Acid-B ase B alan ce

in Ne onate s

Dr Mohd Maghayreh
PRTH-IRBID
Definitions
pH
The negative logarithm of hydrogen ion
concentration, pH= -log {H+}, and
corresponds to a pH of range of 7.35 to
7.45.

Acidosis
A downward shift in pH below 7.35
Alkalosis
An upward shift in pH above 7.45.
Buffer
A substance that can minimize changes in
pH when acid or base are added to the
system
Maintenance of Acid-Base
Balance
The main systems that maintain pH
include:
 The body’s buffer systems.
 The respiratory system.
 The kidneys
Maintenance of Acid-Base
Balance (cont.)
Extracellular buffers include:
 The bicarbonate-carbonic acid system.
 Phosphates.
 Plasma proteins.

Intracellular buffers include:

 Hemoglobin.
 Organic phosphates.
Maintenance of Acid-Base Balance
(cont.)

 The plasma bicarbonate-carbonic acid

buffer system:
 The most important extracellular
buffer.
 The acid component [carbonic acid
(H2CO3)] is regulated by the lungs.
 The base component [bicarbonate
(HCO3-)] is regulated by the kidneys
Maintenanc e of Acid- Bas e
Balanc e (cont.)

 Maintenance of normal pH depends on

excretion of volatile acids (e.g. carbonic
acid) from the lungs.
 Kidneys contribute to maintenance of the
acid-base balance by reabsorbing the
filtered bicarbonate, secreting hydrogen
ions as titratable acids, and excreting
ammonium ions
Classification of Acid-Base
Disorders

Metabolic acidosis
Occurs as a result of increased amounts of
nonvolatile acid or decreased amounts of
HCO3- in the extracellular fluid.
Metabolic alkalosis
Occurs as a result of increased amounts of
HCO3- in the extracellular fluid
Classification of Acid-Base
Disorders (cont.)

Respiratory acidosis
Due to hypoventilation and decreased
excretion of volatile acid (CO2).
Respiratory alkalosis
Due to hyperventilation and increased
excretion of volatile acid (CO2).
Evaluation of Acid-Base Balance
 Blood gas measurement should be the
starting point for the evaluation of any
acid-base disorders;
 pH and PaCO2 are directly measured,
and from these HCO3- is calculated.
Evaluation of Acid-Base Balance
(cont.)

Important parameters in diagnosing acid-

base disturbance:
 Type: acidosis or alkalosis (by pH).
 Cause: metabolic or respiratory (by PaCO2
and bicarbonate)
 Response: uncompensated or compensated.
 Form: simple or mixed.
Classification of Acid-Base
Disorders (cont.)
Acid-base disorders are also classified according
to the number of causes giving rise to the disorder:

Simple acid-base disorder

When only one primary acid-base abnormality and its
compensatory mechanism occur.
Mixed acid-base disorder
When a combination of simple acid-base disturbances
occurs.
Evaluation of Acid-Base Balance

Metabolic Respiratory

Decrease Increased PaCO2 Acidosis

d HCO3-

Increased Decreased Alkalosis

HCO3- PaCO2
Evaluation of Acid-Base Balance
(cont.)
 A nomogram can help in the diagnosis of
primary disturbance; it describes the expected
compensatory response to a primary
abnormality in either PaCO2 or HCO3-.
 If compensation in a given patient differs
from that predicted, the patient either has not
had enough time to compensate for a simple
acid-base disturbance or has a mixed acid-
base disorder
Evaluation of Acid-Base Balance
(cont.)
 Analysisof blood gas values must be
considered according to patient history
and physical findings and with
understanding of expected
compensatory responses to identify the
primary disturbance
Nomogram for Diagnosis of Simple Acid-Base
Disorders
Compensatory Mechanisms in Primary
Acid-Base Disorders

Acid-base Primary Compensatio Rate of

disorder event n compensatio
n
Metabolic acidosis
Normal Decreased Decreased For 1meq/l ↓ in
anion gap HCO3- PaCO2 HCO3-
→Pco2 ↓ by 1-
1.5mmHg
Increased  Increased Decreased For 1meq/l ↓in
anion gap acid PaCO2 HCO3-
production →Pco2↓ by 1-
 Increased 1.5mmHg
acid intake
Compensatory Mechanisms in Primary
Acid-Base Disorders (cont.)

Acid-base Primary Compensatio Rate of

disorder event n compensation

Respiratory alkalosis
Acute decreased decreased For 10mmHg ↓in
PCO2 HCO3 PCO2 →HCO3
↓by 1 meq/l

Chronic decreased decreased For 10mmHg ↓in

PCO2 HCO3 PCO2 →HCO3 ↓s
by 2-5meq/l
Types of Acid-Base Disorders
Metabolic acidosis
 Common problem, especially in critically
ill newborn.
 Occurs either when the fall in pH is
caused by the accumulation of acid other
than H2CO3 and thus results in loss of
available HCO3-, or alternatively, by the
direct loss of HCO3- from body fluids.
Metabolic Acidosis
Causes of metabolic acidosis are
divided
into:
 Metabolicacidosis with an elevated
anion gap.
 Metabolic acidosis with a normal anion
gap.
Metabolic Acidosis (cont.)
 The anion gap reflects the difference
between the unmeasured cations and
the unmeasured anions.
 The unmeasured cations are serum
potassium, calcium and magnesium.
 The unmeasured anions normally
include the serum proteins, phosphates,
sulfates and organic acids
Metabolic Acidosis (cont.)
 The anion gap is estimated using the
following formula:
Anion gap= [Na+] – ([Cl -] + [HCO3-]
 Thenormal range of serum anion gap in
newborns is 8 to 16 meq/L with slightly
higher values in very premature
newborns.
Metabolic Acidosis with an
Elevated Anion Gap
 Itindicates the accumulation of strong
acids due to increased intake or
production, or to decreased excretion.
 It is most frequently due to:
 Lacticacidosis secondary to tissue
hypoxia
Metabolic Acidosis with an
Elevated Anion Gap (cont.)
 Inborn error of metabolism.
 Renal failure.

 Late metabolic acidosis.

 Toxins such as benzyl alcohol .

Metabolic Acidosis with a
Normal Anion Gap

 It occurs as a result of HCO3- loss from the

extracellular space through the kidneys or
gastrointestinal tract.
 It is most frequently due to:
• Renal bicarbonate loss:
• Bicarbonate wasting due to immaturity.
• Renal tubular acidosis.
• Carbonic anhydrase inhibitors.
Metabolic Acidosis with a Normal
Anion Gap (cont.)

• Gastrointestinal bicarbonate loss:

• Small bowel drainage such as ileostomy and
fistula.
• Diarrhea.
• Aldosterone deficiency.
• Excessive chloride in intravenous fluids
Complications of Acidosis

 Arteriolar vasoconstriction followed by

dilatation.
 Depression of cardiac contractility.

 Systemic hypotension.

 Pulmonary edema.

 Arrhythmias.
Management of Metabolic Acidosis

 The most important approach to treat

metabolic acidosis is correcting the underlying
cause, usually by improving circulating blood
volume and/or cardiac output.
 In cases of significant metabolic acidosis (base
deficit >10-12, arterial PH < 7.25), it may be
useful to give exogenous base (buffer) to
correct pH. The most widely used buffer is
sodium bicarbonate (NaHCO3).
Management of Metabolic Acidosis
(cont.)

 The dose of sodium bicarbonate required to

correct the pH can be estimated using the
following formula:

NaHCO3 (mEq) = base deficit X body weight

X 0.3
 NaHCO3 should not be given if ventilation is
inadequate because its administration results
in an increase in PaCO2 with no improvement
in pH .
Management of Metabolic
Acidosis (cont.)
 NaHCO3 should be administered slowly and
diluted 1:1 with D5 or sterile water.
 Give half of the calculated total correction dose
for initial therapy to avoid overcorrection of
metabolic acidosis.
 Subsequent doses of sodium bicarbonate are
then based on the results of repeated blood
gas measurements.
Metabolic Alkalosis

It is characterized by a primary increase

in the extracellular HCO3-
concentration, sufficient to raise the
arterial pH above 7.45.
Causes of Metabolic Alkalosis in
Newborns

 Excessive loss of hydrogen from the

gastrointestinal tract or kidneys as a result of:
• Continuous nasogastric aspiration.
• Persistent vomiting.
• Diuretics treatment (This will induce equivalent rise
in extracellular HCO3-).
 Gain of bicarbonate as occurs during
administration of NaHCO3 in attempting to
correct metabolic acidosis.
Respiratory Acidosis (cont.)

 The initial increase in PaCO2 is buffered by

the non-HCO3- intracellular buffers without
noticeable renal compensation for at least
12-24 hours.
 Renal metabolic compensation reaches its
maximum levels within 3 to 5 days, and its
effectiveness is influenced by the functional
maturity of proximal tubular HCO3- transport.
Respiratory Acidosis (cont.)

 Directed towards improving alveolar

ventilation and treating the underlying
disorder.
 Adequate ventilation often must be
provided by mechanical ventilation in
sick patients.
Respiratory Alkalosis

 Occurs when a primary decrease in PaCO2 results in

an increase in the arterial pH > 7.45.
 The initial hypocapnea is acutely titrated by
intracellular buffers, and metabolic compensation by
the kidneys returns pH towards normal within 1 to 2
days.
 This is the only simple acid-base disorder in which the
pH may be completely normalized by the
compensatory mechanisms.
Causes of Respiratory Alkalosis

Hyperventilation: In spontaneously breathing

newborns it is most often caused by:
 Fever.
 Sepsis.
 Retained fetal lung fluid.
 Mild aspiration pneumonia.
 Central nervous system disorders.
Causes of Respiratory Alkalosis
(cont.)

 In the NICU, the most frequent cause of

respiratory alkalosis is increased alveolar
ventilation secondary to hyperventilation
of the intubated newborn.
Complications of Respiratory Alkalosis

 There is a suggested association

between hypocapnia and development of
periventricular leukomalacia and
bronchopulmonary dysplasia in
ventilated preterm infants.
Management of Respiratory
Alkalosis

 Treatment of neonatal respiratory

alkalosis consists of specific
management of the underlying process
causing hyperventilation.
Respiratory Acidosis

 Occurs when a primary increase in PaCO2

develops secondary to impairments in
alveolar ventilation resulting in an arterial pH
of less than 7.35.
 Common problem in newborns, and can be
due to many causes such as HMD,
pneumonia, PDA and bronchopulmonary
dysplasia.