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C HAP TE R 7 / Fluid and Electrolyte and Acid–Base Balance and Imbalance 171

Respiratory alkalosis causes increased pH inside myocardial cells The initial clinical manifestations of metabolic alkalosis are of-
and increases cardiac contractility by increasing the calcium sensitiv- ten milder than those of respiratory alkalosis because bicarbonate
ity of myofibrils as shown in classic work by Hunjan et al. 162 The im- ions cross membranes (and thus alter CSF and intracellular pH)
balance also increases sympathetic nervous system activity and circu- less rapidly than does carbon dioxide. These clinical manifesta-
lating catecholamines that may cause cardiac arrhythmias. Although tions may include light-headedness, paresthesias, muscle cramps,
respiratory alkalosis may cause a transient peripheral vasodilation, carpal and pedal spasms, and cardiac arrhythmias. An initial CNS
which decreases peripheral vascular resistance, it is most likely to excitation is followed by the CNS depression of severe metabolic
cause peripheral vasoconstriction and increased peripheral vascular alkalosis: confusion, lethargy, and coma. The plasma bicarbonate
resistance. 163,164 Respiratory alkalosis also causes coronary and cere- ion concentration is elevated.
bral vasoconstriction. 164,165 This latter effect reduces intracranial Correction of metabolic alkalosis must be accomplished by the
pressure and cerebral blood flow and may be the reason for the light- kidneys because they are the excretory organs for bicarbonate ions.
headedness and syncope experienced by some individuals with res- Compensation for the disorder, therefore, is the role of the lungs.
piratory alkalosis. In contrast to its effect on other blood vessels, res- Because the bicarbonate ion concentration is increased in meta-
piratory alkalosis causes pulmonary vasodilation. 147 This effect is bolic alkalosis, the 20:1 ratio of bicarbonate ion to carbonic acid
decreased in conditions with chronically increased pulmonary blood that creates a normal pH can be restored by increasing the amount
flow, such as some congenital heart defects. 166 of carbonic acid in the blood. Thus, the respiratory compensation
for metabolic alkalosis is decreased rate and depth of respira-
Metabolic Alkalosis tion. 169 This compensatory hypoventilation retains carbonic acid
Metabolic alkalosis is caused by relatively too little metabolic acid. It (carbon dioxide and water) in the body, which tends to normal-
can be due to a loss of acid or a gain of base. 139 Acid can be lost ize the pH. Compensatory hypoventilation, however, is limited
through the gastrointestinal tract or in the urine. Acid may also be by the body’s need for oxygen, so full compensation for meta-
shifted into cells and thus “lost” from the blood. Base (bicarbonate bolic alkalosis is not common. Compensated metabolic alkalosis
ions) may be gained from intake of bicarbonate or of substances that is characterized by an increased Pa CO2 (the sign of the respiratory
are converted to bicarbonate in the body. More commonly, base is compensation), an increased bicarbonate ion concentration (the
gained through renal bicarbonate reabsorption. For example, di- sign of the primary problem), and a pH that is somewhat in-
uretic therapy often causes a mild “contraction alkalosis,” metabolic creased (partially compensated).
3
alkalosis associated with extracellular volume contraction. Contrac- Metabolic alkalosis causes increased cardiac contractility by
tion alkalosis is especially common with loop and thiazide diuretic increasing calcium sensitivity, although intracellular pH does not
therapy for heart failure because a high volume of sodium is deliv- increase in myocardial cells as it does in respiratory alkalosis. 162
ered to the distal tubules by the diuretic in the presence of excessive Cardiac arrhythmias may occur. Vascular effects are likely to include
stimulation of distal tubule mineralocorticoid receptors from the peripheral vasoconstriction. Other vascular effects of metabolic al-
elevated aldosterone that is a compensatory mechanism in heart fail- kalosis are coronary vasoconstriction, pulmonary vasodilation, and
ure. 167,168 In an individual with hypovolemic shock from hemor- cerebral vasoconstriction with resulting decreased cerebral blood
rhage, a metabolic alkalosis may develop if eight or more units of flow and light-headedness. 147
packed red cells or other forms of blood are infused in a short time
because the liver metabolizes the citrate in the blood into bicarbon- Principles of Interpreting Arterial
ate. Additional causes of metabolic alkalosis are listed in Table 7-21.
Blood Gas Reports
Arterial blood gases are used to assess an individual’s acid–base sta-
tus. The material presented earlier in this chapter provides the ba-
Table 7-21 ■ CAUSES OF METABOLIC ALKALOSIS
sis for understanding and interpreting acid–base aspects of arterial
Category Clinical Examples blood gases. The principles are summarized in this section. The
Pa O2 , a measure of oxygenation, is discussed in Chapter 2.
Decrease of acid Emesis 170
Gastric suction The first laboratory value to consider is the pH. If the pH
Hyperaldosteronism (increases renal excretion is below the normal range (i.e., less than 7.35 or the reported lab-
of acid) oratory normal), then the individual has acidosis. If the pH is
Chronic excessive ingestion of black licorice above the normal range (greater than 7.45 or the reported labora-
(contains aldosterone-like compounds) tory normal), then the individual has alkalosis. If the pH is within
Glucocorticoid excess
Loop or thiazide diuretics the normal range, there may be no acid–base imbalance, or the in-
Hypokalemia (acid moves into cells) dividual may have a fully compensated imbalance. For purposes of
Increase of base Excess ingestion of baking soda or bicarbonate interpretation, then, if the pH is less than 7.40, the individual is
(bicarbonate ions) antacids tentatively considered to have acidosis; if the pH is greater than
Excess infusion of NaHCO 3 7.40, the individual is tentatively considered to have alkalosis.
Excess administration of lactate or acetate
(convert to bicarbonate) The next value to consider is the Pa CO2 . If the Pa CO2 is above
Massive blood transfusion (citrate converts to the normal range, then the individual has respiratory acidosis.
bicarbonate) This respiratory acidosis may be the primary problem, or it may
Citrate anticoagulation during chronic renal be compensatory. On the other hand, if the Pa CO2 is below the
replacement therapy (citrate converts to
bicarbonate) normal range, then the individual has respiratory alkalosis. This
Extracellular fluid volume deficit (contraction respiratory alkalosis may be the primary problem or it may be
alkalosis) compensatory. If the Pa CO2 is within the normal range, then the
individual does not have a respiratory acid–base disorder.