acidbase balance in body. pediatrics

1. ACID BASE BALANCE
-DR. NAGESH LONIKAR

5. NORMAL VALUES
PH= 7.35-7.45
PCO2 35-45 mmHg
BICARB( HCO3-) = 20-28 mEq/L
CHLORIDE
ANION GAP 4-11

6. HAH+ +A-

10. The bicarbonate buffer system is very effective
BECAUSE OF -
1.HIGHconcentration of bicarbonate in the body (24 mEq/L) .
2.it is an open system.
The remaining body buffers are in a closed system.
The bicarbonate buffer system is an open system because the lungs
increase carbon dioxide excretion when the blood carbon dioxide
concentration increases.
When acid is added to the body, the following
reaction occurs:
H+ +HCO3- CO2 +H2O
The higher CO2 concentration
would lead to an increase in the reverse reaction:
CO2 +H2O H+ +HCO3−
This would increase the concentration of hydrogen ions, limiting the
buffering capacity of bicarbonate.
However, because the lungs excretethe excess carbon dioxide, the reverse
reaction does not increase

14. Carbon dioxide generated during normal metabolism is a weak acid.
Lungs prevent an increase in the Pco2 in the blood by excreting
the CO2 that the body produces.
An increase in ventilation decreases the Pco2, and
a decrease in ventilation increases the Pco2.

15. HOW ARE ACIDS ( H+ IONS) GENERATED IN BODY??
The 3 principal sources of hydrogen ions
1. dietary protein metabolism
2.incomplete metabolism of carbohydrates and fat
3. and stool losses of bicarbonate
Incomplete glucose metabolism can produce lactic acid. ( LACTIC ACIDOSIS)
incomplete triglyceride metabolism can produce
keto acids = such as β-hydroxybutyric acid and acetoacetic acid.
( DIABETIC KETOACIDOSIS)
For each bicarbonate molecule lost in the stool, the body gains 1 hydrogen ion.
may increase dramatically in a patient with diarrhea.

16. The hydrogen ions formed from endogenous acid production are neutralized by
bicarbonate, potentially causing the bicarbonate concentration
to decrease.
The kidneys regenerate this bicarbonate by secreting hydrogen ions.

17. -- Excretion of hydrogen ions by binding with
1.phosphate H2PO4--
2. and ammonia NH3

19. REABSORPTION OF BICARBONATE IONS
BICARBONATE IONS ARE REGENERATED IN EXCHANGE OF SECRETING HYDROGEN
IONS.

20. STIMULI FOR INCREASED BICARBONATE ION ABSORPTION
AND HYDROGEH ION EXCRETION
1. Volume Depletion – Which Stimulates Production Of Renin- Angiotensin
Angiotensin –II stimulates this
hence metabolic alkalosis can occur in volume deplition ( persistent vomitings)
2. Hypokalemia---- causes metabolic alkalosis
3. Increased pco2----- leading to retention of bicarb by kidneys.
 compensatory metabolic alkalosis.
STIMULI FOR DECREASEDBICARBONATE ION ABSORPTION
AND HYDROGEH ION EXCRETION.
1. Decreased pco2--- ---- leading to more excretion of bicarb by kidneys.
 compensatory metabolic acidosis.
2. Hyperparathyroidism
3. Drugs – acetazolamide

21. STIMULI THAT INCREASE H+ ( ACID ) EXCRETION
1. Metabolic acidosis
2. Aldosterone  thats why there is metabolic alkalosis in hyperaldosteronism
3. Hypokalemia  it also causes metabolic alkalosis
HYDROGEN ION EXCRETION

24. IN PRIMARY METABOLIC ACIDOSIS  WHERE EXTRA ACID H+ IS ADDED TO SYETEM.
1. DECREASE IN PH STIMULATES RESPIRATORY DRIVE CAUSING MORE
WASHOUT OF PCO2 .
SO EVEN THOUGH PCO2 IS BELOW THE NORMAL RANGE OF 35-45 mmHg it is not a
respiratory alkalosis.
If pco2 falls below the expected change then it will be labelled as respiratory alkalosis
IN PRIMARY RESPIRATORY PROCESS  WHERE DECREASED RESPIRATORY
DRIVE CAUSES RETENTION OF CO2 LEADING TO FALL IN PH.
Kidneys respond by increasing H+ excretion.
generating more bicarb. ( expected increase of bicarb)
So this rise in bicarb within the certain limit is also not metabolic alkalosis .

26. 3 STEPS FOR EVALUATING ABG INTERPRETATION

28. PARAMETER
PH 7.2 6.9 7.2 7.2 7.6 7.6 6.95
PCO2 ( mmHg) 24 18 20 62 15 52 70
HCO3-( mEq/L) 12 6 12 30 18 40 10

29. METABOLIC ACIDOSIS
3 BASIC MECHANISMS
1. Loss of bicarbonate from body
2. Impaired ability to excrete acid by kidneys
3. Addition of acid to body ( endogenous or exogenous)
CAUSES
A). NORMAL ANION GAP
Diarrhea
Renal tubular acidosis (RTA):
Distal (type I) RTA URINE PH > 5.5
Proximal (type II) URINE PH < 5.5
Hyperkalemic (type IV) RTA
Urinary tract diversions
Posthypocapnia
Ammonium chloride intake

30. B.) INCREASED ANION GAP
Lactic acidosis
Tissue hypoxia
Shock
Hypoxemia
Severe anemia
Liver failure
Malignancy
Intestinal bacterial overgrowth
Inborn errors of metabolism
Medications
Nucleoside reverse transcriptase inhibitors
Metformin
Propofol
Ketoacidosis
Diabetic ketoacidosis
Starvation ketoacidosis
Kidney failure
Poisoning
Ethylene glycol
Methanol
Salicylate
Toluene
Paraldehyde

31. The anion gap, which is the difference between the
sodium concentration and the combined concentrations of chloride
and bicarbonate
Anion gap =[Na+ ]−[Cl− ]−[HCO3− ]

32. UNMEASURED CATIONS (+ IONS)
K+, MAGNESIUM, CALCIUM.
UNMEASURED ANIONS (- VE IONS)
ALBUMIN PHOSPHATE, URATE SULPHATES
LACTATE- IN LACTIC ACIDOSIS
keto acids β-hydroxybutyrate , acetoacetate
A normal anion gap metabolic acidosis occurs when there is a
decrease in the bicarbonate concentration without an increase
in the unmeasured anions .
serum chloride concentration increases to maintain electrical
Neutrality .

33. MECHANISM OF METABOLIC ACIDOSIS IN DIFFERENT ETIOLOGIES
DIARRHEA .
BICARBONATE LOSS IN STOOLS
LACTIC ACIDOSIS SECONDARY TO VOLUME DEPLITION.
TYPE I ( DISTAL ) RTA URINE PH > 5.5
DEFECT TO EXCRETE H+ ION
hypokalemia, hypercalciuria, nephrolithiasis, and
nephrocalcinosis.
Failure to thrive because of chronic metabolic acidosis .
TYPE II ( PROXIMAL ) RTA ) URINE PH < 5.5
DEFECT IN ABSORBING BICARBONATE
glycosuria, aminoaciduria,
and excessive urinary losses of phosphate and uric acid.
Chronic hypophosphatemia leads to rickets .
TYPE IV ( HYPERKALEMIC) RTA
RENAL EXCRETION OF ACID AND POTASSIUM IS IMPAIRED.
hyperkalemia + metabolic acidosis + hyponatremia + volume depletion
from renal salt wasting .
CAUSE ALDOSTERONE DEFICIENCY OR RESISTENCE
E.G. congenital adrenal hyperplasia because of 21α-hydroxylase deficiency .

34. Symptoms of metabolic acidosis

35. TREATMENT OF METABOLIC ACIDOSIS
repair of the underlying disorder,
The administration of insulin in diabetic ketoacidosis .
restoration of adequate perfusion with intravenous fluids in lactic acidosis.
Indications For Bicarbonate Therapy
1. RTA or chronic renal failure require longterm base therapy.
2. Acute renal failure and metabolicacidosis need base therapy until their kidneys’
ability to excrete hydrogennormalizes.
3. salicylate poisoning, alkali administration increases renal clearance of salicylate .
4. Some inborn errors of metabolism require long-term base therapy.
The use of base therapy in diabetic ketoacidosis and lactic acidosis is
controversial; there is little evidence that it improves patient outcome,
and it has a variety of potential side effects.

36. METABOLIC ALKALOSIS

37. CHLORIDE-RESPONSIVE (URINARY CHLORIDE <15 MEQ/L)
The volume depletion in these patients is caused by losses of
sodium and potassium, but the loss of chloride is usually greater than
the losses of sodium and potassium combined .
These patients requirechloride to correct the volume depletion and
metabolic alkalosis; they are said to have chloride-responsive metabolic alkalosis.
Diuretic use leads to volume depletion, which increases
angiotensin II, aldosterone, and adrenergic stimulation of the kidney.
Diuretic use increases chloride excretion in the urine.
urine chloride level is typically high (>20 mEq/L).
After the diuretic effect has worn off, the urinary
chloride level is low (<15 mEq/L)
However, the metabolic alkalosis from diuretics
is clearly chloride responsive;

38. CHLORIDE-RESISTANT (URINARY CHLORIDE >20 MEQ/L)
INCREASED ALDOSTERONE
HYPERNATREMIA
HYPOKALEMIA
HYPERTENSION
LIDDLE SYNDROME: DUE TO MUTATED Na+ channel
hence hypernatremia+ hypokalemia+ hypertension
but aldosterone levels are normal.
Bartter and Gitelman syndrome.
secondary to defect of Na+ Cl- reabsorption
normal blood pressure + matabolic alkalosis+ hypokalemia
Gitelman syndrome is responsive to thiazide diuretics .

39. Clinical manifestations of metabolic alkalosis
Decreased ionised calcium leading to tetany ( carpopedal spasm).

40. Treatment of metabolic alkalosis CHLORIDE RESPONSIVE
1. nasogastric suction may be decreased or discontinued.
2. addition of a gastric proton pump inhibitor reduces gastric secretion
and losses of HCl.
3. Stop diureics if possible.
4. add potassium sparing diuretics. ALDACTONE
5. ACETAZOLAMIDE
A carbonicanhydrase inhibitor, acetazolamide decreases resorption of
Bicarbonate in the proximal tubule, causing significant bicarbonate loss in the
urine.
Most children with a metabolic alkalosis have one of the chlorideresponsive
etiologies. In these situations, administration of sufficient
sodium chloride and potassium chloride to correct the volume deficit
and the potassium deficit is necessary to correct the metabolic alkalosis.

41. TREATMENT OF CHLORIDE RESISTENT METABOLIC ALKALOSIS
1. Adrenal adenomas can be resected,
2.renovascular disease can be repaired.
3. Glucocorticoids for
Glucocorticoid-remediable aldosteronism,
17α-hydroxylase deficiency
11β-hydroxylase deficiency.
4. Spironolactone for hyperaldosteronism
5. triamterene or amiloride
effective therapy because both agents block the sodium
that is constitutively active in Liddle syndrome.
6. In Bartter syndrome and Gitelman syndrome
oral potassium supplementation and potassium-sparing
diuretics.
magnesium supplimentation in GITELMAN SYNDROME
severe Bartter syndrome often indomethacin.