2. Metabolic Disorders
• Processes that directly alter
bicarbonate concentration
Metabolic acidosis: decreased
bicarbonate
• Metabolic alkalosis: increased
bicarbonate
3. Respiratory Disorders
• Processes that directly alter CO2
• Respiratory acidosis: increased CO2
• Respiratory alkalosis: decreased CO2
• Buffer effect: slightly increased HCO3
with respiratory acidosis. Slightly
decreased HCO3 with respiratory
alkalosis.
4. Metabolic acidosis
• Process that reduces plasma bicarbonate
concentration
• Etiology:
• Decreased renal acid excretion
• Direct bicarbonate losses (GI tract or urine)
• Increased acid generation (exogenous or
endogenous)
5. Causes of metabolic acidosis
• 1) increased acid generation
• Lactic acidosis, Ketoacidosis, ingestion of
acids (aspirin, ethylene glycol, methanol),
dietary protein intake (animal source)
• 2) loss of bicarbonate
• Gastrointestinal (diarrhea, intestinal
fistulas)
• Renal: type 2 proximal renal tubular
acidosis
6. Causes of metabolic acidosis
• 1) decreased acid excretion (impaired
NH4+ excretion)
• Renal failure (reduced GFR) decreased
ammonium excretion
• Type I (distal) renal tubular acidosis
• Type 4 renal tubular acidosis
(hypoaldosteronism)
7. Respiratory acidosis
• Induced by hypercapnia (decreased alveolar
ventilation)
• Buffering mechanisms raise plasma bicarbonate
concentration (rapid but limited response, ~1-2
meq/l)
• Kidney minimizes the change in extracellular pH
by increasing acid excretion (NH4+) generating
new bicarbonate ions (delayed response, 2-3
days).
8. Respiratory alkalosis
• Reduced carbon dioxide due to increased
alveolar ventilation
• Buffering processes lower plasma
bicarbonate concentration (rapid but
limited response, ~1-2 meq/l)
• Kidney response is to reduce net acid
excretion (eliminate bicarbonate into the
urine or decrease ammonium excretion).
Delayed response, 1-2 days)
9. Respiratory disorders
• Acute respiratory acid base disorders
always have a greater change in pH than
chronic disorders
• Plasma Cl changes equally and inversely
with plasma HCO3.
• Plasma anion gap does not change with
respiratory disorders
• Plasma sodium is not directly altered by
acid base disorders
10. Metabolic alkalosis
• Processes that raise plasma bicarbonate
concentration
• Etiology: Loss of hydrogen ion from the GI
tract (vomiting) or into the urine (diuretic
therapy)
• Excessive urinary net acid excretion
(primary hyperaldosteronism)
12. Expected pH Changes for
Respiratory Disorders
• Acute Respiratory Acidosis:
HCO3
- increases 1 mEq for each 10 mm increase in PCO2
• Chronic Respiratory Acidosis:
HCO3
- increases 4 mEq for each 10 mm increase in
PCO2
• Acute Respiratory Alkalosis:
HCO3
- decreases 2 mEq for each 10 mm decrease in
PCO2
• Chronic Respiratory Alkalosis:
HCO3
- decreases 5 mEq for each 10 mm decrease in
PCO
13. Plasma anion gap
Strong acids (HA) fully dissociate at physiologic
pH (7.40) into H+ and A-
H+ is buffered by HC03-
A- is either excreted into the urine (normal plasma
anion gap, increased plasma chloride
concentration)
Or, A- is reabsorbed by the kidney and retained in
plasma, as an unmeasured anion (increased
plasma anion gap, minimal change in plasma
chloride concentration)
14.
15.
16. Renal acid excretion
• All of the filter of bicarbonate must be
reabsorbed (primarily in the proximal
tubule and loop of Henle)
• Final excretion of the daily acid load
occurs primarily in the collecting duct
(approximately 50-100 meq/d)
17. Titratable acidity
• Phosphate homeostasis is maintained by
urinary excretion of dietary phosphate
• Monobasic phosphate is an effective
urinary buffer, esp. at lower urinary pH
• Accounts for excretion of 10 to 40 mEq of
hydrogen ion daily
• Cannot be increased beyond this due to
the fixed amount of phosphate in urine
18. Ammonium excretion
• Contributes the major adaptive response
to an acid load
• Can be increased in response to
physiologic needs
• Normally 30-40 mEq/d and maximal
excretion is approximately 300 mEq/d
• NH4+ is lipid soluble and therefore trapped
in the urinary lumen
19. Urine anion gap
• An indirect estimate of urinary NH4+
excretion
• Urine Na + K minus urine Cl
• Normally, ~ 10 meq/l
• Becomes less positive and may even
become neg with incr urinary NH4
excretion (Cl- must accomany NH4+)
20. Sodium and Chloride relationship
• Law of electroneutrality:
• Sodium concentration is not directly altered by
acid base disorders
• Plasma Cl is altered in all acid base disorders
(except increased plasma anion gap metaboic
acidosis)
• Conclusion: If sodium concetration stays
constant but chloride conc changes, an acid
base disorder is present
21. Mixed Acid-base disorders
• The presence of more than one simple acid-
base disorder simultaneously:
• Respiratory acidosis and metabolic acidosis
(profound acidemia)
• Respiratory alkalosis and metabolic alkalosis
(profound alkalemia)
• Metabolic alkalosis and respiratory acidosis
• Metabolic acidosis and respiratory alkalosis
