Acid base disorder in neonate

1. Welcome To Seminar
on
Acid – Base disorder
Dr. Tareq Rahman
(Resident phase – B , year 4)
Dr. Bipin Karki
(Resident phase – B , year 5)
Bangabandhu Sheikh Mujib Medical
University,Dhaka , Bangladesh.

2. Concerning matter ?
• Acid-base balance is one of the body’s most
important homeostatic mechanisms –
- It represents equilibrium, balance, and a steady state.
- Without acid-base balance, the cells cannot function properly.
- The body can tolerate slight deviations in balance for short
periods of time
- Chronic imbalances can result in pronounced, potentially fatal
changes in metabolic activity and essential body functions.
- Structural shapes of proteins and/or protein functions are
altered.
- Enzymatic activity is diminished.
- Chemical reactions may cease.

3. Neonatal status
• Due to higher metabolism, production of acid
is three times more than adult.
• Respiratory and renal function can not
maintain acid base balance properly like adult.
• In the premature or sick newborn, buffers may
be blunted or insufficient.

4. Terminology
 Acid
 Any substance that can yield a hydron (proton or
hydrogen ion H+)when dissolved in water
 Base
 Substance that can yield hydroxyl ions (OH-)
 Accept proton or H+

5. Acid Production
• Volatile acid –
- CO2 is produced from aerobic metabolism of
cells.
- CO2 combines with H2O to form the weak
acid H2CO3 , which dissociates into H+ and
HCO3 by the following reaction –
CO2 + H2O – H2CO3 - H+ + HCO3-

6. • Non-volatile acid –
- Sufuric acid ( a product of protein
metabolism).
- Phosphoric acid ( a product of phospholipid
metabolism ).
- Ketoacid , lactic acid and salicyclic acid are
other acids , are overproduced in disease or may be
ingested.

7.  pH
 Negative log of the hydrogen ion concentration
 Measure of acidity
 pH= pK + log([base]/[acid])
 Represents the hydrogen concentration
 Normal pH of body fluid is 7.35-7.45
 pK
 Negative log of the ionization constant of an acid
 The pH at which a buffer is 50% dissociated is it’s pK.
The best physiologic buffers have pK close to 7.4.

8. Henderson–Hasselbalch equation
• Henderson–Hasselbalch equation describes the
derivation of pH as a measure of acidity.
• The equation is given by:
pH = pKa + log ([A-]/[HA])
• [A-] = molar concentration of a conjugate base
• [HA] = molar concentration of a undissociated
weak acid (M)

9. Estimating blood pH
pH = pKa + log ([HCO3
−]/[H2CO3])
= 6.1 + log ([HCO3
−]/[H2CO3])
= 6.1 + log ([HCO3
−]/0.03x pCO2)
where:
• pKa is the logarithm of the acid dissociation constant of carbonic acid. It is
equal to 6.1.
• [HCO3
−] is the concentration of bicarbonate in the blood
• [H2CO3] is the concentration of carbonic acid in the blood
• 0.03 is the solubility factor of CO2
• pCO2 - Partial pressure of CO2 in blood

10.  Acidemia -
 Blood pH less than 7.35 ( < 7.4 is acidotic)
Alkalemia -
 Blood PH greater than 7.45 ( > 7.4 is alkaline)
Acidosis: pathological process that causes an
increase in hydrogen ion concentration.
Alkalosis: pathological process that causes a
decrease in hydrogen ion concentration.

12. • Base Excess (BE) :
- It refers to the change in the concentration of buffer
base ( BB ) from it’s normal value . Base excess refers
principally to the [ HCO3- ].
BE are only influenced only by metabolic process.
Normal range : -5 to + 5 mEq/L in arterial blood.
Increase HCO3- : positive base excess ( metabolic
alkalosis)
Decrease HCO3- : negative base excess ( metabolic
acidosis )

13. Regulation of pH
 Mechanism :
- Buffers 1st line defense.
- Respiratory Center and Lungs
2nd line defense.
- Renal system

14. Buffer -
Combination of a weak acid and /or a weak base
and its salt
 What does it do?
 Resists changes in pH

15. • Extracellular buffers –
- HCO3 is major extracellular buffer produced from CO2 and
H2O
- Phosphate is a minor urinary buffer and most important
urinary buffer .
• Intracellular buffers –
 Proteins
- Hemoglobin is a major intracellular buffer.
- Imidazole and alfa amino groups
 Organic acid - AMP , ADP , ATP , 2,3-
diphosphoglycerate .

16. • Bone –
- Bone represents an important site of buffering acid
load.
- An acid load, is associated with the uptake of excess H+
ions by bone which occurs in exchange for surface Na+ and K+
and by the dissolution of bone mineral
- It has been estimated that at least 40% of the buffering
of an acute acid load takes place in bone.
- Chronic acidosis can have very adverse effects on bone
mineraliz can result in bone diseases such as rickets,
osteomalacia and osteopenia.

17. Mechanism of Buffer
• Buffers combine with the strong acids
replacing them with weaker acids, and vice
versa.
-Buffers do not actually rid the body of H+ or CO2
but combine with them until another system can
excrete them from the body.
-Depending on whether an acid or base state exists,
chemical buffer reactions are reversible.

18. Bicarbonate buffer
• Is a mixture of carbonic acid
(H2CO3) and its salt, sodium
bicarbonate (NaHCO3) and the
reversible reaction catalyzed by
carbonic anhydrase
• If strong acid is added-
-Hydrogen ions released combine
with the bicarbonate ions and
form carbonic acid (a weak acid)
- The pH of the solution decreases
only slightly
• If strong base is added –
- It reacts with the carbonic acid
to form sodium bicarbonate (a
weak base)
- The pH of the solution rises
only slightly

19. Hemoglobin buffer
• In RBC CO2 binds with Hb
to form carbamino-Hb
• CO2 also converted into
H2CO3 which dissociates to
HCO3
- and H+ .
• HCO3
- exchanged for
chloride ions (Cl-) into
plasma called chloride
shift.
• H+ combines
with oxyhemoglobin
stimulating the release of
the oxygen

20. Renal Regulation System :
• The renal buffer system uses bicarbonate,
phosphate and ammonium buffers.
• It takes hours to days
• Kidney maintain acid-base balance in three ways:
- secrete H+,
- reabsorb bicarbonate,
- produce new bicarbonate.

21. Cont…
• The renal responses to abnormal acid load are –
 increases secretion of H+
 increases HCO3
- reabsorption and HCO3
- generation
 increases excretion of titrable acid and NH4+ ( mainly )
• The renal responses to abnormal alkali load are –
 increases HCO3
- excretion in urine
 increases excretion of phosphate buffer base
 Suppression of ammonia secretion

22. Reabsorption of bicarbonate

23. Excretion of titrable acid

24. Excretion of ammonium

25. Respiratory system regulation
• Acts within min to hours maximal within 12-24 hrs.
• H2CO3 produced converted to CO2, and excreted by
the lungs.
• Powerful, but works with volatile acids
• Exhalation / accumulation of carbon dioxide.
• Body pH can be adjusted by changing rate and depth
of breathing.
• CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3
-
• Metabolic acidosis – hyperventilation – exhalation
of CO2
• Metabolic alkalosis – hypoventilation –
accumulation of CO2

26. Anion gap
 The anion gap is the difference in the measured
cation ( Sodium and potassium) and the measured
anions ( Bicarbonate and chloride) in plasma.
 Anion gap= ([Na+] + [K+]) − ([Cl−] - [HCO3
−])
 Normal value: 8-16 mmol/L
 It is also the difference between unmeasured anions
and unmeasured cations.
 Anion gap is increased when there is increase in
unmeasured anions.

27. Acid- Base disorders
 Metabolic acidosis
 Metabolic alkalosis
 Respiratory acidosis
 Respiratory alkalosis
 Mixed disorder

28. Metabolic acidosis
 Bicarbonate deficit - blood concentrations of
bicarbonate drop below 24 mmol/L
 3 basic mechanisms:
1. Loss of bicarbonate from body
2. Impaired ability to excrete acid by kidney
3. Addition of acid to the body
 Causes:
1. Normal anion gap
2. Increased anion gap

29. Metabolic alkalosis
  Metabolic alkalosis is elevation
of arterial pH , an increase in
serum {HCO3-} .

30. RESPIRATORY ACIDOSIS
• Caused by hypercapnia due to hypoventilation
• Characterized by a pH decrease and an increase
in CO2
30
CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2 CO2
CO2
pH
pH

31. RESPIRATORY ALKALOSIS
• Cause is Hyperventilation
– Leads to eliminating excessive amounts of CO2
– Decrease in H+
31
CO2 CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2

32. Mixed Acid-Base Disorders
• Mixed- when compensation is inappropriate
• Mixed respiratory alkalosis & metabolic acidosis
– Sepsis
• Mixed respiratory acidosis & metabolic alkalosis
– Excessive use of diuretics , BPD

33. Metabolic acidosis
Increased anion gap metabolic acidosis (Normal Chloride)
 Lactic acidosis associated with clinical evidence of
decreased tissue perfusion
• Asphyxia
• Hypoxia
• Respiratory distress syndrome (RDS)
• Sepsis
• Anemia
• Hypothermia/cold stress
• Patent ductus arteriosus
• Necrotizing enterocolitis

34. Inborn errors of metabolism
Renal failure
Toxins and medications
• Maternal use of salicylates acetaminophen,
cocaine, nitroprusside, ibuprofen, iron,
isoniazid, paraldehyde, sulfasalazine, valproic
acid.

35. Normal or non–anion gap metabolic acidosis
Renal loss of bicarbonate
(a) Immature kidneys
(b) RTA
(c) Renal failure
(d) Medications Carbonic anhydrase inhibitors
(acetazolamide)

36.  GI loss of bicarbonate
(a) Diarrhea (usually secretory)
(b) Urologic and GI procedures
Surgery for NEC, ileostomy, Enterocutaneous or
bowel fistula

37. Effects of metabolic acidosis
• Hyperventilation (Kussmaul respiration)
• Depression of myocardial contractility
(PH≤7.2)
• Resistance to the effects of catecholamines
• Vasoconstriction of pulmonary arteries
• Shift of K+ out of cells causing hyperkalaemia

38. Management
Metabolic acidosis.
• The primary treatment is to treat the underlying
cause. Correct hypoxia, hypovolemia, low cardiac
output, and anemia.
• Fluid therapy for metabolic acidosis Volume
expansion should not be used to treat acidosis
unless there are signs of hypovolemia.
• Treatment with bicarbonate is not recommended
as a supportive therapy and its use is very
controversial.

39. • Cochrane review states there are insufficient data
to make a recommendation on using sodium
bicarbonate during resuscitation. (Beveridge et al
2006)
• There is insufficient evidence from randomised
controlled trials to determine whether infusion of
base or fluid bolus reduces morbidity and
mortality in preterm infants with metabolic
acidosis. (Cochrane review 2005)

40. • Some institutions treat acidosis if severe with
an alkali infusion if the base excess is > –5 to –
10 or if the pH is ≤7.25
• Total requirement=0.4× wt in kg× base excess
• 1 st1/3rd mixed with same amount of distilled
H2O IV stat
• 2 nd 1/3rd mixed with 24 hrs IV fluid
• Rest 1/3rd : Auto-correction, if renal functions
is in normal limit

41. Side effect of Sodium Bicarbonate
• Hypernatremia
• IVH
• Alkalosis
• Hypocalcaemia
• Extravasation cause tissue injury
• ability to generate CO2 and actually lower the
intracellular pH and cerebrospinal fluid pH. (HCO3-
+H+→H2CO3→H2O+CO2)
Prerequisite
Adequate ventilation

42. • Tromethamine (THAM) can be used in infants who have a
severe metabolic acidosis but have a high serum sodium
(>150 mEq/L) or high Pco2 (>65 mm Hg) despite aggressive
assisted ventilation.
• Use only in infants with good urine output (hyperkalemia
risk) and monitor for hypoglycemia
• Polycitrate (Polycitra) (oral solution).
 Chronic renal insufficiency
 intrinsic renal disease
 RTA
 Each 1 mEq citrate equals 1 mEq bicarbonate. Dose adjust
to maintain a normal pH.

43. Metabolic alkalosis
Common causes of metabolic alkalosis in the
newborn
• Prolonged NG/OG suction
• Pyloric stenosis (persistent vomiting)
• Diuretic therapy (especially Lasix in patients with
bronchopulmonary dysplasia)
• Excess alkali administration (eg, sodium
bicarbonate, citrate, acetate, or lactate infusion)
• Potassium depletion

44. Effects of metabolic alkalosis
• Decreased myocardial contractility
• Decreased cerebral blood flow(cerebral
vasoconstriction)
• Pulmonary vasodilation
• Confusion
• Mental obtundation
• Impaired peripheral oxygen unloading (due
shift of oxygen dissociation curve to left).

45. Management of metabolic alkalosis
• Mild or even moderate alkalosis may not
require correction.
• Because volume depletion is common so,
infusion of isotonic saline (0.9% sodium
chloride) is the most common method of
chloride replacement in this condition.

46. Management of metabolic alkalosis
a. Excess administered alkali. Adjust or discontinue the dose
of THAM, sodium bicarbonate
b. Hypokalemia. The infant’s potassium level should be
corrected
c. Prolonged nasogastric suction. Treated with IV fluid
replacement, usually
with 1/2 normal saline with 10–20 mEq KCl/L, replaced mL/mL
each shift.
d. Vomiting and loss of chloride from diarrhea. Give IV fluids
and replace deficits.
e. Diuretics. Stop the dose temporarily, or decrease the
diuretic dose if necessary, or add a potassium-sparing diuretic
such as spironolactone.

47. Respiratory acidosis
• Increasing respiratory failure; lung diseases such as RDS,
pneumonia, transient tachypnea (TTN), BPD/CLD, pulmonary
hypoplasia, atelectasis.
• Obstructed ETT (eg, mucus plug).
• Improper ETT position. An endotracheal tube positioned in the
oropharynx, down the right main stem bronchus, or at the carina.
• Pneumothorax.
• Hypoventilation or poor respiratory effort from maternal
anesthesia, PNA, medications, neuromuscular disorders, sepsis,
intracranial hemorrhage, hypoglycemia.
• PDA with pulmonary edema
• Others: Congenital diaphragmatic hernia, phrenic nerve paralysis

48. Effects of respiratory acidosis
• Acidemia, no matter the etiology, affects the
cardiovascular system. An arterial pH <7.2
impairs cardiac contractility
• Hypercapnia causes cerebral vasculature
vasodilation
• Hypercapnia produces vasoconstriction of the
pulmonary circulation
• Central depression at very high levels of pCO2

49. Respiratory alkalosis
• Overventilation by the ventilator. Most common cause in
NICU.
• Air bubble in the blood gas collection syringe. This can
falsely lower the Pao2 and Paco2
• Hyperventilation therapy. As used in persistent pulmonary
hypertension.
• Central hyperventilation. Central nervous system (CNS)
stimulation of the respiratory drive caused by a CNS
disorder or transient hyperammonemia
• Hypoxemia can cause a low CO2. Respiratory centers are
stimulated through chemoreceptors.
• Hyperventilation. Seen in a spontaneously breathing infant
secondary to sepsis, fever.

50. Effects of respiratory alkalosis
• Decreased intracranial pressure (secondary to
cerebral vasoconstriction)
• Inhibition of respiratory drive via the central &
peripheral chemoreceptors
• Decreased myocardial contractility
• Shift of the haemoglobin oxygen dissociation
curve to the left (impairing peripheral oxygen
unloading)
• Slight fall in plasma [K+]

51. Management of Respiratory acidosis
and alkalosis
• ETT problem
• Ventilator issues
• Treatment of underlying disease
Sudden respiratory acidosis in MV
• D – Dislodged
• O – Obstructed
• P – Pneumothorax
• E – Equipment

52. Three-step process for interpreting acid–base
disturbances.
• Step 1: Determine whether the pH is low
(acidemia) or high (alkalemia).
• Step 2: Establish an explanation for the
acidemia or alkalemia.
• Step 3: Calculate the expected compensation
and determine whether a mixed disturbance is
present

56. Quiz 1
• Baby boy, 28 wks GA, admitted 3 hrs ago, intubated initially,
given surfactant, then extubated immediately to nasal
CPAP, pressure 5 cm H2O, FiO2 0.5.
• ABG now: pH=7.20, PCO2=68, PO2=40, HCO3=22, SaO2=85%
• Interpret above blood gas
Acidosis
Respiratory
Exp Hco3: 29
Metabolic Acidosis
Hypoxemia

57. Quiz 2
• Baby girl, born at term by emergency CS, because of
cord prolapse and severe fetal distress. She was flat,
needed thorough resuscitation (intubation, UVC, 2
doses of epinephrine)
• Now she is 6 hrs old, ventilated, FiO2 0.3, and had
focal seizure.
• ABG: pH=7.15, PCO2=30, PO2=60, HCO3=6, SaO2=92%
• Interpret above blood gas
• Acidosis
• Metabolic
• Exp Pco2 15-18
• Respiratory acidosis

58. Quiz 3
• Hundred day-old baby girl, was born at 27 wks GA, had
stormy course.
• Now she is on NC 1 LPM, FiO2 0.3
• ABG: pH=7.34, PCO2=65, PO2=60, HCO3=35, SaO2=92%
• Interpret above blood gas
Acidosis
Respiratory
Exp Hco3: 32.5
Metabolic alkalosis

59. Quiz 4
• Seven day-old, baby boy, born at 29 wks GA.
• He had large PDA, led to pulmonary
hemorrhage, which treated conservatively.
• Indomethacin cannot be given because of Lt
side grade 4 IVH, TFI was restricted to 120
ml/kg/d and furosemide was given 1.2 mg q12
hrs.
• ABG: pH=7.47, PCO2=40, PO2=60, HCO3=30,
SaO2=92%
• Alkalosis
• Metabolic
• Exp Pco2: 44
• Respiratory alkalosis

60. Thank you all