Acid Base Disorders Apply acid base physiology to identify acid base d/o Respiratory acidosis/alkalosis Classify types of metabolic acidosis “anion gap”

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Presentation transcript:

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 HCO 3 from body Metabolic alkalosis

pH = log [HCO 3 - ] = log kidney PCO 2 lung

HCO 3 - H + added to NH 3 becomes NH 4 + Urine pH 4.5 Still [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 HCO 3 - 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 PCO 2 ) metabolic (means starts with change in [HCO 3 - ]) simple mixed pH = log [HCO 3 - ] = log kidney PCO 2 lung

[HCO 3 - ] = 8 mEq/l PCO 2 = 27 mmHg pH = 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 PCO 2 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 + + HCO 3   H 2 CO 3    CO 2

The low side: what can make the [HCO 3 - ] fall below 24 mEq/l (What are the causes of “metabolic” acidosis?)

AG=Na + -HCO 3 -Cl -

Anion-Gap Acidosis Lactic acidosis Ketoacidosis Ingestion –Salicylates –Methanol –Ethylene glycol Renal Failure

pH 7.0 AG=22 pH 6.91 pCO 2 12 mmHg HCO 3 < 5 mEq/L AG=26

Normal-Gap Acidosis GI loss of HCO 3 –Diarrhea Renal loss of HCO 3 –Proximal Renal Tubular Acidosis –Distal Renal Tubular Acidosis AG=Na + -HCO 3 -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)

HCO 3 - H + added to NH 3 becomes NH 4 + RTA (more important for distal) Cannot acidify the urine: Urine pH is high (>6.0) Urine buffers (NH 4 + ) are low Putting a H + ion into the urine puts a HCO 3 - ion back into the ECF

[HCO 3 - ] = 14 mEq/l PCO 2 = 29 mmHg pH = 7.31 The acid base disorder is: 1.1 o low bicarb, normal respiratory response 2.1 o low bicarb, impaired respiratory response 3.1 o low PCO 2, normal kidney response 4.1 o low PC0 2, impaired kidney response

Bicarbonate is missing -- where did it go? [HCO 3 - ] = 14 mEq/lNa + = 140 mEq/l PCO 2 = 29 mmHgCl - = 114 mEq/l pH = 7.31“anion gap” = 12 meq/l

If there was no extra acid, why did the bicarbonate go down? [HCO 3 - ] = 11 mEq/l “Anion gap” = 12 mEq/l PCO 2 = 25 mmHg Urine pH = 6.5 pH = Lactic Acidosis 2.Chronic Diarrhea 3.Renal Tubular Acidosis (“RTA”)

[HCO 3 - ] = 30 mEq/l PCO 2 = 44 mmHg pH = 7.46 What is the acid base disorder? 1.1 o increase in bicarb and normal respiratory function 2.1 o increase in bicarb and impaired respiratory function 3. 1 o increase in PC0 2 due to impaired respiratory function

[HCO 3 - ] = 30 mEq/l PCO 2 = 44 mmHg pH = 7.46 What made this happen? Clues: the blood pressure is low the serum potassium is 2.8 mEq/l 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+ HCO

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