3. Introduction...
• Buffers : substances that resist change in pH
when acid or alkali is added
» Bicarbonate buffer
» Phosphate
» Protein
» Ammonia
• Levels of compensation
• Chemical Buffers
• Respiratory
• Renal
5. Metabolic acidosis
• Decrease in serum pH due to loss of plasma HCO3
- or
increase in H+ concentration
• Compensated by hyperventilation
• Causes
– NORMAL ANION GAP
I. Gastrointestinal bicarbonate loss
A. Diarrhea
B. External pancreatic or small-bowel drainage
C. Drugs
1. Calcium chloride (acidifying agent)
2. Magnesium sulfate (diarrhea)
6. II. Renal acidosis
RTA, CA inhibitors, tubular damage due to drugs or
toxins, Potassium-sparing diuretics (amiloride,
triamterene, spironolactone)
III. Others
A. Acid loads (ammonium chloride, hyperalimentation)
B. Loss of potential bicarbonate: ketosis with ketone
excretion
7. • High anion gap MA
• Lactic acidosis
• Ketoacidosis : Diabetic, Alcoholic, Starvation
• Toxins : methanol, ethylene glycol, salicylates
• Renal failure (acute and chronic)
9. Approach to a patient
• Obtain arterial blood gas (ABG) and electrolytes
simultaneously.
• Compare [HCO3
–] on ABG and electrolytes to verify
accuracy.
• Calculate anion gap (AG).
• Know four causes of high-AG acidosis (ketoacidosis,
lactic acid acidosis, renal failure, and toxins).
• Know two causes of hyperchloremic or nongap
acidosis (bicarbonate loss from GI tract, renal tubular
acidosis).
• Estimate compensatory response
10. Management
• Correction of underlying cause
• Alkali therapy : mainly in cases of salicylate
poisoning, inborn errors , pH<7
11. Metabolic alkalosis
• Net gain of HCO3
- or loss of non volatile acids
• Chloride responsive
– Gastric fluid loss
– Volume contraction
– Congenital chloride diarrhoea
– Post hypercapnia syndrome
• Chloride resistant
– Primary aldosteronism
– Renovascular HTN
– Liddle syndrome
12. Clinical features
• Nausea and vomiting
• Hypocalcemia: muscular cramping, tetany
• Hypokalemia : generalized weakness,
aggravation of arrhythmias
• Mental confusion and a predisposition to
seizures, paresthesia,, and hypoxemia in
chronic obstructive pulmonary disease
13. Management
• Correction of underlying etiology
• Severe cases with renal failure may require
dialysis
• Chloride responsive:
– IV infusion of NS ( Volume depletion )
– IV KCl ( edematous state )
– Diuretics if needed ; acetazolamide
• Chloride resistant
– Management of specific cause
– Acetazolamide if GFR adequate
17. Clinical features
• Respiratory: Air hunger, dyspnea
• Neurological symptoms like anxiety,
disorientation ,psychosis, hallucinations, coma
• CVS : tachycardia,
18. Compensation
• Acute
– HCO3
- production from intracellular proteins
– HCO3
- increases 1mEq/L for every 10mm Hg rise in
PaCO2
• Chronic
– Renal retention of HCO3
-
– HCO3
- increases 4mEq/L for every 10 mm Hg
– Takes 2-5 days for renal retention of HCO3
-
– Nearly normalizes pH
19. Management
• Correction of underlying cause
• Correct the minute ventilation
• Establish the airway
• Re-expand the lung
• Correct the CNS disease
• Bronchodilators
• Antibiotics
20. Respiratory alkalosis
• Increased minute ventilation leads to
decreased PaCO2 and alkalosis
• Acute : normal HCO3
-
• Chronic : decreased HCO3
- due to renal
compensation
21. Causes
Central nervous system stimulation
1. Pain
2. Anxiety, psychosis
3. Fever
4. Cerebrovascular accident
5. Meningitis, encephalitis
6. Trauma
B. Hypoxemia or tissue hypoxia
1. High altitude
2. Pneumonia, pulmonary edema
3. Aspiration
4. Severe anemia
22. C. Drugs or hormones
1. Pregnancy, progesterone
2. Salicylates
D. Miscellaneous
1. Septicemia
2. Mechanical hyperventilation
3. Recovery from metabolic acidosis
24. Management
• Correction of underlying disorder
• In case of hyperventilation syndrome :
reassurance, re-breathing into a paper bag
during acute episodes and treatment for
underlying psychological stress.