eMedicine Specialties > Pulmonology > Acid-Base Disorders

Respiratory Alkalosis

Author: April Lambert-Drwiega, DO, Fellow, Department of Pulmonology and Critical Care Medicine, East Tennessee State University
Coauthor(s): Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University; Chief of Pulmonary Medicine, Medical Director of Respiratory Therapy, Intensive Care Unit, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Feb 12, 2009

Introduction

Background

Respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO₂), or partial pressure of carbon dioxide (PCO₂). In turn, the decrease in PCO₂ increases the ratio of bicarbonate concentration to PCO₂ and increases the pH level. The decrease in PCO₂ (hypocapnia) develops when a strong respiratory stimulus causes the lungs to remove more carbon dioxide than is produced metabolically in the tissues. Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PCO₂ level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PCO₂ level is below the lower limit of normal, but the pH level is normal or near normal.

Respiratory alkalosis is the most common acid-base abnormality observed in patients who are critically ill. It is associated with numerous illnesses and is a common finding in patients on mechanical ventilation. Many cardiac and pulmonary disorders can manifest respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be minor; however, more serious disease processes should also be considered in the differential diagnosis.

Pathophysiology

Breathing is the body’s way of providing adequate amounts of oxygen for metabolism and for removing carbon dioxide produced by the tissues. By sensing the body’s partial pressure of oxygen (PO₂) and PCO₂, the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elimination at the lungs is equal to that used and produced by the tissues. PO₂ is not as closely regulated because adequate hemoglobin saturation can be achieved over a wide range of PO₂ levels. Oxygen is dependent on pressure gradients whereas, carbon dioxide diffuses much easier through an aqueous environment, making carbon dioxide regulation more complex. The PCO₂ must be maintained at a level that ensures hydrogen ion concentrations remain in the narrow limits required for optimal protein function.

Metabolism generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide.¹ The carbon dioxide combines with water to form carbonic acid. The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. Significant alterations in ventilation can affect the elimination of carbon dioxide and lead to a respiratory acid-base disorder.

PCO₂ is normally maintained in the range of 37-43 mm Hg. Chemoreceptors in the brain (central chemoreceptors) and in the carotid bodies (peripheral chemoreceptors) sense hydrogen concentrations and influence ventilation to adjust the PCO₂, PO₂, and pH. Under this feedback regulator is how the PCO₂ is maintained within its narrow normal range. When these receptors sense an increase in hydrogen ions, breathing is increased to “blow off” carbon dioxide and subsequently reduce the amount of hydrogen ions. Various disease processes may cause stimulation of ventilation with subsequent hyperventilation. If hyperventilation is persistent, it leads to hypocapnia.

Hyperventilation refers to an increase in the rate of alveolar ventilation that is disproportionate to the rate of metabolic carbon dioxide production, leading to an arterial PCO₂ below the normal range. Two words often used synonymously with hyperventilation are tachypnea, an increase in respiratory frequency, and hyperpnea, an increase in the minute volume of ventilation. These should not be used to describe hyperventilation because they are distinct entities and neither results from nor means a change in PaCO₂. Hyperventilation is often associated with dyspnea, but not all patients who are hyperventilating complain of shortness of breath. Conversely, patients with dyspnea need not be hyperventilating.

Acute hypocapnia causes a reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions. A reduction in free serum calcium also occurs. Calcium reduction is secondary to increased binding of calcium to serum albumin. Many of the symptoms present in persons with respiratory alkalosis are related to the hypocalcemia. Hyponatremia and hypochloremia may also be present.

Acute hyperventilation with hypocapnia causes a small, early reduction in serum bicarbonate levels resulting from cellular uptake of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PCO₂ along a range of 15-40 mm Hg. The relationship of PCO₂ to arterial hydrogen and bicarbonate is 0.7 mmol/L per mm Hg and 0.2 mmol/L per mm Hg, respectively. After 2-6 hours, respiratory alkalosis is renally compensated by a decrease in bicarbonate reabsorption. The kidneys respond more to the decreased PCO₂ rather than the increased pH. Kidney compensation may take several days and requires normal kidney function and intravascular volume status. The expected change in serum bicarbonate concentration can be estimated as follows:

• Acute
  • Bicarbonate (HCO₃ ^-) falls 2 mEq/L for each decrease of 10 mm Hg in the PCO₂
    • That is, ΔHCO₃ = 0.2(ΔPCO₂)
    • Maximum compensation: HCO₃ ^- = 12-20 mEq/L
• Chronic
  • Bicarbonate (HCO₃ ^-) falls 5 mEq/L for each decrease of 10 mm Hg in the PCO₂
    • That is, ΔHCO₃ = 0.5(ΔPCO₂)
    • Maximum compensation: HCO₃ ^- = 12-20 mEq/L

Note that a plasma bicarbonate concentration of less than 12 mmol/L is unusual in pure respiratory alkalosis alone.

The expected change in pH with respiratory alkalosis can be estimated with the following equations:

• Acute respiratory alkalosis: Change in pH = 0.008 X (40 – PCO₂)
• Chronic respiratory alkalosis: Change in pH = 0.017 X (40 – PCO₂)

Frequency

United States

The frequency of respiratory alkalosis varies depending on the etiology. It is the most common acid-base abnormality observed in critically ill patients.

Mortality/Morbidity

Morbidity and mortality of patients with respiratory alkalosis depend on the nature of the underlying cause of the respiratory alkalosis and associated conditions.

Clinical

History

Clinical manifestations of respiratory alkalosis depend on its duration, its severity, and the underlying disease process.

• The hyperventilation syndrome can mimic many conditions that are more serious. Symptoms may include paresthesias, circumoral numbness, chest pain or tightness, dyspnea, and tetany.
• Acute onset of hypocapnia can cause cerebral vasoconstriction. Therefore, an acute decrease in PCO₂ reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, and seizures.
• The first cases of spontaneous hyperventilation with dizziness and tingling leading to tetany were described in 1922 by Goldman in patients with cholecystitis, abdominal distention, and hysteria.²
• Haldane and Poulton described painful tingling in the hands and feet, numbness and sweating of the hands, and cerebral symptoms following voluntary hyperventilation.³

Physical

Physical examination findings in patients with respiratory alkalosis are usually nonspecific and are related to the underlying illness or cause of the respiratory alkalosis.

• Many patients with hyperventilation syndrome appear anxious and are frequently tachycardic. Understandably, tachypnea is a frequent finding.
• In acute hyperventilation, chest wall movement and breathing rate increase. In patients with chronic hyperventilation, these physical findings may not be obvious.
• Positive Chvostek and Trousseau signs may be elicited.
• Patients with underlying pulmonary disease may have signs suggestive of pulmonary disease, such as crackles and rhonchi. Cyanosis may be present if the patient is hypoxic.
• If the underlying pathology is neurologic, the patient may have focal neurologic signs or a depressed level of consciousness.
• Cardiovascular effects of hypocapnia in healthy and alert patients are minimal, but in patients who are anesthetized, critically ill, or receiving mechanical ventilation, the effects can be more significant. Cardiac output and systemic blood pressure may fall as a result of the effects of sedation and positive-pressure ventilation on venous return, systemic vascular resistance, and heart rate.
• Cardiac rhythm disturbances may occur because of increased tissue hypoxia related to the leftward shift of the hemoglobin-oxygen dissociation curve.

Causes

The differential diagnosis of respiratory alkalosis is broad; therefore, a thorough history, physical examination, and laboratory evaluation are helpful in limiting the differential and arriving at the diagnosis.

• Central nervous system
  • Pain
  • Hyperventilation syndrome
  • Anxiety
  • Psychosis
  • Fever
  • Cerebrovascular accident
  • Meningitis
  • Encephalitis
  • Tumor
  • Trauma
• Hypoxia
  • High altitude
  • Severe anemia
  • Right-to-left shunts
• Drugs
  • Progesterone
  • Methylxanthines
  • Salicylates
  • Catecholamines
  • Nicotine
• Endocrine
  • Pregnancy
  • Hyperthyroidism
• Pulmonary
  • Pneumothorax/hemothorax
  • Pneumonia
  • Pulmonary edema
  • Pulmonary embolism
  • Aspiration
  • Interstitial lung disease
  • Asthma
  • Emphysema
  • Chronic bronchitis
• Miscellaneous
  • Sepsis
  • Hepatic failure
  • Mechanical ventilation
  • Heat exhaustion
  • Recovery phase of metabolic acidosis
  • Congestive heart failure

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