SEMINAR

1. Metabolic Acidosis
R.Anusha
PharmD 5th Year
Roll No:07
1

2. Introduction
2
• Acidosis : It is a process that increases [H+]
• Acidemia: When blood pH <7.35
• Metabolic acidosis: When an acid other than carbonic acid
accumulates in the body resulting in fall in HCO3-
• Metabolic acidosis is a clinical disturbance characterized by
an increase in plasma acidity.
• Metabolic acidosis should be considered a sign of an
underlying disease process.
• Identification of this underlying condition is essential to
initiate appropriate therapy.

3. 3
• In body fluids, the concentration of hydrogen ions ([H+]) is
maintained within very narrow limits, with the normal
physiologic concentration being 40 nEq/L.
• The concentration of HCO3
- (24 mEq /L) is 600,000 times
that of [H+].
• The tight regulation of [H+] at this low concentration is
crucial for normal cellular activities because H+ at higher
concentrations can bind strongly to negatively charged
proteins, including enzymes, and impair their function.

4. 4
• Under normal conditions, acids and, to a lesser extent,
bases are being added constantly to the extracellular fluid
compartment, and for the body to maintain a physiologic
[H+] of 40 nEq/L, the following three processes must take
place:
i. Buffering by extracellular and intracellular buffers
ii. Alveolar ventilation, which controls PaCO2
iii. Renal H+ excretion, which controls plasma HCO3
-

5. 5
Metabolic acidosis is acid accumulation due to
 Increased acid production or acid ingestion
 Decreased acid excretion
 GI or renal HCO3 − loss
Results in:
 ↓pH (7.35)
 ↓HCO3- (<22mEq/L)

6. Signs and symptoms
6

7. Anion gap
7
Anion gap = ( [Na+ ] + [K+ ] ) − ( [Cl− ] + [HCO3 − ] )
• Unmeasured anions subtracted by unmeasured cations
(in ECF)
• Omission of potassium has become widely accepted,
as potassium concentrations, being very low, usually
have little effect on the calculated gap.
• Normal value: 3–11 mEq/L

8. High anion gap metabolic acidosis
Causes include:
8
• M-Methanol
• U-Uremia (chronic kidney failure)
• D-Diabetic ketoacidosis
• P-Propylene glycol
• I- Infection, Iron, Isoniazid, Inborn errors of
metabolism
• L-Lactic acidosis
• E-Ethylene glycol

9. Normal anion gap acidosis
Causes include
9
• Longstanding diarrohea (bicarbonate loss)
• Bicarbonate loss due to taking topiramate
• Pancreatic fistula
• Uretero-sigmoidostomy
• Renal tubular acidosis
• Intoxication: ammonium chloride,acetazolamide,bile
acid sequestrants, isopropyl alcohol
• Renal failure (occasionally)
• Inhalant abuse
• Toluene

10. 10
Some examples of specific treatments for
underlying disorders:
• Fluid, insulin and electrolyte replacement is necessary for
diabetic ketoacidosis
• Administration of bicarbonate and/or dialysis may be
required for acidosis associated with renal failure
• Restoration of an adequate intravascular volume and
peripheral perfusion is necessary in lactic acidosis.

11. Diabetic Keto Acidosis
11
• Managing diabetic ketoacidosis (DKA) in an intensive care
unit during the first 24-48 hours always is advisable. When
treating patients with DKA, the following points must be
considered and closely monitored:
• Correction of fluid loss with intravenous fluids
• Correction of hyperglycemia with insulin
• Correction of electrolyte disturbances, particularly
potassium loss
• Correction of acid-base balance
• Treatment of concurrent infection, if present

12. Lactic Acidosis
12
 Blood lactate concentrations >2mmol/L(20mg/dl) results
lactic acidosis.
 Type 1 hypoxia + peripheral generation of Lactate in
patient with circulatory failure+ shock.
• Type 2 impaired metabolism of Lactate in Liver disease and
drug + toxin inhibit lactate metabolism( eg:Metformin).
• Treatment is directed towards correcting the underlying
cause of lactic acidosis and optimizing tissue oxygen
delivery for type A lactic acidosis and the removal of the
offending drug or toxin in type B lactic acidosis.
• Blood lactate concentrations >2mmol/L(20mg/dl) results
lactic acidosis.

13. Renal tubular Acidosis
13
• The treatment of type 1 and type 2 RTA is relatively simple,
requiring the use of sodium bicarbonate or the slightly more
palatable compound Shohl solution (or Bicitra), which
contains citric acid and sodium citrate, providing 1
mEq/mL of alkali.
• Polycitra K solutions contain potassium citrate to provide 2
mEq/mL of alkali and 2 mEq/mL of potassium,designed to
correct both the acidosis and hypokalemia.

14. 14
• Type 4 RTA may require treatment with fludrocortisone 0.1
to 0.3 mg/d (0.05 to 0.15 mg/m 2 per day).
• To reverse the hyperkalemia that characterizes the
metabolic acidosis of type 4 RTA, dietary potassium
restriction and orally administered potassium binders may
be needed. Finally, to increase renal excretion of potassium,
chlorothiazide and furosemide may be required to correct
hyperkalemia.
• To neutralize the metabolic acidosis, bicarbonate therapy of
1.5 to 2.0 mEq/kg per day has been advocated.

15. The ECLS Approach to Management of
Metabolic Acidosis
15
 Emergency: intubation and ventilation for airway or
ventilatory control; cardiopulmonary resuscitation; severe
hyperkalaemia correction.
 Cause: Treat the underlying disorder as the primary
therapeutic goal.Consequently,accurate diagnosis of the
cause of the metabolic acidosis is very important.
 Losses: Replace losses (e.g. of fluids and electrolytes)
where appropriate.Other supportive care (oxygen
administration) is useful. In most cases, IV sodium
bicarbonate is NOT necessary, NOT helpful, and may even
be harmful so is not generally recommended.

16. 16
 Specifics:There are often specific problems or
complications associated with specific causes or specific
cases which require specific management. For example:
 Ethanol blocking treatment with methanol ingestion;
 Rhabdomyolysis requires management for preventing
acute renal failure;
 Haemodialysis can remove some toxins

17. Emergency <7.1(plasma bicarbonate of 8 mEq/L
[mmol/L]
17
• A pH under 7.1 is an emergency, due to the risk of cardiac
arrhythmias, and may warrant treatment with intravenous
bicarbonate. Bicarbonate is given at 50-100 mmol at a time
under monitoring of the arterial blood gas readings. This
intervention, however, has some serious complications in
lactic acidosis and, in those cases, should be used with
great care.
• If the acidosis is particularly severe and/or there may be
intoxication, consultation with the nephrology team is
considered useful, as dialysis may clear both the
intoxication and the acidosis.

18. REFERENCE
18
 Medicine Update 2010 ; Vol. 20 ; Metabolic Acid
Base Disorders ;690-694
 https://emedicine.medscape.com/article/242975-
overview