938
chapter
39
Water, Electrolytes, and Acid-Base Balance
TABLE 39-2
Important Causes o f Mixed Acid-Base Disturbances*
Respiratory acidosis with metabolic acidosis
Example:
Cardiopulmonary arrest
Severe pulmonary edema
Drug ingestion with central nervous
system depression
Respiratory alkalosis and metabolic alkalosis
Example:
Hepatic failure and diuretics
Patients on ventilation given
nasogastric suction
Respiratory alkalosis and metabolic acidosis
Example:
Septic shock
Renal failure with sepsis
Salicylate overdose
Respiratory acidosis and metabolic alkalosis
Example:
Chronic lung disease and diuretic use
Mixed acute and chronic respiratory acidosis
Example:
Chronic lung disease and
superimposed infection
Metabolic acidosis and metabolic alkalosis
Example:
Renal failure and vomiting
Vomiting and hypotension
(lactic acidosis)
*Reproduced, with permission, from M. Bia and S. O. Thier: Mixed
acid-based disturbances: A clinical approach.
M e d . C lin . N o r th A m .
65, 347(1981).
of some diuretics and increased aldosterone production
can cause the hypokalemia that initiates this type of
alkalosis.
In compensation, the respiratory rate decreases, raising
Pco
2
and lowering the pH of blood. This mechanism is
limited because if the respiratory rate falls too low, P
Û2
de-
creases to the point where respiration is again stimulated.
Renal compensation involves decreased reabsorption of
bicarbonate and formation of alkaline urine. Because the
urinary bicarbonate is accompanied by Na+ and K+, if
the alkalosis is accompanied by extracellular fluid deple-
tion, renal compensation by this mechanism may not be
possible.
Treatment consists of fluid and electrolyte replacement
and NH
4
C1 to counteract the alkalosis.
Acid-base disturbances frequently coexist with two or
more simple disorders (Table 39-2). In these settings,
blood pH is either severely depressed (e.g., a patient with
metabolic acidosis and respiratory acidosis) or normal.
Both plasma HCO, and pH may be within normal lim-
its when metabolic alkalosis and metabolic ketoacidosis
coexist, as in a patient with diabetic ketoacidosis who is
vomiting. In this situation, an elevated anion gap may be
the initial abnormality that can be detected in the under-
lying mixed acid-base disturbance.
Supplemental Readings and References
H. J. Adrogue and N. E. Madias: Management of life-threatening acid-base
disorders.
N ew E n g la n d J o u rn a l o f M ed icin e
338, 26 (1998).
D. G. Bichet: Nephrogenic diabetes insipidus.
A m e rica n J o u rn a l o f M ed icin e
105,431 (1998).
S. L. Gluck: Acid-base.
L a n c e t
352,474 (1998).
M. L. Halperin and K. S. Kamel: Potassium.
L a n cet
352, 135 (1998).
V. L. Hood and R. L. Tannen: Protection of acid-base balance by pH reg-
ulation of acid production.
N ew E n g la n d J o u rn a l o f M ed icin e
339, 819
(1998).
S. Klahr and S. B. Miller: Acute oliguria.
N ew E n g la n d Jo u rn a l o f M ed icin e
338,671 (1998).
S. J. Scheinman, L. M. Guay-Woodford, R. V. Thakker, et al.: Genetic dis-
orders of renal electrolyte transport.
N ew E n g la n d J o u rn a l o f M ed icin e
340, 1177(1999).
J. Uribarri, M. S. Oh, and H. J. Carroll: D-Lactic acidosis.
M ed icin e
77, 73
(1998).
K. D. Wrenn, C. M. Slovis, G. E. Minion, et al.: The syndrome of alcoholic
ketoacidosis.
A m erica n J o u rn a l o f M ed icin e
91, 119 (1991).
H. J. Androgue and N. E. Madias: Hyponatremia
N ew E n g la n d J o u rn a l o f
M ed icin e M 2 ,
1581 (2000).
