Water, Electrolytes, and Acid-Base Balance
TABLE 39-2
Important Causes o f Mixed Acid-Base Disturbances*
Respiratory acidosis with metabolic acidosis
Cardiopulmonary arrest
Severe pulmonary edema
Drug ingestion with central nervous
system depression
Respiratory alkalosis and metabolic alkalosis
Hepatic failure and diuretics
Patients on ventilation given
nasogastric suction
Respiratory alkalosis and metabolic acidosis
Septic shock
Renal failure with sepsis
Salicylate overdose
Respiratory acidosis and metabolic alkalosis
Chronic lung disease and diuretic use
Mixed acute and chronic respiratory acidosis
Chronic lung disease and
superimposed infection
Metabolic acidosis and metabolic alkalosis
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
In compensation, the respiratory rate decreases, raising
and lowering the pH of blood. This mechanism is
limited because if the respiratory rate falls too low, P
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
Treatment consists of fluid and electrolyte replacement
and NH
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
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
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
K. D. Wrenn, C. M. Slovis, G. E. Minion, et al.: The syndrome of alcoholic
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).
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