsorption

↑HCO –

↓Bicarbonate

reabsorption

↓HCO –

Metabolic acidosis

Metabolic alkalosis

ate buffer, respiratory and renal systems.



Acidebase disorders, blood gas findings and common causes in neonates

Disorder Blood gas analysis (normal range) Causes

pH

(7.30e7.45)

pCO2

(4.5e6 kPa)

HCO3L

(19e24 mmol/l)

BE

(L3 to D3)

Metabolic acidosis

Uncompensated Y Normal Y Y Increased anion gap (more than 16 mEq/l)

Hypoxaemia/lactic acidosis: sepsis, shock, respiratory or cardiac disorders, anaemia, intraventricular haemorrhage,

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

Compensated Low Y Y Y

Normal

Metabolic alkalosis

Uncompensated [ Normal [ [ Decreased urinary chloride (<10 mEq/l)

Gastric losses: vomiting, pyloric stenosis, excess naso-gastric aspirates

Diuretics

Chloride losing diarrhoea

Hypokalaemia

Increased urinary chloride (>20 mEq/l)

Hyperaldosteronism

Adrenal hyperplasia

Excess alkali administration

Compensated High [ [ [

Normal


Uncompensated Y [ Normal Normal Respiratory abnormalities: respiratory distress syndrome, chronic lung disease, pneumothorax, meconium aspi-

ration, transient tachypnoea of newborn, pneumonia, pulmonary hypoplasia, congenital lung malformations

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

Upper airway obstruction: Pierre-Robin sequence, choanal atresia, laryngeal oedema/spasm/mass etc.

Iatrogenic: inadequate ventilator settings in mechanically ventilated patient

Compensated Low [ [ [

Normal


Uncompensated [ Y Normal Normal Increased sensitivity of respiratory centre: hypoxia due to any cause

Medications: Caffeine

Extra pulmonary CO2 losses: ECMO, dialysis

Iatrogenic: over-ventilation of mechanically ventilated patient

Compensated High Y Y Y

Normal

Table 1

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Normalplasma

UC

UC, unmeasured cations; UA, unmeasured anions.

The anion gap

UA

HCO

Na

UCUA

UC

UA

Cl

HCO

Cl

NaHCO

Cl

Na

Acidosis(no gap)

Acidosis(increased gap)

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.


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


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.


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



Guide for blood gas values in neonates

Analyte Normal reference ranges

(arterial sample)

pH 7.30e7.45

PaCO2 (kPa) 4.5e6.0

PaO2 (kPa) 6.0e8.0

HCO3� (mmol/l) 19e24

BE (mmol/l) �3 to þ3

Table 2


imbalance and whether any respiratory or renal compensation

is taking place.

Blood gas values vary depending on the site of the sample,

i.e., arterial, capillary or venous; arterial samples are the most

informative. The technique of sampling is equally important; the

sample site should be warm if capillary, the sample itself should

be free flowing, un-diluted with no air bubbles and processed in

a timely manner (less than 15 min). Arterial gases provide

information about pulmonary gas exchange, while central

venous samples give information regarding the acidebase status

of tissues in conditions of severe hypoperfusion. If the sample is

taken from an arterial line running heparinized saline solution,

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.

These differences increase in hypoventilation and circulatory

failure, with a pH difference up to 0.1 units and pCO2 difference

of up to 3.2 kPa.

Capillary blood samples are commonly used in the neonatal

unit for blood gas estimation. The capillary values for pH and

pCO2 are usually within 1 kPa of the corresponding arterial

values. However, they have their limitations and are less reli-

able for babies with hypotension, poor perfusion or cold

peripheries. Capillary blood samples also cannot reliably

monitor oxygenation status or predict the degree of hypo-

xaemia. In these settings, an arterial blood gas is more useful,

although invasive.

Non-invasive monitoring using pulse oximetry to monitor

oxygen saturation in blood (SpO2) and transcutaneous moni-

toring are useful adjuncts to blood gas measurements. Pulse

oximeters work on the principle that oxygenated and deoxy-

genated haemoglobin absorb different wavelengths of light. The

oximeter provides a measure of the oxygen saturation of pulsatile

arterial blood compared with that from non-pulsatile venous

blood. It can be unreliable in hypoperfusion or with movement

artefacts. Transcutaneous electrodes measure oxygen (TcPO2)

and CO2 pressures (TcPCO2). They rely on diffusion from vaso-

dilated vessels in heated skin, so are particularly useful in the

newborn period when the skin is thin, but can be unreliable in

hypoperfusion. Transcutaneous levels usually match arterial

blood levels closely, thus careful application can be used to

monitor trends and may allow the frequency of blood gas

sampling to be reduced. Continuous end tidal CO2 monitors can

also be useful for monitoring CO2 levels in infants with stable

ventilation.

Clinical interpretation of blood gases

Blood gas analyzers measure pH, pCO2, PO2 and HCO3� (Table

2). They measure ‘actual’ HCO3� in the blood sample from

which they calculate ‘actual’ BE. Normally all the bicarbonate in

blood is produced by the ‘metabolic’ system, i.e., liver and

kidneys. However hypercapnia increases H2CO3 dissociation into

bicarbonate. ‘Standardised’ figures therefore calculate bicar-

bonate derived from CO2 and subtract this from the actual

measurements to reflect metabolic function. Thus in patients

with respiratory problems, it is advisable to use the ‘standard-

ized’ HCO3� and BE. Normal ranges vary slightly with gestation

& postnatal age and the desired values of these parameters for


any specific medical condition can vary with clinical practice, for

example with approaches such as “permissive hypercarbia” or

“gentle ventilation”. Understanding that pH is maintained by the

ratio of HCO3�/pCO2, a patients’ acidebase status can be readily

ascertained from a blood gas.

The following steps can be used as a guide for blood gas

interpretation (see Table 1):

1. Is there acidaemia or alkalaemia, i.e., pH less than 7.30 or pH

more than 7.45?

2. Is it primarily metabolic, i.e., HCO3� less than 19 or more

than 24 mmol/litre & BE less than �3 or more than þ3? OR

Is it primarily respiratory, i.e., pCO2 less than 4.5 or more

than 6 kPa?

3. Is there any compensation?

4. Is there a mixed disorder present, i.e., values outside the

normal compensation?

Blood gases should always be interpreted in conjunction with

information from a detailed history and thorough clinical

examination, the type of sample and non-invasive monitoring.

The prudent use of blood gas analysis in conjunction with

continuous monitoring allows optimal assessment of the patient

and prompt intervention when required, the response to which

can then be monitored and the blood gas repeated after an

appropriate time period to ensure clinical improvement.

Management should always be directed at the underlying cause

and an understanding of the processes involved in acidebase

balance aids this interpretation. A

FURTHER READING

1 Greenbaum Larry A. Chapter 52.7. Acidebase balance. In:

Kleigman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson text-

book of paediatrics. 18th Edn. WB Saunders, 2007.

2 Quigley R, Baum M. Neonatal acid base balance and disturbances.

Semin Perinatol 2004 Apr; 28: 97e102.

3 Adelman RD, Solhaug MJ. Chapter 52. Hydrogen ion. In: Behrman RE,

Kleigman RM, Jenson HB, eds. Nelson textbook of paediatrics. 16th

Edn. WB Saunders, 2000.

4 Modi N. Chapter 39. In: Rennie JM, Roberton NRC, eds. Textbook of

neonatology. 3rd Edn. Churchill Livingstone, 1999.

5 Cloherty JP, Eichen EC, Stark AR, eds. Manual of neonatal care.

6th Edn. Lippincott Williams & Wilkins, 2008.

6 Woodrow P. Essential principles: blood gas analysis. Nurs Crit Care

2010 MayeJun; 15: 152e6.



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


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 22:4 148 � 2011 Elsevier Ltd. All rights reserved.


understanding blood gases/acid–base balance

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