Adaptation to respiratory alkalosis. Respiratory alkalosis, or primary hypocapnia, is the acid-base disturbance initiated by a decrease in arterial carbon dioxide tension (PaCO2) and entails alkalinization of body fluids. Hypocapnia elicits adaptive decrements in plasma bicarbonate concentration that should be viewed as an integral part of respiratory alkalosis. An immediate decrement in plasma bicarbonate occurs in response to hypocapnia. This acute adaptation is complete within 5 to 10 minutes from the onset of hypocapnia and is accounted for principally by alkaline titration of the nonbicarbonate buffers of the body. To a lesser extent, this acute adaptation reflects increased production of organic acids, notably lactic acid. When hypocapnia is sustained, renal adjustments cause an additional decrease in plasma bicarbonate, further ameliorating the resulting alkalemia. This chronic adaptation requires 2 to 3 days for completion and reflects retention of hydrogen ions by the kidneys as a result of downregulation of renal acidification [2,10]. Shown are the average decreases in plasma bicarbonate and hydrogen ion concentrations per mm Hg decrease in PaCO2after completion of the acute or chronic adaptation to respiratory alkalosis. Empiric observations on these adaptations have been used for constructing 95% confidence intervals for graded degrees of acute or chronic respiratory alkalosis, which are represented by the areas in color in the acid-base template. The black ellipse near the center of the figure indicates the normal range for the acid-base parameters. Note that for the same level of PaCO2, the degree of alkalemia is considerably lower in chronic than it is in acute respiratory alkalosis. Assuming that a steady state is present, values falling within the areas in color are consistent with but not diagnostic of the corresponding simple disorders. Acid-base values falling outside the areas in color denote the presence of a mixed acid-base disturbance [4].

Renal acidification response to chronic hypocapnia. A, Sustained hypocapnia entails a persistent decrease in the renal tubular secretory rate of hydrogen ions and a persistent increase in the chloride reabsorption rate. As a result, transient suppression of net acid excretion occurs. This suppression is largely manifested by a decrease in ammonium excretion and, early on, by an increase in bicarbonate excretion. The transient discrepancy between net acid excretion and endogenous acid production, in turn, leads to positive hydrogen ion balance and a reduction in the bicarbonate stores of the body. Maintenance of the resulting hypobicarbonatemia is ensured by the gradual suppression in the rate of renal bicarbonate reabsorption. This suppression itself is a reflection of the hypocapnia-induced decrease in the hydrogen ion secretory rate. A new steady state emerges when two things occur: the reduced filtered load of bicarbonate is precisely balanced by the dampened rate of bicarbonate reabsorption and net acid excretion returns to the level required to offset daily endogenous acid production. The transient retention of acid during sustained hypocapnia is normally accompanied by a loss of sodium in the urine (and not by a retention of chloride as analogy with chronic respiratory acidosis would dictate). The resulting extracellular fluid loss is responsible for the hyperchloremia that typically accompanies chronic respiratory alkalosis. Hyperchloremia is sustained by the persistently enhanced chloride reabsorption rate. If dietary sodium is restricted, acid retention is achieved in the company of increased potassium excretion. The specific cellular mechanisms mediating the renal acidification response to chronic hypocap-nia are under investigation. Available evidence indicates a parallel decrease in the rates of the luminal sodium ion-hydrogen ion (Na+-H+) exchanger and the basolateral sodium ion-3 bicarbonate ion (Na+-3HCC>3) cotransporter in the proximal tubule. This parallel decrease reflects a decrease in the maximum velocity (Vmax) of each transporter but no change in the substrate concentration at halfmaximal velocity (Km) for sodium (as shown in B for the Na+-H+ exchanger in rabbit renal cortical brush-border membrane vesicles) [11]. Moreover, hypocapnia induces endocytotic retrieval of H+-adenosine triphosphatase (ATPase) pumps from the luminal membrane of the proximal tubule cells as well as type A intercalated cells of the cortical and medullary collecting ducts. It remains unknown whether chronic hypocapnia alters the quantity of the H+-ATPase pumps as well as the kinetics or quantity of other acidification transporters in the renal cortex or medulla [6]. NS—not significant. (B, From Hilden and coworkers [11]; with permission.)

Central Nervous System

Cardiovascular System

Neuromuscular System

Cerebral vasoconstriction

Chest oppression

Numbness and paresthesias

Reduction in intracranial pressure

Angina pectoris

of the extremities


Ischemic electrocardiographic changes

Circumoral numbness


Normal or decreased blood pressure

Laryngeal spasm

Increased deep tendon reflexes

Cardiac arrhythmias

Manifestations of tetany

Generalized seizures

Peripheral vasoconstriction

Muscle cramps

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