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Indian Pediatrics 2001; 38: 1116-1128

Arterial Blood Gas Analysis in Clinical Practice

D. Vijaya Sekaran, L. Subramanyam, A. Balachandran

From the Institute of Child Health and Hospital for Children, Egmore, Chennai 600 008, India
and Kanchi Kamakoti Child Trust Hospital, Nungambakkam, Chennai 600 034, India.
Correspondence to: Dr. D. Vijaya Sekaran, No. 110/3, New Street, Mannady, Chennai 600
001, India.

Knowledge of arterial blood gas analysis (ABG) is important for every physician who is interested in treating
critically ill patients. Many serious acid-base disturbances can co-exist without significant clinical manifesta-
tions. In children with acute disorders of respiratory system, circulatory system, gastrointestinal system and
renal system, underlying acid-base disturbances are inevitable. These should be identified at the earliest
and attempts made to maintain normal homeostasis till the organ function recovers.

Arterial blood gas analysis reveals oxygenation status, adequacy of ventilation and acid-base balance. It
plays a significant role in documenting and monitoring respi-ratory failure, especially during ventilator and
oxygen therapy.

Normal Metabolism and its Dysfunction

Cellular function is ultimately dependent on regular supply of glucose, oxygen and water. Consequently,
volatile acids like carbonic acid (from tissue oxidation) and fixed acids like sulphuric acid, phosphoric acid,
lactic acid, keto acid (products of intermediary metabolism) are constantly poured into the general
circulation. Respi-ratory system plays an important role in eliminating volatile acids while renal mecha-nisms
eliminate fixed acids in the form of hydrogen ions. In pathological states, this homeostasis gets disturbed
causing accu-mulation of the above acids and resulting in acid-base disturbance. Though renal and
respiratory system take the brunt to mitigate the acid-base disturbance, the other important mechanism for
immediate rescue is the buffer base system which includes intra cellular and extra cellular buffers(1).

Clinical Significance of ABG

If the acid base disturbances are mild, the pH variation is also within adjustable limits (7.3 - 7.5) and the
clinical manifestations are not overt. In severe acidosis when pH falls below 7.20 (H+ ion concentration >63
nEq/L), grave features like poor myocardial performance, arrhythmias, hypotension, pulmonary edema and
hyperkalemia occur. Similarly in severe alkalosis when the pH exceeds 7.5 (H+ ion concentration <28 nEq/L)
features like mental confusion, muscular irritability, seizures, arrhythmias, generalized tissue hypoxia and
hypokalemia occur(1). Identification of these clinical features is difficult in a sick child presenting pre-
dominantly with the features of primary disease. Before discussing ABG inter-pretation, a pertinent review of
the normal body homeostasis would be useful.

Hydrogen Ion Homoeostasis

Normal hydrogen ion concentration in our body is 40 nEq/l 000 (0.000 000000 40) and the acceptable range
is 36-44 nEq/L. Deviation from this range may impair vital organ functions. Excessive accumulation of
hydrogen ions (occurs in pathological condi-tions like shock, asphyxia, and keto-acidosis) has to be
eliminated immediately to prevent organ damage. Body buffer and the respi-ratory system mitigate the
harmful effects immediately (within hours) and the renal compensation plays a major role to normalize the
disturbance though it is a delayed process. Water plays an important role by transporting hydrogen ions in
non-toxic form. Carbonic anyhydrase converts excess of hydrogen ions to carbon dioxide by its unique
action and eliminates the same through the lungs. Similarly, the excessive accumulation of CO2 (occurs in
ventilatory failure) is removed by kidney as hydrogen ion.

Hydrogen Ion Concentration and Carbon-dioxide

When organic compounds are oxidized during intermediary metabolism, the released CO2 is constantly
removed by alveolar ventilation. Normal PaCO2 value is 40 mm Hg (5.3K Pa) and the acceptable range is
36-44 mm Hg. When PaCO2 is above the normal value (>44 mm Hg) respiratory acidemia results which is
designated as ventilatory failure and a decrease of PCO2 (<36 mm Hg) results in respiratory alkalosis.
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PaCO2 is a sensitive index of alveolar ventilation to which it is inversely related and is controlled by
chemoreceptors in the hypothalamus. Ninety five per cent of CO2 produced is transported by the RBC and
5% by plasma in which 99.9% is present as physically dissolved (dCO2) and 0.1% as chemically dissolved
(carbonic acid). The pressure exerted by the dCO2 is measured as PaCO2. So the total CO2 (TCO2 )
includes dCO2 and H2CO3. In respiratory disturbances, PaCO2 is not affected initially as the diffusion
capacity of CO2 is 20 times more than that of oxygen. For every 20 mm of Hg increase of PaCO2, pH falls
by 0.1 unit and for every 10 mm of Hg fall of PaCO2, pH increases by 0.1. Thus the value of pH also
depends upon CO2 level(2).

Hydrogen Ion Concentration and Bicarbonate

At normal H+ ion concentration of 40 nEq/L (pH 7.4), HCO3– level is 24 mEq/L and the normal range is 22-
26. When HCO3– level falls below 22 mEq/L (in conditions like acute watery diarrhea, renal tubular acidosis,
addition of lactic acid and ketoacids) metabolic acidosis results. When the HCO3– levels exceeds 26 mEq/L
(in conditions like persistent vomiting, increased renin-angio-tensin activity, loop diuretics) it is termed as
metabolic alkalosis. Kidney regulates HCO3– homeostasis by reabsorbing or regenerating HCO3– of which
the latter mechanism is the desired one to correct metabolic problems(3).

Hydrogen Ion Concentration and pH

Since the amount of H+ in our body is too small to express easily, the pH notation was put forward by
Henderson. pH is the negative logarithm of hydrogen ion concentration which gives more meaningful
numbers for easy understanding. pH denotes either acidity or alkalinity and it has no units. Lower the pH,
higher the hydrogen ion concentration and vice versa. Normal pH is 7.4 which is equivalent to H+
concentration of 40 nEq/L and permissible range is 7.36-7.44.

Relationship of pH with CO2 and Bicarbonate

The pH of our body ultimately depends upon the levels of PaCO2 and HCO3 derived by Henderson-
Hasselbalch equation as follows(4):

pH = HCO3/PaCO2 = Rental compensation / Pulmonary compensation

Looking at the equation, it is the ratio of PCO2 to HCO3 that really decides the pH (hydrogen ion
concentration) more than the absolute value.

Acid-Base Disorders

Disturbance of the relationship of HCO3– with H2CO3 results in four (simple) acid-base disorders namely
metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis (Table I).

In simple disorders both PCO2 and HCO3– change in the same direction. Among the four simple disorders
metabolic acidosis is common. In some clinical conditions, these simple disorders may co-exist resulting in a
mixed disorder, when both PCO2 and HCO3– are either reduced or increased resulting in near normal pH,
though the clinical situa- tion is actually ominous. (for example, coexistence of metabolic acidosis with
respiratory alkalosis in salicylate poisoning). Metabolic alkalosis is the most important one to be managed
judiciously as a rise of pH above 7.5 may cause arrhythmias.

Primary Distrubance pH HCO3– PCO2

Metabolic Acidoses
Acute ¯ ¯ N
Partially compensated ¯ ¯ ¯
Fully compensated N ¯ ¯
Respiratory Acidosis
Acute ¯ N
Partially compensated ¯ ­
Fully compensated N ­
Respiratory Alkalosis
Acute ­ N ¯
Partially compensated ­ ¯ ¯
Fully compensated N ¯ ¯
Metabolic Alkalosis

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Acute ­ ­ N
Partially compensated ­ ­
Fully compensated N ­

Buffers and Physiological Compensation

The ultimate aim of the body is to maintain the pH within near normal limits. Chemical buffers and
physiological compensation work together to achieve this. Chemical buffers are built in stabilizers that
mitigate the sudden changes of body pH and include extra-cellular and intra-cellular buffers. Extracellular
buffers are the first line defense (act within minutes) and include bicarbonate and serum proteins.
Intracellular buffers act at a slower rate (within hours) and include intra-cellular proteins, phosphates and
hemoglobin(4). When chemical buffer-ing is not enough, physiological compensa-tion starts.

When HCO3– loss occurs from the body (primary event) the respiratory system comes to rescue by
eliminating CO2 (compensatory) from the body quickly (12-24 h) till the pH approaches normal value along
with body buffers. Similarly, when CO2 accumulates in the body (primary event), kidneys retain HCO3–
(compensatory) and along with buffers normalize the pH in 3 to 5 days. Thus depending upon the stage of
compensa-tion, the given acid base disorder may be either acute (uncompensated), subacute (partially
compensated) or chronic (fully compensated).

So the clinical picture of acid base disturbances may show either one of three stages (Table I): (a) Acute
stage (where either HCO3– or PaCO2 is altered with altered pH); (b) Partially compensated stage (where
both HCO3– and PaCO2 are altered with altered pH); and (c) Fully compensated (where both HCO3– and
PaCO2 are altered with near normal pH).

Metabolic Acidosis

It is commonest acid base disorder which results due to loss of HCO3 from the body (gastro-intestinal tract
or kidney) or due to addition of acids (lactic acid, keto acids) or due to administration of fluid devoid of
bicarbonate (total parenteral nutrition, massive transfusion). Many acute pediatric problems may result in
metabolic acidosis and their individual management differs. Effective management of metabolic acidosis
needs anion gap calculation(5). Anion gap helps to categorize metabolic acidosis into two broad groups, i.e.,
metabolic acidosis with increased anion gap and metabolic acidosis with normal anion gap (Table II).

Table II - Metabolic Acidosis

Increased anion gap (Normochloremic
Normal anion gap (Hyperchloremic acidosis)
acidosis)
Lactic acidosis Diarrhea
Shock Rental tubular acidosis
Asphyxia Uretero sigmoidostomy
Cyanide Poisoning Parenteral alimentation
Salicylate poisoning Rapid ECF expansion
Paraldehyde poisoning Exogenous chlorides
Biguanides poisoning CaCl2, MgCl2, NH4Cl
Organic acidemias Cholestyramine
Inborn errors of carbohydrate and Carbolic anhydrase inhibitors
pyruvate metabolism Small bowel/biliary fistula
Ketoacids
Diabetes mellitus
Starvation

Sulphuric/phosphoric acids
Renal failure

Anion Gap

According to electrochemical law, equal number of anions balance equal number of cations giving electrical
neutrality. A small amount of anion that cannot be measured by biochemical investigations is named as
anion gap:
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(Na+ + K+) = (Cl– + HCO3–) +

(Unmeasured anions) (Anion gap)

(135 + 04) = (100 + 24) + 8 to 16

In some type of metabolic acidosis, addition of acids results in fall of HCO3 . In this condition to maintain the
anionic charge, unmeasured anions increase without any alterations of chloride level, known as metabolic
acidosis with increased anion gap also known as "normochloremic acidosis". In metabolic acidosis with
normal anion gap, basic pathology is loss of bicarbonate ions where chloride level is increased, this is
designated as "hyperchloremic acidosis" (Table II).

Since the management of each type of metabolic acidosis grossly differs, anion gap calculation may be
useful apart from the detailed clinical history and evaluation. These children should be subjected to
investigations like serum electrolytes, urea, creatinine, sugar, ketone bodies, etc.

If increased anion gap acidosis (normochloremic acidosis) is evident, the etiology should be identified and
corrected, where administration of HCO3– may be hazardous. In children with normal anion gap acidosis
(hyperchloremic acidosis) bicarbo-nate correction should be done judiciously.

Since acidosis is beneficial to the body homeostasis, correction should be attempted only when HCO3–
goes below 15 mEq/L (pH 7.2 or base deficit reaches 10 mmol/L). Overzealous correction of acidosis with
HCO3 (hypertonic solution) leads to many adverse effects like shifting of the oxygen-hemoglobin
dissociation curve to the left resulting in poor release of O2 at tissue level, precipitation of hypokalemia,
intraventricular hemorrhage, hypernatremia and hypocal-cemic tetany. So the correction of acidosis is
advised only when HCO3– falls below 15 mEq/L.

(15 – measured HCO3–) × 0.6 × Body weight (in kg)

Half of the HCO3– correction can be done immediately by slow intravenous administra-tion after diluting with
5% dextrose, the rest can be added in the maintenance fluid over 24 hours.

Metabolic Alkalosis

Metabolic alkalosis results due to loss of acids (H+ ions) from the gastrointestinal tract, through renal
mechanisms, due to alkali gain or due to disproportionate loss of extracellular fluid. (Table III).

Table III - Metablic Alkalosis - Causes

Acid loss Alkali gain ECF loss Cl >HCO3–
(a)GIT loss
–Vomiting Rapid HCO3– correction Cystic Fibrosis
–Nasogastric tube aspiration Massive transfusion (citrate) Massive diuresis
(b)Mineralocorticoid activity Hyperalimentation (acetate)
–Cushing’s syndrome

–Hyperaldosteronism Antacids-excessive

–Bartter’s syndrome

–Liquorice carbenoxolone

In metabolic alkalosis the child may present with shallow respiration (hypo-ventilation) in an attempt to
conserve CO2 . However the compensation cannot extend beyond physiological limits (PaCO2 may not rise
above 55 mm of Hg). When the alkalosis increases, altered sensorium, muscle cramps, dysarrhythmias and
features of tetany due to low ionized calcium and acetyl choline release, may occur.

Many children with metabolic alkalosis may present with volume loss and or associated hypokalemia. The
correction of these derangements will automatically restore functional derangements. When glomerular
filtration rate (GFR) is maintained with adequate ECF volume, the normally functioning kidney will eliminate
excessive HCO3– (alkali loss), reduce the production of NH3 (acid gain) thereby normalizing the basic
pathology. Contrary to this, if ECF volume is not adequately maintained, low GFR results in HCO3– retention
(alkali gain) and increased aldosterone production resulting in further loss of H+ ion (acid loss) in exchange
of Na+ at the distal convoluted tubule. However, in hypokalemic state, body loses H+ in exchange offer while
retaining sodium resulting in paradoxical aciduria. Thus, the presence of associated hypokalemia

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aggravates the basic pathology. The best way to manage metabolic alkalosis (saline responsive) is to
maintain adequate ECF volume and serum potassium.

Metabolic alkalosis resulting from in-creased aldosterone activity (saline resistant) will respond to
aldosterone antagonists (spironolactone), ACE inhibitors, or at times to amiloride and indomethacin.
Estimation of urinary chloride may help to differentiate saline responsive (urine chloride-level <10 mEq/L)
from saline resistant (urine chloride >10 mEq/L) type of metabolic alkalosis(6).

Respiratory Alkalosis

Mild respiratory disorders causes hypoxemia (oxygenation failure or Type I respiratory failure) resulting in
respiratory alkalosis as the hypoxic drive causes hyperventilation and wasting out of carbon-di-oxide. Other
than lung diseases, heart disease, sepsis, central nervous system infection, and hysterical overbreathing
may result in respiratory alkalosis (Table IV).

Children with respiratory alkalosis need prompt oxygen supplementation apart from correcting the basic
pathological condition. Oxygen is a drug, which should be used judiciously. Since the PaO2 of 60 mm of Hg
saturates 90% of the hemoglobin (SaO2) majority of children with mild lung condi-tions may not require
supplemental oxygen therapy. However, when PaO2 falls below 60 mm of Hg, SaO2 falls steeply hence
oxygen supplementation should be done imme-diately. Majority of the clinical situations can be managed
with nasal catheter or face mask alone with oxygen flow rate of 6-8 litres /minute. Respiratory alkalosis
induced by hysterical breathing is common in adolescent girls and is best managed by rebreathing in paper
bag.

Table IV - Respiratory Alkalosis - Causes

Pathological Physiological
Lung Disease Anxiety
Obstructive Fever
Restrictive Screaming
Embolus
CVS Iatrogenic
Cardic failure Hysterical
Liver cell failure Mechanical venti-lation
CNS Infection
Trauma, tumors
Sepsis
Hypothyroidism
Salicylate poisoning

Respiratory Acidosis

Ventilation is a process, which needs the co-ordinated activity of central nervous system and thoracic cage
(pump) and lungs. Advanced respiratory disease, thoracic cage and neuromuscular dysfunction leads to
carbon-di-oxide retention (PaCO2 >45 mm of Hg) resulting in respiratory acidosis also known as ventilatory
(Type II) failure (Table V).

In ventilatory failure CO2 should be eliminated from the body at the earliest, which can be done by
mechanical ventilatory support. Oxygen supplementation is essential, as oxygenation failure is invariably
present. When respiratory support is not feasible, bag and mask ventilation should be continued till
adequate ventilatory support is made available to eliminate CO2.

Table V - Respiratory Acidosis - Cause(7)

Respiratory Thoracic cage Neuromuscular
(a) Obstructive
Aspiration Flail chest Brain stem lesions
Croup Scoliosis Sedatives (Opium)
Foreign body Pick-wickian syndrome

Epiglottitis Poliomyelitis

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Asthma Guillain Barre syndrome

Bronchiolitis Myasthenia gravis

(b) Parenchymal Muscular dystrophy

Pneumonia Botulism

Respiratory distress
syndrome, Interstitial lung
disease Pulmonary edema

(c) Pleural

Pleural effusion

Pneumothorax

Base Excess/Deficit

In metabolic dysfunction the body buffers take an important role to normalize the pH. In metabolic acidosis,
the buffer base becomes negative which is referred to as "base deficit" or negative base excess. Buffer base
will remain unaffected in respiratory problem. Since there is a constant relationship between PaCO2 and pH
the respiratory pH can be predicted. By finding the difference between respiratory pH (predicted) and
measured pH (laboratory value), base excess and base deficit can be calculated. Though the calculation of
base excess and deficit is not mandatory in all the cases, such calculation is important in the management
of metabolic problems to quantify the contribution of the body buffer base system especially when
administration of HCO3– is desired.

Oxygen Homeostasis

The most important interpretation in ABG is to look for the adequacy of oxygenation status. The normal
partial pressure of O2 in the artrial blood (PaO2 ) is 80-100 mm of Hg in adults on breathing at atmospheric
oxygen (which contains 21% of oxygen = FiO2 21%). When fraction of the inspired O2 (FiO2) concentration
increases, the arterial PaO2 increases by five times (PaO2 = FiO2 × 5). When PaO2 falls below 80 mm of
Hg, hypoxemia results which can be classified as either mild (PaO2 of 60-80 mm), moderate (PaO2 of 40-60
mm) or severe (PaO2 <40 mm).

The tolerance of hypoxemia is better at extremes of ages. Thus in newborn baby, the normal PaO2 is 40-70
mm of Hg and in older age (> 60 years) PaO2 falls by 1 mm of Hg frm the lower limit of normal PaO2 (80
mm Hg) for every year increase of age (e.g., at 90 years of age, PaO2 of 60 mm Hg is normal). Arterial
oxygen tension (PaO2 ) depends upon atmospheric oxygen content and adequacy of ventilation.

Though PaO2 reflects oxygen level in arterial blood, the adequacy of tissue oxygenation ultimately decides
cellular metabolism. Reduction of oxygen at tissue level is called hypoxia. In addition to PaO2, other
parameters like hemoglobin content, circulatory efficiency and mitochondrial function (cytochrome oxidase)
decide ultimate delivery of oxygen to tissues. In ahypoxic child maintenance of the above parameters are
important to ensure normal aerobic metabolism.

Further, the delivery of oxygen at the tissue level is decided by the shift of Oxygen hemoglobin dissociation
curve. Shift to the right is advantageous to the body as the liberation of oxygen at the tissue level is more.
This occurs in acidosis, pyrexia, hypercarbia and increased DPG level.

Oxygen Tension and Oxygen Saturation (SaO2)

Though estimation of PaO2 through ABG is the best investigation to identify oxygena-tion status and acid
base disturbances, it requires arterial puncture every time. Since a constant relationship exists between
PaO2 and oxygen saturation of hemoglobin (PaO2 40 mm of Hg = SaO2 70%; PaO2 50 mm of Hg = SaO2
80%; PaO2 60 mm of Hg = SaO2 90%) real time monitoring of oxygen status by estimating SaO2 with pulse
oximetry is (a non-invasive technique) popularly practiced though it has its own limitations. By placing the
sensor in the arterial catheter, continuous arterial gas monitoring is possible(8). Pulse oxymetry is useful to
assess the oxygenation status in minor cardiopulmonary diseases and procedures; however, at higher
oxygen tension, poor perfusion status and in meth-haemoglobinemia, pulse oximetry fails.

Practical Workup of ABG

Memorizing the normal values of arterial blood gas analysis is an important pre-liminary exercise before
going for actual ABG interpretation (Table VI).

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ABG Specimen Collection

The radial artery at the wrist is the most preferred site of ABG specimen collection as it has adequate
collaterals where inadvertent puncture of veins is unlikely. When this is not feasible, popliteal, brachial or
femoral arteries can be chosen. The injection site is cleansed with iodine or alcohol. The index and middle
finger of the other hand can be used to palplate the artery. Heparinized syringe with 22 gauge needle should
be held like a pen with 45º angle (with beveled edge of the tip facing downwards) and the artery should be
punctured just 2 cm above the wrist crease.

ABG syringes are the most advantageous where the arterial blood gets filled on its own without any
application of suction force and ensure anaerobic collection. Presence of air bubbles may increase oxygen
values and lower CO2 values. If ordinary syringes are used, the nozzle should be stoppered immediately
and transported to the laboratory by placing on an ice slush or refrigerated to reduce metabolism of red
blood cells(9). Estimation should be done immediately otherwise values of oxygen and CO2 may be altered
due to cellular metabolism. Though 0.05 ml of heparin is enough for 1 ml of blood, upto 0.1 ml of heparin
may not interfere with blood gas values. Excess of heparin should be avoided as it may increase the acidity
because of its high hydrogen ion concentration. After arterial puncture, the site should be compressed tightly
for 3 to 5 minutes to prevent hematoma formation.

Table VI - ABG Symbols and Values

Term Symbol Normal value Range Unit
H+ H+ 40 36-44 nmol/L
pH pH 7.4 7.36-7.44 -
CO2 tension PaCO2 40 36-44 mm Hg
Base exces BE 0 –2 to +2 mmol/L
Total CO2 TCO2 25 23-27 mmol/L
Actual HCO3 HCO3 24 22-26 mmol/L
Standard HCO3 SBC 24 22-26 mmol/L
O2 saturation SaO2 98 95-100 %
O2 tension PaO2 95 80-100 mmHg

ABG Interpretation - Step by Step Approach(9)

I. pH: Acidosis/alkalosis
II. Respiratory/Metabolic
III. Stages of compensation
IV. Oxygenation status
V. Simple disorder/Mixed disorder
VI. Acute/chronic
VII. Laboratory error

Step I: pH - Acidosis/Alkalosis

By looking at the pH we will be able to differentiate normal pH from acidemia and alkalemia. Normal pH
ranges between 7.36 to 7.44; pH less than 7.36 denotes acidemia and above 7.44 alkalemia.

Step II: Respiratory/Metabolic

Acidemia would be either due to increase of PaCO2 or fall of HCO3–. Alkalemia would be either due to
decrease of PaCO2 or increase of HCO3–.

In respiratory acidosis kidney regenerates HCO3– and increase the HCO3– level as a compensatory
response in addition to hyper-ventilation. Similarly, in respiratory alkalosis loss of HCO3– occurs through
kidney as a compensatory event.

Metabolic acidosis is compensated by hyperventilation (Kussmaul’s breathing), when elimination of CO2

increases the pH to alkaline side. Metabolic alkalosis occurs when HCO3– level exceeds the normal limit,
which is compensated by hypoventilation to increase CO2 level.

Step III: Stages of Compensation

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During initial stage of acid-base disturbance there is no time for compensa-tion this phase is known as acute
or uncompensated stage where pH and one of the parameters PaCO2 or HCO3– is abnormal. To normalize
the pH, compensation occurs where body buffers come first (within minutes) followed by respiratory (within
hours) and renal system buffering (within days). The initial compensation is not complete and is known as
subacute or partially compensated stage where both the parameters (CO2 and HCO3–) change in the same
direction. In fully compensated stage (chronic state), pH becomes near normal with abnormally altered
PCO2 or HCO3–. Accord-ingly the ABG disorder may either be acute (uncompensated), subacute (partially
com-pensated) or chronic (fully compen-sated).

Step IV: Oxygenation Status

While assessing the oxygentation status, knowledge regarding age of child and the inspired oxygen
concentaration (FiO2) are very important. The normal value of PaO2 is 80-100 mm of Hg in children and
adults whereas in a normal newborn it ranges from 40-70 mm of Hg. In older age, the normal PaO2 comes
down from the adult level. In children with supplemental oxygen therapy the PaO2 will be high (PaO2 = FiO2
× 5).

Irrespective of the oxygen status, if the child is critically ill with cardiopulmonary problem, the child should be
benefited with 100% oxygen. It is advisable to keep the oxygen supplementation below 60% to avoid oxygen
toxicity (bronchopulmonary dysplasia, retrolental fibroplasia). Another important factor that should be borne
in mind is the hemoglobin status. Even if PaO2 and SaO2 is normal, where the hemoglobin is inadequate
the final delivery of O2 to the tissues will be compromised.

Step V: Simple or Mixed Disorder

In simple acid base disorder, both PaCO2 and HCO3– change in the same direction. If they do not follow
this trend, the possibility of mixed disorder is likely. The expected compensation for simple acid base
disorder is predetermined and if they deviate from the norms there is the possibility of mixed disorder. If the
difference between total carbon dioxide (TCO2) and HCO3– is more than 1.2 in addition to metabolic
problem, the underlying respiratory disturbance should be thought of. When both actual bicarbonate and
standard bicarbonate are not the same, in addition to respiratory added metabolic component should be
thought off. Gross deviation of buffer base reflects the under-lying metabolic problem.

Common problems leading on to mixed disturbance are acute severe asthma, shock, cardiopulmonary
arrest, respiratory distress syndrome in newborn, diarrhea with vomit-ing, decompensated liver disease,
diuretic therapy and salicylate poisoning (10).

Step VI: Acute or Chronic

By knowing the duration of illness, we can easily adjudge whether it is an acute or chronic problem. This
knowledge is important because the compensation that occurs during acute and chronic stage especially in
respiratory disorders grossly differs due to delayed renal compensation that occurs in addition to buffer base
adjustment (Table VII).

Step VII: Laboratory Error

According to the Henderson Hasselbach equation, out of the three measured values (pH, PaCO2, HCO3–) if
two are known, the third can be calculated provided the pH is presented as H+ ion concentration. If there is
discrepancy between the measured value and calculated values one should suspect laboratory error by
applying the following formula: H (nmol/L) = 24 ´ (PCO2 / HCO– ).

ABG Report and Management Guidelines

Application of ABG in day to day clinical practice on a sick child is the secret behind the proficiency of this
complex subject. Examples may illustrate. Let us work out the ABG status in following clinical situations
(Table VIII).

Table VII - ABG Disorder - Expected Compensation

Disorder
Metabolic acidosis (HCO3)
Metabolic alkalosis (HCO3)
Respiratory acidosis (PaCO2)
Acute
Chronic
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Compensation
For every 1 mEq/L fall in HCO3 PaCO2 should fall by
1 mm of Hg (1-1.5)
For every 1 mEq/L increase HCO3– aCO2 should
increase by 1 mm of Hg (0.5-1)
For every 1 mm ­PaCO2, HCO3 ­by 0.2 mEq
For every 1 mm ­PaCO2, HCO3 ­by 0.4 mEq
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Respiratory alkalosis (PaCO2)

Acute For every 1 mm ¯ PaCo2, HCO3 ¯ by 0.2 mEq
Chronic For every 1 mm ¯ PaCO2, HCO3 ¯ by 0.5 mEq
Table VIII- Some Illustrative Situations
(e)
(a) 9/M (b) 1/F (c) 8/12/F (d) 1.5/F
Age / Sex 3/365/M
Acute Severe Bulbar Severe
Respiratory
Clinical distress
asthma diarrhea polio-myelitis vomiting
picture syndrome
pH 7.6 7.24 7.20 7.44 7.12
PaCO2 30 35 60 55 30
HCO3– 24 9 20 36 8
PaO2 65 90 50 90 30
FiO2 21 21 40 21 60

(a) Uncompensated respiratory alkalosis with mild hypoxemia due to alveolor hyperventilation
(simple disorder): Hypoxic drive in acute asthma causes hyperventilation resulting in CO2
washout. Oxygen supplementation should be immediate either through nasal catheter or face
mask.

(b) Partly compensated metabolic acidosis without hypoxemia: Diarrheal dehydra-tion results
in loss of HCO3– in stools (simple disorder). Calculate the HCO3– deficiency (for 15 meq) and
half the same should be given as a slow intravenous bolus.

(c) Uncompensated respiratory acidosis with hypoxemia due to acute ventilatory failure
resulting in mounting of CO2 (simple disorder): This child needs immediate ventilatory support
and oxygen supple-mentation.

(d) Fully compensated metabolic alkalosis: Excessive vomiting results in loss of acid (H+) and
chloride ions with compensatory elevation HCO3– (simple disorder). This child needs
immediate replacement of extracellular volume and maintenance of normal serum potassium.

(e) Uncompensated metabolic acidosis with severe hypoxemia: The fall in PaCO2 is far less
than what is expected (for every 1 mEq/L ¯ HCO3–, PCO2 should fall by 1.2 mg Hg) which
means that there is an independent factor arising the PaCO2 which has to be a respiratory
acidosis. So this is a mixed ABG disorder with both metabolic and respiratory acidosis.

Contributors: All the authors were involved in conceptualising and drafting the manuscript. DVS will act as
the guarantor.
Funding: None
Competing interests: None declared.

Key Messages
Arterial blood gas analysis plays an important role in critically ill children with respiratory
distress.

Many life threatening metabolic or respiratory conditions co-exist making pH near normal
where the role of serial ABG estimation is indispensible.

In mixed disorders if the pH deviation occurs in the same direction, chances of life
threatening complications are imminent.

Knowledge of ABG is essential for any physician who handles a critically ill child.

References

1. Brewer ED. Disorder of acid base balance. Pediatr Clin North Am 1990; 37: 429-448.

2. Shapiro BA. Clinical application of blood gases. In: Pulmonary Artery Blood Gases, III edn.
Eds. Shapiro BA, Harvison RA, Watton JR, Chicago, Year Book Medical Publishers, 1982; pp
201-207.

https://www.indianpediatrics.net/oct2001/oct-1116-1128.htm 9/10
9/2/23, 11:15 AM Indian Pediatrics - Recommendations

3. Subramanyam L, Vijaya Sekaran D, Somu N. Interpretation of blood gas analysis. In:

Essentials of Pediatric Pulmonology, 2nd edn. Eds Somu N, Subramanyam L. M/s. Siva and
Co, 1996; pp 203-215.

4. Kachuny WD, Gabow PA. Pathgenesis and management of metabolic acidosis and
alkalosis. In: Renal and Electrolyte disorders, 3rd edn. Ed. Schrier RW. Boston, Little Brown,
1986; p141.

5. Di Nubile MJ. The increment in the anion gap: Overextension of a concept? Lancet 1988; 2:
951.

6. Isselbacher KA, Braunwald E, Wison JD, Martin JB Fauci AS, Kasper DL. Electrolyte, acid-
base balance. In: Harrisons Principles of Internal Medicine (Companion Handbook): New York,
Mc Graw-Hill Book Co. 1994; pp 83-95.

7. Hope RA, Longmore JM, Memanus SK, Wkkd-Allum CA. Respiratory failure. In: Oxford
Handbook of Clincial Medicine, 4th edn. Eds. Longmore JM, Mcmanus SK, World Alumn CA.
New York, Oxford University Press, 1988; p 352.

8. Weiss IK, Fink S, Edmunds S, Harrison R, Donnelly K. Continuous arterial gas monitor-ing
intensive care medicine 1996; 22: 1414-1417.

9. Aelow B. Arterial Blood Gases in Under-standing acid base. Baltimore Williams and
Williams, 1998; pp 239-252.

10. Subramanyam L. Thangavelu S. Arterial blood gas analysis. Pediatric Pulmonology

Update, 1999; 11: 7-15.

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