Chapter 7, cont…(Page 4)

Acid­base balance

CLINICAL APPROACH TO ACID­BASE DIAGNOSIS

The means to diagnose acid­base disorders, both simple and complicated, have been explained. Acid­base disorders refer to what is happening in the patient and represent physiologic processes, not just blood gas values. This concept allows diagnosis and management of difficult acid­base disorders. A rational approach to acid­base diagnosis and management is suggested below:

1. Find the acid­base disorder­serum HCO₃^- or arterial blood gas measurement.

2. Based on a full clinical assessment (history, physical examination, detailed laboratory review), explain the blood gas values in terms of physiologic processes and underlying clinical conditions.

3. Correct the pH if it is outside the range of 7.30­7.52.

4. Treat the underlying clinical condition.

SUMMARY

To maintain homeostasis, the body tries to keep the hydrogen ion concentration ([H⁺]) at approximately 40 nmoles/L or the pH close to 7.40. Deviation from this [H⁺] is minimized by buffering systems, all of which are in equilibrium with one another; the largest is the bicarbonate buffer system. Any change in acid­base status is reflected in the components of the bicarbonate buffer system­the bicarbonate ion (HCO₃^- ) and the arterial partial pressure of carbon dioxide (PaCO₂). The Henderson­Hasselbalch equation relates pH to HCO₃^- and PaCO₂.

There are four primary acid­base disorders, each with a compensatory response that minimizes the change in pH. Compensatory responses are not named alkalosis or acidosis. Metabolic acidosis tends to lower the pH and the HCO₃^- (compensatory response is hyperventilation). Metabolic alkalosis tends to raise the pH and the HCO₃^- (compensatory response is hypoventilation). Respiratory acidosis tends to raise the PaCO₂ and lower the pH (compensatory response is renal retention of HCO₃^-). Respiratory alkalosis tends to lower the PaCO₂ and raise the pH (compensatory response is renal excretion of HCO₃^-). Compensatory processes do not return the pH to normal; a truly normal pH in the presence of an acid­base disorder (e.g., pH of 7.40 and PaCO₂ of 25 mm Hg) indicates the presence of at least two primary acid­base disorders.

Each primary acid­base disorder should be viewed as a physiologic process caused by a specific clinical problem or disease and not simply as changes in blood gas values. This approach allows for unraveling complex or mixed acid­base disorders, which are particularly common in patients with severe respiratory disease.

REVIEW QUESTIONS

State whether each of the following is true or false.

1. Metabolic acidosis is present whenever the arterial pH is less than 7.35 and PaCO₂ is less than 35 mm Hg.

2. In acute respiratory acidosis, bicarbonate initially rises because of the reaction of carbon dioxide with water and the formation of H2CO3.

3. If every cation and every anion were measured in the serum, there would be no "anion gap."

4. By definition, a patient cannot have a state of metabolic acidosis and a state of metabolic alkalosis at the same time.

5. If pH and PaCO₂ are both above normal, bicarbonate must also be above normal.

6. The denominator of the Henderson­Hasselbalch equation equals 1.2 mEq/L when PaCO₂ equals 40 mm Hg.

7. One reason the measured serum bicarbonate may not agree with the value calculated from the pH and the PaCO₂ is the variation of the bicarbonate buffer system's pK value.

8. Diarrhea leads to metabolic alkalosis through the loss of gastrointestinal hydrogen ions.

9. A serum bicarbonate above normal, if accurate, always indicates an acid­base disorder.

10. The compensation for chronic respiratory acidosis is renal excretion of bicarbonate.

References

Goldberg, M., Green, S.B., Moss, M.L., et al.: Computer-based instruction and diagnosis of acid­base disorders, JAMA 223:269, 1973.

Hood, I., and Campbell, E.J.M.: Is pK OK? (editorial), N. Engl. J. Med. 306:864, 1982.

Mencken, H.L.: Exeunt Omnes, The Smart Set, p. 139, Dec. 1919.

Pierce, N.F., Fedson, D.S., Bingham, K.L., et al.: The ventilatory response to acute base deficit in humans, Ann. Intern. Med. 72:633, 1970.

Schwartz, W.B., and Relman, A.S.: A critique of the parameters used in the evaluation of acid­base disorders, N. Engl. J. Med. 268:1382, 1963.

Suggested readings

General

Brackett, N.C.: An approach to clinical disorders of acid­base balance, South. Med. J. 67:1084, 1974.

Cohen, J.J., and Kassiner, J.P.: Acid/base, Boston, 1982, Little, Brown & Co.

Elkington, J.R.: Acid­base disorders and the clinician, Ann. Intern. Med. 63:893, 1965.

Masoro, E.J., and Siegel, P.D.: Acid­base regulation: its physiology, pathophysiology and the interpretation of blood gas analysis, Philadelphia, 1977. W.B. Saunders Co.

McCurdy, D.K.: Mixed metabolic and respiratory acid­base disturbances: diagnosis and treatment, Chest Suppl. 62:35, 1972.

Winters, R.W.: Terminology of acid­base disorders, Ann. Intern. Med. 63:837, IY65.

See also General References in Appendix G.

Respiratory disorders

Arbus, G.S., Hebert, L.A., Levesque, P.R., et al.: Characterization and clinical application of the ''significance band'' for acute respiratory alkalosis, N. Engl. J. Med. 280:117, 1969.

Brackett, N.C., Cohen, J.J., and Schwartz, W.B.: Carbon dioxide titration curve of normal man, N. Engl. J. Med. 272:6, 1965.

Brackett, N.C., Wingo, F., Muren, O., ct al.: Acid­base response to chronic hypercapnia in man, N. Engl. J. Med. 280:124,1969.

Gennari, F.J., Goldstein, M.B., and Schwartz, W.B.: The nature of the renal adaption to chronic hypocapnia, J. Clin. Invest. 51:1722, 1972.

Ingram, R.H., Jr., Miller, R.B., and Tatc, L.A.: Acid­base response to acute carbon dioxide changes in chronic obstructive pulmonary disease, Am. Rev. Respir. Dis. 108:225, 1973.

Robin, E.D., Bromberg, P.A., and Tushan, F.S.: Carbon dioxide in body fluids, N. Engl. J. Med. 280:162, 1969.

Schwartz, W B., Brackett, N.C., and Cohen. J.J.: The response of extracellular hydrogen ion concentration to graded degrees of chronic hypercapnia: the physiologic limits of the defense of pH, J. Clin. Invest. 44:281, 1965.

van Ypersele de Strihou, C., Brasseur, L., and DeConnick, J.: The carbon dioxide response curve for chronic hypercapnia in man, N. Engl. J. Med. 275:117, 1966.

Metabolic disorders

Albert. M.S., Dell, R.B., and Winters, R.W.: Quantitative displacement of acid­base equilibrium in metabolic acidosis, Ann. Intern. Med. 66:312, 1967.

Emmet, M., and Narins, R.G.: Clinical use of the anion gap, Medicine (Baltimore) 56:38, 1977.

Fulop, M.: The ventilatory response in severe metabolic acidosis, Clin. Sci. Mol. Med. 50:367, 1976.

Fulop, M.: Hypercapnia in metabolic alkalosis, N. Y. State J. Med. 76:19, 1976.

Goldring, R.M., Cannon, P.J., Heinemann, H.O., et al.: Respiratory adjustment to chronic metabolic alkalosis in man, J. Clin. Invest. 47:188. 1968.

Jarboe, T.M., Penman, R.W., and Luke, R.G.: Ventilatory failure due to metabolic alkalosis, Chest Suppl. 61 :6 1, 1 972.

Lifschitz, M.D., Brasch, R., and Buomo, A.J.: Marked hypercapnia secondary to severe metabolic alkalosis, Ann. Intern. Med. 77:405, 1972.

Madias, N.E., Ayus, J.C., and Adrogue, H.J.: Increased anion gap in metabolic alkalosis, N. Engl. J. Med. 300:1421, 1979 .

Oh, M.S., and Carroll, H.J.: The anion gap, N. Engl. J. Med. 297:814, 1977.

Oliva, P.B.: Severe alveolar hypoventilation in a patient with metabolic alkalosis, Am. J. Med. 52:817, 1972.

Perez­Guerra, F.: Hypercapnia during iatrogenically induced metabolic alkalosis, Chest 65:108, 1974.

Tuller, M.A., and Mehdi, F.: Compensatory hypoventilation and hypocapnia in primary metabolic alkalosis, Am. J. Med. 50:281, 1971.

van Ypersele de Strihou, C., and Frans, A.: The respiratory response to chronic metabolic alkalosis and acidosis in disease, Clin. Sci. Mol. Med. 45:439, 1973.

Webb, J.: Severe hypercapnia associated with a nonrespiratory alkalosis, Br. J. Dis. Chest 72:62, 1978.

[Table of Contents][Previous Chapter][Chapter 7, Page 1][Chapter 7, Page 2][Chapter 7, Page 3][Next Chapter]