Acid Base Disorders

• Apply acid base physiology to identify acid base d/o• Respiratory acidosis/alkalosis• Classify types of metabolic acidosis

“anion gap” acidosis: introduction of acid into ECF“non-anion gap” acidosis: loss of HCO3 from body

• Metabolic alkalosis

pH = 6.1 + log [HCO3-] = 6.1 + log kidney

PCO2 lung

HCO3-

H+

added to NH3 becomes NH4+

Urine pH 4.5Still [H+] = 0.03 mEq/L

To excrete 70 mEq of H+,70 mEq/0.03 mEq/L=2,333 L urine per day

Putting a H+ ion into the urine puts a HCO3- ion back into the ECF

On an average diet, your cells dump acid into your ECF every day

Acid Base Disorders

respiratory (means starts with change in PCO2)metabolic (means starts with change in [HCO3

-])

simplemixed

pH = 6.1 + log [HCO3-] = 6.1 + log kidney

PCO2 lung

[HCO3-] = 8 mEq/l

PCO2 = 27 mmHgpH = 7.1

English: the bicarbonate concentration is down, and the blood pH is also down. So the patient has had an acid added to the body or bicarb has been lost. And the PCO2 is down, but it isn’t going down as much as it is does when the bicarbonate goes down in a normal person, so there’s a respiratory problem too.

Medicalese: poorly compensated metabolic acidosis

Respiratory acidosis/alkalosis

H+ + HCO3- H2CO3 H2O + CO2

The low side: what can make the [HCO3-]

fall below 24 mEq/l

(What are the causes of “metabolic” acidosis?)

AG=Na+-HCO3-Cl-

Anion-Gap Acidosis

• Lactic acidosis• Ketoacidosis• Ingestion

– Salicylates– Methanol– Ethylene glycol

• Renal Failure

pH 7.0AG=22

pH 6.91pCO2 12 mmHgHCO3 < 5 mEq/LAG=26

Normal-Gap Acidosis

• GI loss of HCO3

– Diarrhea• Renal loss of HCO3

– Proximal Renal Tubular Acidosis– Distal Renal Tubular Acidosis

AG=Na+-HCO3-Cl-

The renal tubule could have failed to reabsorb bicarbonate and secret H+.. This is called “renal tubular acidosis.”

You can easily think of two types:

distal renal tubular acidosis(type I)

proximal renal tubular acidosis (type II)

HCO3-

H+

added to NH3 becomes NH4+

RTA (more important for distal)

Cannot acidify the urine:Urine pH is high (>6.0)Urine buffers (NH4

+) are low

Putting a H+ ion into the urine puts a HCO3- ion back into the ECF

[HCO3-] = 14 mEq/l

PCO2 = 29 mmHgpH = 7.31

The acid base disorder is:

0%0%0%0%

1. 1o low bicarb, normal respiratory response2. 1o low bicarb, impaired respiratory response3. 1o low PCO2, normal kidney response

4. 1o low PC02, impaired kidney response

Bicarbonate is missing -- where did it go?

[HCO3-] = 14 mEq/l Na+ = 140 mEq/l

PCO2 = 29 mmHg Cl- = 114 mEq/lpH = 7.31 “anion gap” = 12 meq/l

140 114

14

If there was no extra acid, why did the bicarbonate go down?

[HCO3-] = 11 mEq/l “Anion gap” = 12 mEq/l

PCO2 = 25 mmHg Urine pH = 6.5 pH = 7.27

0%0%0%0%1. Lactic Acidosis

2. Chronic Diarrhea3. Renal Tubular Acidosis (“RTA”)

[HCO3-] = 30 mEq/l

PCO2 = 44 mmHgpH = 7.46

What is the acid base disorder?

1. 1o increase in bicarb and normal respiratory function

2. 1o increase in bicarb and impaired respiratory function

3. 1o increase in PC02 due to impaired respiratory function

[HCO3-] = 30 mEq/l

PCO2 = 44 mmHgpH = 7.46

What made this happen? Clues: the blood pressure is low the serum potassium is 2.8 mEq/l

0%0%0%1. use of furosemide in a patient with CHF

2. use of an ACE inhibitor in a patient with CHF

3. use of spironolactone

ALDOSTERONE

Na+

K+H+

HCO3-

- - - - - - - - - - - - - - - - - -

Metabolic alkalosis• Volume depletion

– AII stimulates NHE3 activity– Aldo stimulates H+ pump, ENaC

• Hyperaldosteronism• Chloride depletion

– Renin increases• Hypokalemia

– H+/K+ ATPase in the distal nephron