Acid Base Disorders in Children

1. ACID BASE DISORDER
Presenter : Dr. Sneha Das
Moderator : Dr. Some Suvra Bose

2. ACID BASE BALANCE PHYSIOLOGY
• Human body is always pro acidic as every living cell needs energy
molecule i.e. ATP molecules.
• During ATP production in cell , acid is generated .
• But, the normal blood pH is 7.35-7.45 ( slightly basic ) and the urine pH is
6.5-7.0 (slightly acidic).
• Mechanisms of Acid Base Balance Regulating pH
1. Buffering ( Tissue level)
Extracellular: HCO3- (most imp), albumin
Intracellular: PO42-(bones), Haemoglobin
2. Respiratory Regulation ( minor role )
3. Renal regulation (most potent) by acidification of urine.

3. BUFFERS
• Buffers are substances that attenuate the change in pH that occurs when acids
or bases are added to the body.
• Extracellular buffers accomplish buffering of metabolic causes and intracellular
buffers to that of respiratory causes.
• The pH at which a buffer is 50% dissociated is its pKa ( ionization constant
of acid).
• The best physiologic buffers have a pKa close to 7.40 .When a pH is lower
than pKa of a buffer ,there is more acid than base and vice versa.
• pH of body fluids is calculated using the Henderson-Hasselbach equation
which expresses the relationship among pH , pKa and the concentrations of an
acid and its conjugate base. This relationship is valid for any buffer.
• Equation: pH = 6.1 + 𝑙𝑜𝑔
[𝐻𝐶𝑂3
−]
[𝐶𝑂2]

4. BICARBONATE BUFFER SYSTEM
• It is based on the relationship between CO2 and HCO3¯
• CO2+H2O H+ + HCO3¯
• CO2 acts as an acid which after combining with water releases H+, bicarbonate
acts as its conjugate base in that it accepts an H+.
• The pKa of this reaction is 6.1 .
• The bicarbonate buffer system is very effective because of the high
concentration in the body (24 meq/l) and because it is an open system. The
remaining body buffers are in closed system.
• As the lungs increase CO2 excretion when the blood CO2 concentration
increases.

5. BICARBONATE BUFFER SYSTEM
• When acid is added to the body, following reaction occurs:
H+ + HCO3¯ CO2 + H2O
• In closed system, the CO2 would increase. The higher CO2 concentration
would lead to an increase in the reverse reaction
CO2 + H2O H+ + HCO3¯
This will increase H+, limiting the buffering capacity of bicarbonate.
As the lungs excrete excess CO2 , the reverse reaction doesn’t occur thus
enhancing the buffering capacity of bicarbonate.
Same mechanism holds with addition of base.

6. NON BICARBONATE BUFFERS
1. Phosphate
• Can bind upto 3 hydrogen molecules so it can exist as PO4 3¯, HPO4 2¯,
H2PO4¯, H3PO4 . However, at a physiological pH most phosphate exists either
as HPO4 2¯ or H2PO4
-
• H2PO4¯ = H+ + HPO4¯
• The pKa of this reaction is 6.8, making it an effective buffer.
2. Protein
• Large numbers of histidine in the Hb makes it an effective buffer. pKa of this
reaction is 6.8.
• Plasma proteins have lesser number of histidine residues than hemoglobin
and hence they are not very effective. pKa of this reaction is 6.8.

7. ENDOGENOUS ACID PRODUCTION
• Normally when food is metabolized, 2 types of acids are added to ECF
1. Volatile acid in the form of carbonic acid ( H2co3), which determines the
level of CO2 in the blood ( PaCO2) and is excreted by lung.
2. Non volatile acids like sulphuric acid and phosphoric acids are produced
by dietary and endogenous protein catabolism. They are excreted by the
kidney.

8. RESPIRATORY REGULATION
• The respiratory compensation begins almost immediately within minutes and
is fully established by 24 hr.
• The lungs participate in regulating pH by increasing or decreasing the
elimination of CO2.
• With acidosis, pH changes around the brainstem stimulate hyperventilation
and the reverse is observed with alkalosis.
• However, the respiratory compensation is not completely effective in restoring
pH as only volatile acids i.e CO2 is taken care by the lungs.
• Failure of respiratory regulation results in respiratory acidosis or
alkalosis.

9. RENAL REGULATION
• It is the most powerful buffering system, which starts within hours and takes
5-6 days for peak effect.
• Involved in the removal of non volatile acids or bases through several active
transport mechanism.
• In response to acidosis-
1. Renal tubules reabsorb bicarbonate that is filtered at the glomerulus
2. Tubular secretion of H+ mostly in the collecting duct, with a small role in
distal tubule.
• Adequate excretion of endogenous acids requires presence of 2 urinary
buffers – Phosphate and ammonia.

10. BICARBONATE REABSORPTION IN PROXIMAL TUBULE
• The reabsorption of filtered bicarbonate is
first step in renal regulation of acid base
balance.
• The proximal tubule reclaims approximately
85% of the filtered bicarbonate.
• Remaining 15% is reclaimed mostly in the
ascending limb of the loop of Henle.

11. BICARBONATE REABSORPTION IN PROXIMAL TUBULE
• Increased HCO3- reabsorption
occurs in
1. Volume depletion
2. Hypokalemia
3. Increased PCO2 (Respiratory
Acidosis)
• Decreased HCO3- reabsorption
occurs in
1. Decreased PCO2 ( Respiratory
Alkalosis)
2. Hyperparathyroidsm ( PTH decreases
HCO3- reabsorption).
3. Carbonic anhydrase inhibitors such as
as acetazolamide
4. Disorders that can cause proximal
RTA.

12. DISTAL TUBULE ACIDIFIACTION
• Distal tubule acidification requires 2
urinary buffers- Phosphate and ammonia.
• Almost 15% of the filtered HCO3- is
absorbed in TAL via apical Na/H
exchanger.
• Type A IC cells in the distal tubule
secretes H+ via H-ATPase and H+/K+
ATPase present in the apical membrane.
• The secreted H+ combines with HPO42- to
form H2PO4- , a titrable acid which is
excreted.
• H+ ATPase is stimulated by aldosterone

13. AMMONIUM EXCRETION
• In the proximal tubule, NH3 is
produced from glutamine in the
renal cells.
• H+ is secreted by Na+-H+ exchanger
and NH3 diffuses into the lumen.
• NH4
+ is reabsorbed by Na+-K+-
2Cl− cotransporter in the TALH and
deposited in the medullary
interstitial fluid.
• In the collecting ducts, NH3 diffuses
from the medullary interstitium into
the lumen, combines with secreted
H+ in the lumen, and is excreted as
NH4
+.

14. AMMONIUM EXCRETION
• Acid excretion by the
collecting duct increases in
1. Primary
hyperaldosteronism and
secondary
hyperaldosteronism due
to volume depletion
2. Hypokalemia ( stimulates
NH3 production in
proximal tubule and
increases H+ secretion in
the collecting duct).

15. INDICATION OF ABG
• Severe respiratory or metabolic disorders
• Clinical features of hypoxia or hypercarbia
• Shock
• Sepsis
• Decreased urine output
• Renal failure
• Monitoring of babies in ventilator

16. ALGORITHM FOR SIMPLE ACID BASE DISORDER
Blood
pH
Acidemi
a
(↓pH)
Alkalemi
a
(↑pH)
Respiratory
Acidosis
Metaboli
c
Acidosis
Respiratory
Acidosis with
compensatory
metabolic
alkalosis
Metabolic
Acidosis with
compensatory
respiratory
alkalosis
Respiratory
Alkalosis
Metaboli
c
Alkalosis
Respiratory
Alkalosis with
compensatory
metabolic
acidosis
Metabolic
Alkalosis with
compensatory
respiratory
acidosis
↑pCO2
↑pCO2
↓pCO2
↓HCO3
¯ ↑HCO3
¯
↑HCO3
¯ ↓pCO2 ↓HCO3
¯

17. STEPS OF ABG INTERPRETATION
1. Is there an acid base disorder?- Look at the PaCO2 and HCO3 to
determine whether they are in the normal range.
Normal values- pH-7.35-7.45(7.40) , HCO3 – 22-26 meq/l (24), PaCO2-
35-45mm of Hg(40)
2. Is there acidosis or alkalosis?
pH<7.35 -Acidosis
pH>7.45 -Alkalosis

18. 3. What is the primary acid base disorder?
Determine the primary defect from the pH, HCO3 and PaCO2
If pH <7.35 – acidosis , may be either
• Metabolic acidosis- Low HCO3
• Respiratory acidosis- High PaCO2
If pH >7.45- alkalosis , may be either
• Metabolic alkalosis – High HCO3
• Respiratory alkalosis- Low PaCO2
STEPS OF ABG INTERPRETATION

19. COMPENSATIONS
Disorder Primary Event Compensation
Metabolic Acidosis ↓ [HCO3
¯] ↓ pCO2
Metabolic Alkalosis ↑ [HCO3
¯] ↑ pCO2
Respiratory Acidosis
Acute (<24 hours) ↑ pCO2 ↑ [HCO3
¯]
Chronic (3-5 days) ↑ pCO2 ↑↑ [HCO3
¯]
Respiratory Alkalosis
Acute (<24 hours) ↓ pCO2 ↓ [HCO3
¯]
Chronic (3-5 days) ↓ pCO2 ↓↓ [HCO3
¯]

20. 4. Calculate the expected compensation
 Metabolic Acidosis
WINTER’S formula-Expected CO2= (1.5xHCO3)+ 8 ±2
 Metabolic Alkalosis
Expected CO2= (HCO3 + 15 )
 Respiratory Acidosis
• Acute- For every 10 mm increase in pCO2 , HCO3 increases by 1.
• Chronic- For every 10 mm increase in pC02, HCO3 increases by 3.5.
 Respiratory Alkalosis
• Acute- For every 10 mm decrease in pCO2, HCO3 decreases by 2.
• Chronic- For every 10 mm decrease in pC02, HCO3 decreases by 4.
STEPS OF ABG INTERPRETATION

21. 5 . Determine the presence of mixed acid base disorder
• If either of the pH or PaCO2 is normal and the other abnormal, then there
is a mixed metabolic and respiratory disorder.
• If the pH is normal in a setting of acid base disorder , there is always a
mixed acid base disorder in the opposite direction.
• In metabolic acidosis, there may be mixed HAGMA and NAGMA or a mixed
HAGMA + metabolic alkalosis ( or pre existing compensated respiratory
acidosis )
• Delta Ratio is measured in high anion gap metabolic acidosis.
6. Clinical correlation and to establish the etiological diagnosis
STEPS OF ABG INTERPRETATION

22. SAME MIXED DISORDERS
Same Mixed Disorders – Which came first?
• If the trend of change in PaCO2 and HCO3 is the same, check the percent
difference. The one , with greater % difference between the two is the one
that is the dominant disorder.
• Eg : pH=7.25, HCO3=16, PaCO2=60
• Here, the pH is acidotic and both PaCO2 and HCO3 explain its acidosis, so
look at the % difference
• HCO3 % difference= (24-16)/24 = 0.33
• PaCO2 % difference= (60-40)/40= 0.5
• So, respiratory acidosis is the dominant disorder

23. PLASMA ANION GAP
• Plasma Anion gap is the difference between measured cations (Na+) and the
measured anions (Cl-+ HCO3
-). It is also the difference between unmeasured
cations (K , Mg , Ca) and the unmeasured anions ( albumin, phosphate, urate,
sulfate).
• Formula : Na – (Cl – HCO3)
• Normal value 8-12 meq/l or 12±2meq/l
• A 1g/dl decrease in albumin concentration decreases anion gap by 2.5 meq/l. So,
anion gap corrected for albumin is
[Na]-[Cl+HCO3]+2.5(4-albumin)
• High anion gap metabolic acidosis(HAGMA)-AG is high as HCO3 gets
overconsumed to neutralise accumulated acids and increase in unmeasured
anions.
• Normal anion gap metabolic acidosis(NAGMA)- AG is normal as HCO3 loss is
accompanied by Cl reabsorption ( hyperchloremic metabolic acidosis)

25. IMPORTANCE OF ANION GAP
• Useful to establish the etiological diagnosis of metabolic acidosis.
• Useful in diagnosis of mixed disorder.

26. DELTA RATIO
• If there is high anion gap metabolic acidosis then calculate the delta ratio or delta
gap to determine additional hidden metabolic acidosis or metabolic alkalosis.
• Formula : (AG-12)/(24-HCO3)
• <0.4 –Pure NAGMA
• 0.4-0.8- Mixed NAGMA+HAGMA
• 0.8-2- Pure HAGMA
• >2- Mixed HAGMA + metabolic alkalosis

27. METABOLIC ACIDOSIS
• It is characterized by fall in plasma HCO3- and fall in pH (<7.35). The PaCO2 is
reduced secondarily by hyperventilation , which minimizes fall in pH.
• 3 basic mechanisms-
1. Loss of bicarbonate from the body
2. Impaired ability to excrete acid by the kidney
3. Addition of acid to the body ( endogenous or exogenous)

28. CLASSIFICATION AND CAUSES OF METABOLIC ACIDOSIS
I. Overproduction of H+
1. Toxins and drugs –methanol ,
ethylene glycol, salicylate etc
2. Ketoacidosis- DKA, starvation
3. Lactic acidosis-
• Type A – shock, anaemia, CO
poisoning
• Type B- Liver failure, renal failure ,
metformin , zidovudine, INH
II. Underexcretion of H+
Renal failure- uraemic acidosis(
GFR<15ml/1.73m2/min)
III. Excess loss of HCO3
1. GIT causes- diarrhea, pancreatic
fistula, ureterosigmoidostomy
2. Renal causes- RTA , drugs such
as ACEi, aldosterone antagonist,
CA inhibitors
I, II- HAGMA
III- NAGMA

29. URINARY ANION GAP
• It helps in differentiating the causes of normal anion gap metabolic acidosis.
• Urinary anion gap reflects the ability of the kidney to excrete NH4Cl
• Formula – Urinary (Na+K-Cl) =80 –NH4
• Normally UAG is zero or has a positive value around 30-35meq/l, due to the
presence of dissolved anions.
• UAG is negative in GIT causes of metabolic acidosis due to intact mechanism
of renal acidification resulting in enhanced NH4Cl excretion.
• UAG is positive in all forms of RTA due to low renal NH4+ excretion.

30. CLINICAL FEATURES OF METABOLIC ACIDOSIS
I. Manifestations of underlying disorder
II. Manifestations of metabolic acidosis
• Pulmonary changes- Kussmauls breathing
• Cardiovascular changes- In severe acidemia (pH <7.2), there is increased
susceptibility for arrythmias, decreased response to inotropes, secondary
hypotension due to depressed myocardial contractility and arterial vasodilation.
• Neurological changes- Ranges from headache, confusion, lethargy, drowsiness
to coma.
• Chronic acidemia as with renal failure can cause rickets.

31. APPROACH TO METABOLIC ACIDOSIS
I. History
II. Investigations
III. Management
History- Kussmaul’s breathing is the
most important diagnostic
presentation. H/o diabetes, toxin
ingestion, diarrhoea, FTT, rickets, bone
pains, recurrent episode of
dehydration, vomiting etc
Investigations-
• ABG- Low HCO3, low pH,
compensatory fall in PaCO2.
• Plasma AG
• Delta Gap
• Urinary AG
Management
• Specific management of underlying
disorder
• Correct volume and electrolyte
deficits
• Alkali therapy with NaHCO3 and
Tromethamine
• Amount of IV NaHCO3 required is
calculated as –
B.W x base deficit x0.3

32. ALKALI THERAPY IN METABOLIC ACIDOSIS
 Indication of bicarbonate therapy
• Serum pH <7.10 and/or plasma HCO3 <10 meq/l in conditions of
normal anion gap metabolic acidosis.
Disadvantages of bicarbonate therapy
• Hypernatremia and volume overload especially in CHF or renal
failure.
• Increased PaCO2. Therefore, patients ventilatory status should be
assessed before administration.
• Hypokalemia and hypocalcemia
• Overshoot or rebound alkalosis in organic acidosis (i.e
ketoacidosis , lactic acidosis ) due to conversion of accumulated
organic anions into bicarbonate .

33. APPROACH TO METABOLIC ACIDOSIS
Metabolic Acidosis (pH<7.35, HCO3<22meq/l, PaCO2<35mmHg)
Calculate plasma pH
HAGMA
• Toxins
• Ketoacidosis
• Lactic
acidosis
NAGMA
GIT CAUSES
• Diarrhoea
• Pancreatic fistula
• Ureterosigmoidost
omy
RENAL CAUSES
• RTA
UAG
NEGATIVE POSITIVE
GIT CAUSES RTA

34. APPROACH TO METABOLIC ACIDOSIS
NAGMA
UAG POSITIVE
N / ↓K+ ↑K+
Urine pH Urine pH
pH < 5.3 pH > 5.3 pH < 5.3
pH > 5.3
PRTA Distal RTA RTA
Type IV
Hyper K+
Distal RTA

35. CAUSES AND CLASSIFICATION OF METABOLIC ALKALOSIS
Metabolic
Alkalosis
Urine
Chloride
Diuretics
Persistant vomiting, NG
suction
Villous adenoma
Cystic fibrosis
Post hypercapnia
Chloride diarrhea
Blood
pressure
Plasma renin,
aldosterone
Bartter syndrome
Gitelman
syndrome
High renin
High
aldosterone
Low renin
High
aldosterone
Low renin
Low
aldosterone
Renovascular
stenosis
Renin secreting
tumor
Adrenal hyperplasia,
adenoma, carcinoma
GRA
Liddle syndrome
AME, Cushing
syndrome
Exogenous steroids
CAH (11β- or 17α-
Chloride Responsive
Low (<20mEq/L)
Chloride
Unresponsive
High (>20mEq/L)
High Normal

38. APPROACH TO METABOLIC ALKALOSIS
I. History
II. Investigations
III. Management
History-H/o vomiting, swelling of
the body, recurrent respiratory
infections , polyuria, dehydration
urine output, diarrhoea in newborn,
FTT, shock, HTN etc.
Investigations
• ABG- High HCO3, high pH,
compensatory increase in
PaCO2
• Urine Cl levels
• Serum renin and aldosterone
levels
• BP

39. CAUSES AND CLASSIFICATION OF METABOLIC ALKALOSIS
Management of metabolic alkalosis
Cl responsive
• Administration of
sufficient NaCl,KCl.
Replacement of NG
suction.
• Diuretics usage-
potassium
supplementation or
potassium sparing
diuretics is used
• Rarely acetazolamide can
be helpful in severe
metabolic alkalosis
Cl resistant
 With HTN
• Volume repletion is C/I
• Adrenal adenomas- resected
• Renovascular dis- can be repaired
• Glucocorticoid remediable aldosteronism,
CAH- glucocorticoid administration
• Cushing syndrome- spironolactone
• Liddle syndrome- Triamterene, amiloride
 Without HTN
• Barter and Gitelman syndrome- includes
oral potassium and sodium supplements

40. RESPIRATORY ACIDOSIS
Causes of Respiratory
Acidosis
Central Nervous System Depression
• Pacephalities
• Head Trauma
• Brain Tumor
• Central sleep apnea
• Primary pulmonary
hypoventilation(Ondine curse)
• Stroke
• Hypoxic Brain Damage
• Obesity-
hypoventilation(pickwickian)
syndrome
• Increased Intracranial pressure
• Medications
 Narcotics
 Barbiturates
 Anaesthesia
 Benzodiazepines
 Propofol
 Alcohols
Respiratory Muscle Weakness
• Muscular dystrophy
• Hypothyroidism
• Malnutrition
• Hypokalemia
• Hypophosphatemia
• Medications
 Succinylcholine
 Corticosteroids
Disorders of Spinal Cord, Peripheral
Nerves, or Neuromuscular Junction
• Diaphragmatic paralysis
• Guillain-Barre syndrome
• Poliomyelitis
• Acute flaccid myelitis
• Spinal muscular atrophies
• Tick paralysis
• Botulism
• Myasthenia
• Multiple sclerosis
• Spinal cord injury
• Medications
 Vecuronium
 Aminoglycosides
 Organophosphates(pesticides)

41. RESPIRATORY ACIDOSIS
Causes of Respiratory
Acidosis
Pulmonary Disease
• Pneumonia
• Pneumothorax
• Asthma
• Bronchiolitis
• Pulmonary edema
• Pulmonary hemorrhage
• Acute respiratory distress
syndrome
• Neonatal respiratory distress
syndrome
• Cystic fibrosis
• Bronchopulmonary dysplasia
• Hypoplastic lungs
• Meconium aspiration
• Pulmonary thromboembolus
• Intestinal fibrosis
Miscellaneous
• Flail Chest
• Cardiac Arrest
• Kyphoscoliosis
• Decreased
diaphragmatic
movement due to
ascites
 dialysis
Upper Airway Disease
• Aspiration
• Laryngospasm
• Angioedema
• Obstructive sleep apnea
• Tonsillar hypertrophy
• Vocal cord paralysis
• Extrinsic tumor
• Extrinsic or intrinsic hemangioma

42. TREATMENT OF RESPIRATORY ACIDOSIS
Respiratory acidosis is best managed by treatment of underlying etiology.
All patients with acute respiratory acidosis are hypoxic and need
supplemental oxygen or mechanical ventilation ( PaCO2 >60).
• Respiratory acidosis caused by CNS disease require mechanical ventilation
as hypercarbia causes cerebral vasodilation and raised ICT. This is
dangerous for the child.
Patients with chronic respiratory acidosis, oxygen should be used
cautiously as it blunts the respiratory drive and further increases PaCO2.
• It is best to avoid mechanical ventilation in chronic respiratory acidosis as
extubation is difficult.
• When intubation is necessary , the PaCO2 should be lowered only to the
patients normal baseline.

43. RESPIRATORY ALKALOSIS
Causes of Respiratory
Alkalosis
Hypoxia and Hypoxemia
• High altitude or low
fraction of inspired
oxygen
• Anemia
• Hypotension or lung
disease
Pulmonary disorders
• Pulmonary edema
• Embolism
• Airway obstruction
• Pneumonia
• Interstitial lung disease
• Mechanical ventilation
(ventilatory rate or tidal
volume too high)
Extrapulmonary disorders
(severe respiratory alkalosis)
• Stress
• Neurologic disease (stroke,
infection, trauma, tumor)
• Medications
 Catecholamines
 Progesterone
 Methylxanthines
 Salicylates
 Doxapram
 Nicotine
• Hyperthermia
• Hepatic encephalopathy
• Sepsis
• Recovery from metabolic
acidosis

44. EXAMPLES
1. A child with DKA has the following ABG
pH-7.1, HCO3- 8 mEq/l , PaCO2- 20 mm of Hg , Na 140 mEq/l , Cl- 106
mEq/l and urinary ketones 3+
• pH is low- so acidosis
• Low HCO3 – suggestive of metabolic acidosis and low PaCO2 – suggestive
of compensation ( same direction rule).
• Expected PaCO2 is (1.5x8)+8±2 = 20±2 which matches with the expected
PaCO2.
• AG is 140-106-8 =26
• Delta gap: 26-12/24-8 =0.8 s/o pure HAGMA
• So, this patient has HAGMA with respiratory compensation.

45. 2. A 12 yr old girl K/c/o Type 1 DM presented with fever , nausea, vomiting
and abdominal pain for 1 day. Lab inv suggests pH- 7.28, PaCO2-27, HCO3-
12, Na- 140 , Cl – 98 , BSL – 400.
• Low pH – so acidosis
• Low HCO3- s/o metabolic acidosis
• Expected PaCO2 – (1.5x12)+8±2=26±2
• AG- 140-98-12 =30 s/o HAGMA
• Delta ratio- 30-12/24-12= 1.5 s/o mixed HAGMA+ metabolic alkalosis
• This girl has HAGMA( DKA) + met alkalosis (vomiting) with respiratory
alkalosis.
EXAMPLES

46. 3. ABG of patient with CHF on furosemide is pH-7.48, HCO3- 34 , PaCO2-49.
• pH is high – so alkalosis
• High HCO3 s/o metabolic alkalosis and high PaCO2 s/o respiratory
compensation (same direction rule)
• Expected PaCO2 = 34+15=49 which matches with the given PaCO2 s/o
simple acid base disorder.
• So, this patient has metabolic alkalosis with respiratory compensation.
EXAMPLES

47. 4. A 11 yr old boy was admitted with high grade fever and hypotension after
a prolonged course of diarrhoea. Lab values showed pH-7.32 , HCO3-6,
PCO2- 20, Na- 139, Cl- 106.
• pH is low- so acidosis
• HCO3 is low – primary defect metabolic acidosis
• Expected PaCO2- (1.5x6)+8 ±2= 17±2 s/o respiratory compensation.
• AG : 139-106-6=27 . So , HAGMA.
• Delta gap 27-12/24-6= 0.8 s/o mixed HAGMA + NAGMA
• So this boy has HAGMA( lactic acidosis) + NAGMA ( diarrhoea) with
respiratory alkalosis
EXAMPLES

48. 5. A 3 yr old comatose child with h/o accidental ingestion of several tablets
of phenobarbitone is intubated and ventilation started with 30% oxygen.
ABG after 6 hr showed pH-7.28 , PaCO2- 56 mm of Hg, HCO3 -26
• Low pH- so acidosis
• High PaCO2 – primary defect is respiratory acidosis and high HCO3 s/o
metabolic compensation(Opposite direction rule)
• It is acute. Increase in CO2 = (56-40)=16
Increase in HCO3 =(24+1.6)=25.6
• So, the patient has respiratory acidosis with metabolic compensation.
EXAMPLES

49. EXAMPLES
6. K/c/o chronic lung disease develops severe vomiting . pH -7.4 , HCO3- 36 ,
PaCO2 – 60.
• pH is normal so patient has either no disorder or has mixed acid base
disorder.
• However, abnormal value of HCO3 and PaCO2 is s/o mixed disorders.
• High HCO3 suggests metabolic alkalosis ( due to vomiting). High PaCO2 is
s/o respiratory acidosis (due to CLD).
• Metabolic alkalosis is expected to increase the pH, while respiratory acidosis
is expected to decrease the pH.
• Normal pH can be explained as an end result of opposite changes caused by
both primary disorders.

50. THANK YOU