The document discusses acid-base disorders, emphasizing the importance of arterial blood gas analysis in diagnosing and managing respiratory failure and acid-base homeostasis. It outlines key components like pH, PaO2, PCO2, HCO3, and their roles in diagnosing acidosis and alkalosis, as well as mechanisms of compensation and treatment strategies for various conditions. The document concludes with management approaches for metabolic and respiratory acidosis, highlighting the need to address underlying causes and correct imbalances appropriately.

1. ACID BASE
DISORDERS
Dr.Mohd Javed,MD
Department of Medicine
FHMC Agra

2. DEFINITION
An arterial blood gas analysis is a blood
test , that measures the amount of oxygen
and carbon dioxide in the blood.
Importance:
1) Aids in establishing a diagnosis and
severity of respiratory failure.
2) Assess adequacy of ventilation and
oxygenation.

3. Importance:
1) Aids in establishing a diagnosis and severity of respiratory failure.
2) Assess adequacy of ventilation and oxygenation.
3) Adequacy of co2 excretion.
4) Assess changes in acid base homeostasis.
5) Helps to guide treatment plan.

4. COMPONENTS
pH: Measurement of acidity or alkalinity,
based on the hydrogen (H+). 7.35 –
7.45
Pao2 :The partial pressure oxygen that is
dissolved in arterial blood. 80-100 mm
Hg.
PCO2: The amount of carbon dioxide
dissolved in arterial blood. 35– 45
mmHg
HCO3 : The calculated value of the
amount of bicarbonate in the blood. 22 –
26 mmol/L .
SaO2:The arterial oxygen saturation.
>95%.

5. The normal ECF pH is 7.40 ± 0.03.
Henderson-Hasselbalch equation:
The hydrogen ion concentration [H+] in extracellular fluid
is determined by the balance between the PCO2 and
the bicarbonate concentration [HCO3]. The relationship between these
variables is defined in HENDERSON Equation.
[H+] = 24 x PCO2 /[HCO3]
The normal [H+] in arterial blood is calculated using a PCO2 of 40 mm
Hg and a [HCO3] of 24 mEq/ L.
[H+] = 24 x (40/24) = 40 nEq /L

6. Maintenance of pH is essential for normal cellular function.
Three general mechanisms to keep it within a narrow window:
 Chemical buffering is mediated by HCO3 in the ECF and by
protein and phosphate buffers in the ICF.
The normal [HCO3] is 24 ± 2 mEq/L.
 Alveolar ventilation minimizes variations in the pH by
altering the partial pressure of carbon dioxide (pCO2).
The normal pCO2 is 40 ± 5 mm Hg.
 Renal H1 handling allows the kidney to adapt to changes in
acid–base status via HCO3 reabsorption and excretion of
titratable acid.

7. DEFINITIO
NS
Acidosis: the process which tends to
decrease the pH by gain of H+ or loss of
HCO3_ .
Alkalosis: process which tends to
increase the pH by loss of H+ or gain of
HCO3_.
acidemia and alkalemia refer to
processes that lower and raise pH
regardless of mechanism. They can be
caused by metabolic or respiratory
disturbances:
Metabolic acidosis is characterized by
a decrease in the plasma [HCO3] due to
either HCO3 loss or the accumulation of
acid.
Respiratory acidosis is characterized
by an elevation in pCO2 resulting from
alveolar hypoventilation.

8. DIAGNOSIS
Step 1.
Look at Ph
Acidemia , when pH is <7.37
Alkalemia when pH >7.43.
Step 2. Respiratory or Metabolic
Increase pH increase PCO2 OR decrease pH and decrease
PCO2- METABOLIC
Increase pH decrease PCO2 OR decrease pH and increase
PCO2 -RESPIRATORY
A combined disorder is present when pH is normal but the pCO2 and
HCO3 are both abnormal. Changes in both pCO2 and [HCO2] can cause
the change in pH.

9. Step 3: compensatory mechanism
A respiratory process that shifts the
pH in one direction will be
compensated by a metabolic process
that shifts the pH in the other and
vice versa.
 The effect of compensation is to
attenuate, but not completely correct,
the primary change in pH.
(1) primary metabolic disturbances:
last two digits of pH will generally
reflect PaCO2
Metabolic acidosis (min 7.10) eg pH
7.23 reflects PaCO2 25mmhg.
Metabolic alkalosis (max 7.60) eg pH
7.58 reflects PaCO2 57mmhg.

10. (2) Primary respiratory acidosis:
Increase in HCO3-1mmol/L per 10mmhg increase in PaCO2 above 40.
(3) Chronic respiratory acidosis: increase in HCO3 – 4mmol/L per 10 mmhg
increase in PaCO2 above 40.
An inappropriate compensatory response suggests the presence of a
combined disorder.
 Example: In a patient with metabolic acidosis, respiratory
compensation attenuates the metabolic disturbance to pH by lowering
pCO2. However, if the pCO2 is higher than expected, respiratory
compensation is insufficient, revealing a respiratory acidosis with the
primary metabolic acidosis. If pCO2 is lower than expected,
compensation is excessive, revealing a concomitant respiratory
alkalosis.

11. Anion GAP:
= measured cations – measured anions
AG=Na-(HC03+CL)
Normal value=12+/- 4(8-16meq/l)
Measured anion gap=12
If anion gap is positive or >16: metabolic acidosis.
If anion gap is negative or low:
Reduction in unmeasured anions (hypoproteinemia)
Excess of unmeasured cations (lithium toxicity)
Albumin is the major unmeasured anion.
The anion gap should be corrected if there are gross
changes in serum albumin level.
AG Corrected = AG+(4-(ALBUMIN)x2.5

12. The causes of a metabolic acidosis can
be divided into those that cause an
Elevated anion gap
Normal anion gap.
High AG acidosis results from
exposure to acids, which contribute an
unmeasured anion to the ECF.
Common causes are
diabetic ketoacidosis,
lactic acidosis, and toxic
alcohol ingestions.
Uremia-ARF/CRF

13. Normal anion gap metabolic acidosis
1) hypokalemic
A) GI losses of HCO3-
Diarrhea,ileostomy.
b) Renal losses of HCO3-
Proximal RTA, carbonic anhydrase inhibitors.
2) Normokalemic or Hyperkalemic
Acute tubular necrosis
Distal RTA
Hypoaldosteronism.

14. DECREASED
ANION GAP
ACIDOSIS
1) Hypoalbuminemia
2) Hypermagnesemia.
3) Spurious hyperchloremia

15. MANAGEMENT
High anion gap:
Treat the underlying
cause
No indication for
HCO3.
Normal anion gap:
Treat the underlying
cause.
Replace HCO3 as per
serum level and losses.
Approx. deficit =(24-
(HCO3)X(body
wt.x0.6)mmol/l.
Eg. For a 70kg pt with
a (HCO3)=4mmol/l
Deficit=(24-
4)x(70x0.6)=840mmol
/l=ml of soda bicarb
solution.
Replace 1/3-1/2 of
this amount then
remeasure blood
gases.

16. TREATMENT OF
THE RTAS
In distal (type 1) RTA, correction of the metabolic
acidosis requires oral HCO3 replacement on the order
of 1 to 2 mEq/kg/d with NaHCO3 or sodium citrate.
Potassium citrate replacement may be necessary for
patients with hypokalemia,nephrolithiasis,.
Underlying conditions should be sought and treated.
 In proximal (type 2) RTA, much larger amounts of
alkali (10 to 15 mEq/kg/d) are required to reverse the
acidosis. Administration of potassium salts minimizes
the degree of hypokalemia associated with alkali 
Type 4 RTA - correction of the underlying
hyperkalemia.
This consists of dietary K1 restriction (40 to 60 mEq/d)
and possibly a loop diuretic with or without oral
NaHCO3 (0.5 to 1 mEq/kg/d).
Mineralocorticoid administration (fludrocortisone, 50
to 200 mcmg PO daily) should be used in patients with
primary adrenal insufficiency and may be considered
in other causes
of hypoaldosteronismtherapy.

17. RESPIRATORY
ACIDOSIS
The causes of respiratory acidosis can be divided into
hypoventilation from
(a) respiratory center depression,
(b) neuromuscular failure,
(c) decreased respiratory system compliance,
(d) increased airway resistance, and
(e) increased dead space
DIAGNOSIS
Symptoms of respiratory acidosis result from
changes in the cerebrospinal fluid (CSF) pH.
A very severe hypercapnia may be well tolerated if it is
accompanied
by renal compensation and a relatively normal pH.
Conversely, a modest rise in pCO2 can be very
symptomatic if acute.
Initial symptoms and signs may include headache
and restlessness, which may progress to generalized
hyperreflexia/asterixis and coma.

18. TREATMEN
T
correct the underlying disorder
and improve ventilation.
Administration of NaHCO3 in
order to improve the acidemia may
paradoxically worsen the pH in
situations of limited ventilation.
The administered HCO3 will
combine with H1 in the tissues and
form pCO2 and water. If ventilation is
fixed, this extra CO2 generated
cannot be blown off and worsening
hypercapnia will result.
Therefore, HCO3 should, in general,
be avoided in pure respiratory
acidosis.

19. THANK YOU