BLOOD GASES AND

ACIDBASE DISORDERS

Dr. Wan Nedra Sp. A

Pediatricts Departement
University of YARSI
 LEARNING OBJECTIVES
By the end of the session, the student will be
able to:
1. Identify the causes of acid base imbalance in
children.
2. Recognise the clinical manifestations that
may be seen in a child with acid base
imbalance.
3. Interpret blood gas analysis.
CAPILLARY BLOOD GASES:
pH: Same as arterial or slightly lower (Normal = 7.35-7.40)
pCO2: Same as arterial or slightly higher (Normal = 40-45)
pO2: Lower than arterial (Normal = 45-60)
O2 Saturation: >70% is acceptable.
 blood gas machines
The blood gas machines in most labs
actually measure the pH ,the pCO2 and the
pO2.
The [HCO3-] and the base difference are
calculated values using the Henderson-
Hasselbalch equation
 For a rough estimate of [H+]
[H+] = (7.80 -pH) x100.
This is accurate from a pH 7.25 to 7.48;
40 mEq/L = [H+] at the normal pH of 7.40.
pH is a log scale, and for every change of 0.3 in
pH from 7.40 the [H+] doubles or halves.
For pH 7.10 the [H+] = 2 x 40, or 80 nmol/L, and
for pH 7.70 the [H+] = 1/2 x40, or 20 nmol/L.
 pCO2 and pH
A change in pCO2 up or down 10 mm Hg is
associated with an increase or decrease in
pH of 0.08 units.
As the pCO2 decreases, the pH increases;
as the pCO2 increases, the pH decreases.
 base deficit and base excess
A pH change of 0.15 is equivalent to a base
change of 10 mEq/L.
A decrease in base (i.e, [HCO3-]) is termed
a base deficit, and an increase in base is
termed a base excess.
 Acidosis and alkalosis
Acid-base disorders are very common clinical
problems.
Acidemia is a pH <7.37, and
alkalemia is a pH >7.44.
Acidosis and alkalosis are used to describe how
the pH changes.
The primary causes of acid-base disturbances are
abnormalities in the respiratory system and in the
metabolic or renal system.
normal compensatory response
Any primary disturbance in acid-base homeostasis
invokes a normal compensatory response.
A primary metabolic disorder leads to respiratory
compensation, and a primary respiratory disorder
leads to an acute metabolic response due to the
buffering capacity of body fluids.
A more chronic compensation (1-2 days) due to
alterations in renal function.
 Mixed acid-base disorder
Most acid-base disorders result from a single primary disturbance
with the normal physiologic compensatory response and are called
simple acid-base disorders.

In certain cases, however, particularly in seriously ill patients, two

or more different primary disorders may occur simultaneously,
resulting in a mixed acid-base disorder.

The net effect of mixed disorders may be additive (eg, metabolic

acidosis and respiratory acidosis) and result in extreme alteration
of pH;

or they may be opposite (eg, metabolic acidosis and respiratory

alkalosis) and nullify each others effects on the pH.
INTERPRETATION OF BLOOD GASES

Step 1:
Determine if the numbers fit.
The right side of the equation should be within about
10% of the left side.
If the numbers do not fit, you need to obtain another
ABG
INTERPRETATION OF BLOOD GASES

Step 2:
determine if an acidemia (pH <7.37)
or an alkalemia (pH >7.44) is present.
 Step 3: Identify the primary disturbance as
metabolic or respiratory.

For example, if acidemia is present, is the pCO2 >44 mm Hg (respiratory

acidosis), or is the [HCO3 -] <22 mmol/L (metabolic acidosis).

In other words, identify which component, respiratory or metabolic, is

altered in the same direction as the pH abnormality.

If both components act in the same direction (eg, both respiratory [pCO2 >
44 mm Hg] and metabolic [HCO3 - <22 mmol/L] acidosis are present),
then this is a mixed acid-base problem.

The primary disturbance will be the one that varies from normal the
greatest, that is, with a [HCO3 -] = 6 mmol/L and pCO2 = 50 mm Hg, the
primary disturbance would be a metabolic acidosis, the [HCO3 -] is about
one-quarter normal, whereas the increase in pCO2 is only 25%.
 Step 4:

Calculate the anion gap.

Anion gap = Na+ - (Cl- + HCO3 -).
Normal anion gap is 8-12 mmol.
 Step 5:
If the anion gap is elevated
Then compare the changes from normal between the
anion gap and [HCO3 -].
If the change in the anion gap is greater than the
change in the [HCO3 -] from normal, then a metabolic
alkalosis is present in addition to a gap metabolic
acidosis.
If the change in the anion gap is less than the change in
the [HCO3 -] from normal, then a non gap metabolic
acidosis is present in addition to a gap metabolic
acidosis.
 METABOLIC ACIDOSIS: DIAGNOSIS AND
TREATMENT

Metabolic acidosis represents an increase in

acid in body fluids .
Reflected by a decrease in [HCO3 -] and a
compensatory decrease in pCO2.
 Anion Gap Acidosis:
Anion gap >12 mmol/L; caused by a
decrease in [HCO3 -]
balanced by an increase in an unmeasured
acid ion from either endogenous production
or exogenous ingestion (normochloremic
acidosis).
 Treatment of Metabolic Acidosis
1. Correct any underlying disorder (control diarrhea, etc).
2. Treatment with bicarbonate should be reserved for severe
metabolic gap acidosis.
If the pH <7.20, correct with sodium bicarbonate.
The total replacement dose of [HCO3 -] can be calculated as
follows:
3. Replace with one-half the total amount of bicarbonate over 8-
12 h and reevaluate.
Be aware of sodium and volume overload during replacement.
Normal or isotonic bicarbonate drip is made with 3 ampules
NaHCO3 (50 mmol NaHCO3/ampule) in 1 L D5W.
 METABOLIC ALKALOSIS:
Metabolic alkalosis represents an increase
in [HCO3 -] with a compensatory rise in
pCO2.
 Treatment of Metabolic Alkalosis

Correct the underlying disorder.

1. Chloride-responsive
a. Replace volume with NaCl if depleted.
b. Correct hypokalemia if present.
c. NH4Cl and HCl should be reserved for extreme
cases.
2. Chloride-resistant
a. Treat underlying problem, such as stopping
exogenous steroids.
 RESPIRATORY ACIDOSIS:
DIAGNOSIS AND TREATMENT

Respiratory acidosis is a primary rise in pCO2

with a compensatory rise in plasma [HCO3 -].
Increased pCO2 occurs in clinical situations in
which decreased alveolar ventilation occurs.
 Differential Diagnosis

1. Neuromuscular Abnormalities with Ventilatory Failure

2. Central Nervous System Drugs, Sedative,,Central sleep apnea
3. Airway Obstruction
a. Chronic (COPD)
b. Acute (asthma)
c. Upper airway obstruction
d. Obstructive sleep apnea
4. Thoracic/Pulmonary Disorders
a. Bony thoracic cage: Flail chest, kyphoscoliosis
b. Parenchymal lesions: Pneumothorax, pulmonary edema,
c. Large pleural effusions
d. Scleroderma
e. Marked obesity (Pickwickian syndrome)
Treatment of Respiratory Acidosis

Improve Ventilation:
Intubate patient and place on ventilator,
increase ventilator rate, reverse narcotic
sedation with naloxone (Narcan), etc
 RESPIRATORY ALKALOSIS:

Respiratory alkalosis is a primary fall in

pCO2 with a compensatory decrease in
plasma [HCO3 -].
Respiratory alkalosis occurs with increased
alveolar ventilation.
 Differential Diagnosis
1. Central stimulation
a. Anxiety, hyperventilation syndrome, pain
b. Head trauma or CVA with central neurogenic hyperventilation
c. Tumors
d. Salicylate overdose
e. Fever, early sepsis
2. Peripheral stimulation
a. PE
b. CHF (mild)
c. Interstitial lung disease
d. Pneumonia
e. Altitude
f. Hypoxemia:
3. Miscellaneous
a. Hepatic insufficiency
b. Pregnancy
c. Progesterone
d. Hyperthyroidism
e. Iatrogenic mechanical overventilation
 Treatment of Respiratory
Alkalosis

Correct the underlying disorder.

Hyperventilation Syndrome: Best treated
by having the patient rebreathe into a paper
bag to increase pCO2, decrease ventilator
rate
 LIVER
METABOLISM
PRODUCES H+
Protein buffers
H +
synthesised
BLOOD METABOLISM
BUFFERS
Protein, CO2 H+
Bicarbonate &
HCO3- Phosphate
H+
KIDNEYS
Excrete / reabsorb LUNGS
H+ / HCO3- Eliminate CO2
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PCO2 in
more CO2
arterial PCO2 in
crosses
blood blood brain CSF
barrier

PCO2 in RESPONSE TO
H+ in CSF
arterial HYPERCAPNIA
blood

stimulation of
expiration central
chemoreceptors
of PCO2

frequency of
impulses to
rate and medullary
depth of rhythm
generator
ventilation 33
 Blood Gas Case Studies.

1. Anna is a 3 month old baby who has been in hospital for

one week. She has been tested RSV +ve. She is having
severe difficulty in breathing.

PH 7.15
Paco2 9.25 kPa
BE -1 mmol

What is Annas acid base status?

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2. Badu is a 15 year old who has been involved in a RTA. He
was driving a stolen car. He has been admitted to your ward
awaiting police investigation. He is very anxious. He begins
to hyperventilate.

PH 7.6
Paco2 3.15 kPa
BE +3 mmol

What is Budus acid base status?

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3. Rani is a 10 year old newly diagnosed diabetic. She has
presented to A & E. She has been acutely unwell since this
morning. It is now 2pm.

PH 7.10
Paco2 4.2 kPa
BE -10 mmol

What is Ranis acid base status?

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4. Andrew is a 4 week old baby. He has vomited post
feeds since 1 week old. This vomiting has worsened, he
has come to your ward for investigation into pyloric
stenosis.

PH 7.75
Paco2 5.8 kPa
BE +8.7 mmol
What is Andrews acid base status?

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 5. Jessica is a 10 year old newly diagnosed
diabetic. She has presented to A & E. She has been
acutely unwell since Monday morning but her parents
felt she would get better today. It is now Tuesday
2pm.

PH 7.3
Paco2 3.35 kPa
BE -5.9 mmol
What is Jessicas acid base status?

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 END OF SESSION EVALUATION
Please answer the following questions:
1. How has your ability to relate theory to practice
changed as a result of this session?
2. What was the most valuable aspect of this
session?
3. What was the most unclear aspect of this
session?

Selamat Belajar..

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