1. Acid Base Anthony R Mato, MD

2. Basics Normal pH is 7.38 to 7.42 Key players are CO2 and HCO3 – concentrations “emia” : refers to blood pH Acidemia : pH < 7.38 Alkalemia : pH > 7.42 pH of 7.4 = 40 neq / L H+ A change of.1 pH = 1 neq / L (7.1 – 7.5 range)

3. Basics Acidosis / Alkalosis : refer to processes which cause acid / alkali to accumulate. They do not imply any abnormality in the pH. Buffer: substance which can absorb / donate ions and mitigate but not prevent changes in pH. Compensation is a not a perfect process. If we were to correct an acid/base disturbance it would be removing the stimulus to do so.

4. Modified Henderson and Hasselbalch Equation H+ = 24 x PCO2/HCO3 Equation emphasizes that the [H] depends on a ratio and not absolute concentrations.

5. The Anion Gap Na – (Cl + HCO3) NaHCO3 + HCL  NaCL + H2CO3 NaHCO3 + HX  NaX+ H2CO3 Unmeasured cations: calcium, magnesium, gamma globulins, potassium. Unmeasured anions: albumin, phosphate, sulfate, lactate.

6. Decreased anion gap Decrease in unmeasured anions –Hypoalbuminemia Increase in unmeasured cations –Hypercalcemia –Hypermagnesemia –Hyperkalemia –Multiple myeloma –Lithium toxicity

7. Potassium Potassium : weather vein : The serum K can be used as a poor man’s pH meter in the absence of pH measure. This can help to differentiate between acidosis vs. compensated alkalosis for example in the setting of a low HCO3. This effect is stronger for inorganic acidoses.

8. Simple Acidoses

9. Respiratory Acidosis Elevation of CO2 above normal with a drop in extracellular pH. This is a disorder of ventilation. Rate of CO2 elimination is lower than the production 5 main categories: –CNS depression –Pleural disease –Lung diseases such as COPD and ARDS –Musculoskeletal disorders –Compensatory mechanism for metabolic alkalosis

10. Respiratory Acidosis Acute or Chronic: has the kidney had enough time to partially compensate? The source of the BUFFER (we need to produce bicarb) is different in these states and thus we need to make this distinction.

11. Respiratory Acidosis Acute : H is titrated by non HCO3 organic tissue buffers. Hb is an example. The kidney has little involvement in this phase. –10 mm Hg increase in CO2 / pH should decrease by.08 Chronic: The mechanism here is the renal synthesis and retention of bicarbonate. As HCO3 is added to the blood we see that [Cl] will decrease to balance charges. –This is the hypochloremia of chronic metabolic acidosis. –10 mm H increase in CO2 / pH should decrease by.03

12. Respiratory Alkalosis Initiated by a fall in the CO2  activate processes which lower HCO3. Associated with mild hypokalemia. Cl is retained to offset the loss of HCO3 negative charge. Acute response is independent of renal HCO3 wasting. The chronic compensation is governed by renal HCO3 wasting. Causes –Intracerebral hemorrhage –Drug use : salicylates and progesterone –Decreased lung compliance Anxiety –Liver cirrhosis –Sepsis

13. Respiratory Alkalosis Acute or Chronic: has the kidney had enough time to partially compensate? –Acute : 10 mm Hg decrease in CO2 / pH should increase by.08 –Chronic : 10 mm H decrease in CO2 / pH should increase by.03 After two weeks we may have a complete compensation at the level of the kidney. This is demonstrated in people living at high altitudes (hypoxia induced hyperventilation).

14. Metabolic Acidosis Gap vs. Non-Gap Where does the normal gap of 12 come from? –It is the difference between unmeasured cations and anions. Anion gap acidosis: 4 major categories –Renal failure –Ketoacidosis : diabetes / alcohol withdrawal –Drugs or Poisons : methanol, salicylates, paraldehyde, ethylene glycol. –Lactic acidosis: associated with inadequate tissue perfusion.

15. Non Gap Acidosis H: hyperalimentation A: acetazolamide R: RTA D: diarrhea U: rectosigmoidostomy P: pancreatic fistula

16. Metabolic Acidosis Respiratory compensation process takes 12-24 hours to become fully active. Protons are slow to diffuse across the blood brain barrier. In the case of LA this will be faster because LA is produced in the brain. The degree of compensation can be assessed by using Winter’s Formula. It is INAPPROPRIATE to use this formula before the acidosis has existed for 12-24 hours. –PCO2 = 1.5 (HCO3) + 8 +/-2. –In steady state chronic metabolic acidoses the pCO2 almost invariably approximates the last two digits of the measured arterial pH.

17. Metabolic Alkalosis Generation by gain of HCO3 and maintained by abnormal renal HCO3 absorption. This is almost always secondary to volume contraction (low Cl in urine, responsive to NaCl, maintained at proximal tubule) –Vomiting: net loss of H+ and gain of HCO3. –Diuretics: ECFV depletion –Chronic diarrhea: ECFV depletion –Profound hypokalemia –Renal failure: if we cannot filter HCO3 we cannot excrete it. Mineralocorticoid excess: increased H secretion, hypokalemia (Na/K exchanger), saline resistant).

18. Metabolic Alkalosis The compensation will be to depress the respiratory drive and return the ratio towards normal by a rising PCO2. This is NOT as consistent as the linear PCO2 response seen in MA. Winter’s formula does not apply here. –PCO2 =.9 (HCO3) + 9 –If the CO2 is < normal: we clearly have a resp alkalosis additionally. –Rarely will pCO2 be > 55 in pure compensation, so a CO2 that is more elevated then expected will indicate respiratory acidosis.

19. 5 Step Approach Acidemic or Alkalemic : Check and ABG Is the overriding disturbance respiratory or metabolic? –If respiratory, is it acute or chronic? : equations 1-4. –If metabolic acidosis is present, is there an elevated AG. If metabolic acidosis disturbance is present is the respiratory system compensating adequately? WINTER’S FORMULA. Are other metabolic disturbances present in a patient with a anion gap metabolic acidosis? –This is the famous delta delta approach which aims at calculating the bicarbonate level before the generation of the anion gap acidosis. –Measured bicarbontae + (AG – 12)