1. ACID BASE IMBALANCE AND COMPENSATION
Dr T V Chaitanya Kumar
Assistant professor
Dept of Vety Biochemistry
CVSc, Tirupati
2. pH = - log [H+]
Range is from 0 - 14
If [H+] is high, the
solution is acidic; pH <
7
If [H+] is low, the
solution is basic or
alkaline ; pH > 7
What is pH?
3. 3
The Body and pH
• Extracellular fluid = 7.4
• Blood = 7.35 – 7.45
• < 6.8 or > 8.0 death occurs
• Acidosis (acidemia) below 7.35
• Alkalosis (alkalemia) above 7.45
• Homeostasis of pH is tightly
controlled
4. Homeostasis of pH
1. Extracellular and intracellular
buffering
2. Regulation of the rate of alveolar
ventilation to control
carbon dioxide concentration
3. Regulation of renal hydrogen
excretion
5. How ECF and Cellular Buffers work
Protein Buffer system
7. ACID BASE IMBALANCE
•Metabolic acidosis
• Metabolic acidosis is characterized by a decrease in pH and bicarbonate.
• Addition of hydrogen ions or a loss of bicarbonate ions.
• The initial buffering of an acid load is by the ECF buffers, primarily the
bicarbonate-carbonic acid pair
• Intracellular buffers, protein and phosphate, assist in the buffering
process.
• “ Cation shift ” results in hyperkalemia
8. Causes
• Common causes include lactic acidosis; ketoacidosis
• Gastrointestinal problems
• Indigestion colic or diarrhea
• Renal failure, which may result in a decreased ability to
excrete hydrogen and thus to retain bicarbonate
• Acidosis in calves and goat kids associated with diarrhea.
• Increased anion gap.
• Ingestion of certain salicylate, methanol, ethylene glycol, or
paraldehyde
9. Compensation
• Increased ventilation
• Renal excretion of
hydrogen ions
• K+ exchanges with
excess H+ in ECF
( H+ into cells, K+ out
of cells)
Respiratory response is a reduction of p CO 2 by 0.7 mmHg for each mEq/l decrease in bicarbonate
10. Respiratory Acidosis
• Decrease in pH and an increase in p CO 2 .
• decreased effective alveolar ventilation or breathing an atmosphere
with elevated CO 2 .
• Intracellular buffers.
• The principal ECF buffer, the bicarbonate-carbonic acid buffer pair,
cannot buffer a respiratory acidosis.
• Carbon dioxide diffuses through the lung much more readily than O2
thus, diseases that compromise ventilation normally result in
decreases in p O 2 before significant increases in p CO 2
11. • Causes
• Primary pulmonary diseases :
Acute upper respiratory obstruction, pneumonia, pneumothorax,
chronic obstructive lung disease.
• Diseases or drugs that inhibit the medullary respiratory center
• General anesthesia with volatile agents using a closed system.
• Emphysema
• Compensation
• Increased excretion of hydrogen ion, chronic respiratory acidosis.
• 0.35 mEq/l of bicarbonate is anticipated for each mm Hg increase in p CO 2
• Exogenous bicarbonate is unnecessary, and should bicarbonate be administered
to patients with a respiratory acidosis, it would be excreted without affecting the
final plasma bicarbonate concentration.
12. Metabolic Alkalosis
• Increase in pH and bicarbonate.
• Digestive disturbances in ruminants.
• Metabolic alkalosis requires an initiating process and maintaining the
alkalosis.
• Generation of metabolic alkalosis
• excessive hydrogen loss,
• Bicarbonate retention,
• Contraction alkalosis: Excess loss of ECF (sodium and
chloride)
13. Causes
• Gastrointestinal losses of chloride-rich fluids associated with
vomiting in small animals or sequestration of chloride-rich fluid in
the abomasum and fore stomach of ruminants
• Mineralocorticoid excess
• Diuretic usage , low chloride intake cause or contribute to the
generation of a metabolic alkalosis
• Decreased effective circulating volume induce are central features
of the processes
• Potassium depletion (hypokalemia)
• Decreased glomerular filtration of bicarbonate
14. Compensation
• Chemoreceptors in the respiratory center sense the alkalosis, and the
respiratory response to a metabolic alkalosis is hypoventilation resulting
in an increase in p CO 2 . In dogs, the expected compensating response
is an increase of p CO 2 of 0.7 mmHg for each mEq/l increase in
bicarbonate.
15. Respiratory Alkalosis
• Increase in pH and a decrease in p CO 2 .
• Causes:
• Respiratory alkalosis is due to hyperventilation due to hypoxemia (Anemia)
• Hyperventilation may also be associated with psychogenic disturbances or
neurological disorders that stimulate the medullary respiratory center
• Salicylate intoxication
• Gram-negative sepsis.
• Hyperventilation may occur in dogs and other nonsweating animals as they
employ respiratory evaporative processes for heat loss to prevent
overheating
16. Compensation
• Cellular buffering
• Renal responses result in decreased ECF bicarbonate concentration through
reduced renal bicarbonate reabsorption.
• The decline in bicarbonate is partially offset by chloride retention in order to
retain electro neutrality. Thus, hyperchloremia
• In dogs, anticipated renal compensation for a chronic respiratory alkalosis results
in a decrease of bicarbonate of 0.55 mEq/l for each mmHg decrease in p CO 2
17. Mixed acid base imbalance
• Overcompensation
• Anion gap = (sodium + potassium) - (chloride + bicarbonate)
18. 18
Diagnosis of Acid-Base Imbalances
1. Note whether the pH is low (acidosis) or high (alkalosis)
2. Decide which value, pCO2 or HCO3
- , is outside the normal range
and could be the cause of the problem. If the cause is a change in
pCO2, the problem is respiratory. If the cause is HCO3
- the problem
is metabolic.
3. Look at the value that doesn’t correspond to the observed pH
change. If it is inside the normal range, there is no compensation
occurring. If it is outside the normal range, the body is partially
compensating for the problem.
19. 19
Example
• A patient is in intensive care because he suffered a severe myocardial
infarction 3 days ago. The lab reports the following values from an
arterial blood sample:
• pH 7.3
• HCO3- = 20 mEq / L ( 22 - 26)
• pCO2 = 32 mm Hg (35 - 45)
Diagnosis
• Metabolic acidosis
• With compensation