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974 PART 8: Renal and Metabolic Disorders

mineralocorticoid activity. Treatment requires that the underlying
disorder be addressed. KEY REFERENCES
• De Backer D, Creteur J, Zhang H, et al. Lactate production by the
OTHER CAUSES OF METABOLIC ALKALOSIS lungs in acute lung injury. Am J Resp Cirt Care Med. 1997;156:1099.
• Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment
Rarely, an increased SID (and therefore metabolic alkalosis) occurs sec-
ondary to cation administration rather than anion depletion. Examples of lactic acidosis. Chest. 2000;117:260.
of these disorders include milk-alkali syndrome and intravenous admin- • Gattinoni L, Lissoni A. Respiratory acid-base disturbances in
istration of strong cations without strong anions. The latter occurs with patients with critical illness. In: Ronco C, Bellomo R, eds. Critical
massive blood transfusion or plasma exchange because Na is given with Care Nephrology. Dordrecht, the Netherlands: Kluwer Academic
+
citrate (a weak anion) instead of Cl . Similar results occur when paren- Publishers; 1998:297.
−
teral nutrition formulations contain too much acetate and not enough • Kellum JA. Determinants of blood pH in health and disease. Crit
Cl to balance the Na load. Care. 2000;4:6.
+
−
• Kellum JA, Kramer DJ, Lee KH, et al. Release of lactate by the lung
RESPIRATORY ACID-BASE DISORDERS in acute lung injury. Chest. 1997;1111:1301.
■ PATHOPHYSIOLOGY OF RESPIRATORY ACID-BASE DISORDERS • Kellum JA, Song M, Venkataraman R. Effects of hyperchloremic
acidosis on arterial pressure and circulating inflammatory mol-
CO production by the body (at 220 mL/min) is equal to 15,000 mM/day ecules in experimental sepsis. Chest. 2004;125:243.
2
of carbonic acid. This compares with less than 500 mM/day (depend- • Levy B, Bollaert P-E, Charpentier C, et al. Comparison of norepi-
39
ing on diet) for all nonrespiratory acids, which are managed by the nephrine and dobutamine to epinephrine for hemodynamics, lac-
kidney and gut. Pulmonary ventilation is adjusted by the respiratory tate metabolism, and gastric tonometric variables in septic shock:
, as well as some
center in response to signals from P CO 2 , pH, and P O 2 a prospective, randomized study. Intensive Care Med. 1997;23:282.
of 40 mm Hg
from exercise, anxiety, and wakefulness. The normal P CO 2 • Stacpoole PW. Lactic acidosis and other mitochondrial disorders.
is attained by a precise match of alveolar ventilation to metabolic CO Metab Clin Exp. 1997;46:306.
2
changes in a “compensatory” ventilatory response
production. P CO 2 • Stewart PA. How to Understand Acid-Base: A Quantitative Acid-
to altered arterial pH produced by metabolic acidosis or alkalosis in
predictable ways. Base Primer for Biology and Medicine. New York: Elsevier; 1981.
■ DISEASES OF VENTILATORY IMPAIRMENT • Van Lambalgen AA, Runge HC, van den Bos GC, Thijs LG.
Reginal lactate production in early canine endotoxin shock. Am J
As for virtually all acid-base disorders, treatment begins with address- Physiol. 1988;254:E45.
ing the underlying disorder. Acute respiratory acidosis can be caused by • Wrenn KD, Slovis CM, Minion GE, Rutkowski R. The syndrome
CNS suppression, neuromuscular disease or impairment (eg, myasthenia of alcoholic ketoacidosis. Am J Med. 1991;91:119.
gravis, hypophosphatemia/hypokalemia), severe mechanical derange-
ments of the chest wall, or airway and parenchymal lung disease REFERENCES
(eg, asthma, acute respiratory distress syndrome [ARDS], etc). This last
category of conditions also produces primary hypoxia, not just alveolar Complete references available online at www.mhprofessional.com/hall
hypoventilation. The two can be distinguished by the alveolar gas equation:
/R
P AO 2 = P IO 2 − P CO 2 CHAPTER Hyperglycemic Crisis
where R is the respiratory exchange coefficient (generally taken as and Hypoglycemia
is the inspired oxygen tension (room air is approximately 101
0.8), P IO 2
increases the
150 mm Hg), and P AO 2 is the alveolar P O 2 . Thus, as P CO 2 David Carmody
is significantly
P AO 2 will decrease in a predictable fashion. If the P AO 2 Louis Philipson
, there is a defect in gas exchange.
lower than the calculated P AO 2
Chronic respiratory acidosis is caused most often by chronic lung
disease (eg, chronic obstructive pulmonary disease [COPD]) or chest INTRODUCTION
wall disease (eg, kyphoscoliosis). Rarely, its cause is central hypoventila-
tion or chronic neuromuscular disease. Hyperglycemia crisis and hypoglycemia are both life-threatening
medical emergencies but are usually readily treatable if recognized
■ RESPIRATORY ALKALOSIS early. Hyperglycemic crises comprise diabetic ketoacidosis (DKA) and
Respiratory alkalosis may be the most frequently encountered acid- hyperosmolar hyperglycemic state (HHS). While some elements of
their clinical presentation and pathophysiology are distinct, the general
base disorder. It occurs in residents at high altitude and in a number of principles of treatment are similar. They will be discussed together.
pathologic conditions, the most important of which include salicylate Hypoglycemia is a problem commonly seen in patients with diabetes
intoxication, early sepsis, hepatic failure, and hypoxic respiratory disorders. mellitus (DM) and requires prompt treatment. The common causes and
Respiratory alkalosis also occurs with pregnancy and with pain or anxiety. treatment regimens will be outlined here.
Hypocapnia appears to be a particularly bad prognostic indicator in
patients with critical illness. As in acute respiratory acidosis, acute HYPERGLYCEMIC CRISIS
40
respiratory alkalosis results in a small change in [HCO ], as dictated by
−
3
the Henderson-Hasselbalch equation. If hypocapnia persists, the SID
will begin to decrease as a result of renal Cl reabsorption. After 2 to KEY POINTS
−
3 days, the SID will assume a new, lower steady state. Severe alkalemia • Hyperglycemic crisis has a high mortality, particularly in the elderly.
41
is unusual in respiratory alkalosis, and management therefore is directed
to the underlying cause of the acid-base disorder. Typically, these mild • Mortality rates are falling due to improved recognition and medi-
acid-base changes are more important clinically as an alarm than as any cal care.
threat they pose to the patient.

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