Respiratory Alkalosis

PaCO

120 100 90 80 70 60 50

PaCO

120 100 90 80 70 60 50

Arterial blood pH

Arterial blood pH

Steady-state relationships in respiratory alkalosis: average decrease per mm Hg fall in PaCO2

Acute adaptation Chronic adaptation

FIGURE 6-9

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+-3HCO3) 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

Light-headedness

Ischemic electrocardiographic changes

Circumoral numbness

Confusion

Normal or decreased blood pressure

Laryngeal spasm

Increased deep tendon reflexes

Cardiac arrhythmias

Manifestations of tetany

Generalized seizures

Peripheral vasoconstriction

Muscle cramps

Carpopedal spasm

Trousseau's sign

Chvostek's sign

SIGNS AND SYMPTOMS OF RESPIRATORY ALKALOSIS

FIGURE 6-11

Signs and symptoms of respiratory alkalosis. The manifestations of primary hypocapnia frequently occur in the acute phase, but seldom are evident in chronic respiratory alkalosis. Several mechanisms mediate these clinical manifestations, including cerebral hypoperfusion, alkalemia, hypocalcemia, hypokalemia, and decreased release of oxygen to the tissues by hemoglobin. The cardiovascular effects of respiratory alkalosis are more prominent in patients undergoing mechanical ventilation and those with ischemic heart disease [2].

CAUSES OF RESPIRATORY ALKALOSIS

Hypoxemia or Tissue Hypoxia

Central Nervous System Stimulation

Drugs or Hormones

Stimulation of Chest Receptors

Miscellaneous

Decreased inspired oxygen tension

Voluntary

Nikethamide, ethamivan

Pneumonia

Pregnancy

High altitude

Pain

Doxapram

Asthma

Gram-positive septicemia

Bacterial or viral pneumonia

Anxiety syndrome-

Xanthines

Pneumothorax

Gram-negative septicemia

Aspiration of food, foreign object,

hyperventilation syndrome

Salicylates

Hemothorax

Hepatic failure

or vomitus

Psychosis

Catecholamines

Flail chest

Mechanical hyperventilation

Laryngospasm

Fever

Angiotensin II

Acute respiratory distress syndrome

Heat exposure

Drowning

Subarachnoid hemorrhage

Vasopressor agents

Cardiogenic and noncardiogenic

Recovery from metabolic acidosis

Cyanotic heart disease

Cerebrovascular accident

Progesterone

pulmonary edema

Severe anemia

Meningoencephalitis

Medroxyprogesterone

Pulmonary embolism

Left shift deviation of

Tumor

Dinitrophenol

Pulmonary fibrosis

oxyhemoglobin curve

Trauma

Nicotine

Hypotension

Severe circulatory failure

Pulmonary edema

Respiratory alkalosis is the most frequent acid-base disorder encountered because it occurs in normal pregnancy and high-altitude residence. Pathologic causes of respiratory alkalosis include various hypoxemic conditions, pulmonary disorders, central nervous system diseases, pharmacologic or hormonal stimulation of ventilation, hepatic failure, sepsis, the anxiety-hyper-ventilation syndrome, and other entities. Most of these causes are associated with the abrupt occurrence of hypocapnia; however, in many instances, the process might be sufficiently prolonged to permit full chronic adaptation to occur. Consequently, no attempt has been made to separate these conditions into acute and chronic categories. Some of the major causes of respiratory alkalosis are benign, whereas others are life-threatening. Primary hypocapnia is particularly common among the critically ill, occurring either as the simple disorder or as a component of mixed disturbances. Its presence constitutes an ominous prognostic sign, with mortality increasing in direct proportion to the severity of the hypocapnia [2].

FIGURE 6-13

Respiratory alkalosis management. Because chronic respiratory alka-losis poses a low risk to health and produces few or no symptoms, measures for treating the acid-base disorder itself are not required. In contrast, severe alkalemia caused by acute primary hypocapnia requires corrective measures that depend on whether serious clinical manifestations are present. Such measures can be directed at reducing plasma bicarbonate concentration ([HCO3]), increasing the arterial carbon dioxide tension (PaCO2), or both. Even if the baseline plasma bicarbonate is moderately decreased, reducing it further can be particularly rewarding in this setting. In addition, this maneuver combines effectiveness with relatively little risk [1,2].

Pseudorespiratory alkalosis. This entity develops in patients with profound depression of cardiac function and pulmonary perfusion but relative preservation of alveolar ventilation. Patients include those with advanced circulatory failure and those undergoing cardiopulmonary resuscitation. The severely reduced pulmonary blood flow limits the amount of carbon dioxide delivered to the lungs for excretion, thereby increasing the venous carbon dioxide tension (PCO2). In contrast, the increased ventilation-to-perfusion ratio causes a larger than normal removal of carbon dioxide per unit of blood traversing the pulmonary circulation, thereby giving rise to arterial hypocapnia [12,13]. Note a progressive widening of the arteriovenous difference in pH and PCO2 in the two settings of cardiac dysfunction. The hypobicarbonatemia in the setting of cardiac arrest represents a complicating element of lactic acidosis. Despite the presence of arterial hypocapnia, pseudorespiratory alkalosis represents a special case of respiratory acidosis, as absolute carbon dioxide excretion is decreased and body carbon dioxide balance is positive. Furthermore, the extreme oxygen deprivation prevailing in the tissues might be completely disguised by the reasonably preserved arterial oxygen values. Appropriate monitoring of acid-base composition and oxygenation in patients with advanced cardiac dysfunction requires mixed (or central) venous blood sampling in addition to arterial blood sampling. Management of pseudorespiratory alkalosis must be directed at optimizing systemic hemodynamics [1,13].

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