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Respiratory Alkalosis

  • Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Jul 31, 2015
 

Background

Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO2). In turn, the decrease in PaCO2 increases the ratio of bicarbonate concentration to PaCO2 and, thereby, increases the pH level, thus the descriptive term of respiratory alkalosis. The decrease in PaCO2 (hypocapnia) develops when a strong respiratory stimulus causes the respiratory system to remove more carbon dioxide than is produced metabolically in the tissues.

Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PaCO2 level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PaCO2 level is below the lower limit of normal, but the pH level is relatively 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 with respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be a minor non – life-threatening disorder. However, more serious disease processes should also be considered in the differential diagnosis.

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Pathophysiology

Breathing or alveolar ventilation is the body’s way of providing adequate amounts of oxygen for metabolism while removing carbon dioxide produced in the tissues. By sensing the body’s partial pressure of arterial oxygen (PaO2) and PaCO2, the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elimination at the lungs is balanced to that used and produced by the tissues.

The PaCO2 must be maintained at a level that ensures hydrogen ion concentrations remain in the narrow limits required for optimal protein and enzymatic function. PaO2 is not as closely regulated as the PaCO2. Adequate hemoglobin saturation can be achieved over a wide range of PaO2 levels. The movement of oxygen from the alveoli to the vascular system is dependent on pressure gradients. On the other hand, carbon dioxide diffuses much easier through an aqueous environment.

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.

PaCO2 is normally maintained in the range of 35-45 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 and pH. This feedback regulator is how the PaCO2 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 alveolar ventilation that is disproportionate to the rate of metabolic carbon dioxide production, leading to a PaCO2 level 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. However, these terms should not be used to describe hyperventilation because they are distinct entities and neither necessarily results in 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 due to the change in pH. Many of the symptoms present in persons with respiratory alkalosis are related to hypocalcemia.[2] Hyponatremia and hypochloremia may also be present.

Acute hyperventilation with hypocapnia causes a small, early reduction in serum bicarbonate levels resulting from cellular shift of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PaCO2 along a range of 15-40 mm Hg. The relationship of PaCO2 to arterial hydrogen and bicarbonate is 0.7 mmol/L per mm Hg and 0.2 mmol/L per mm Hg, respectively.[3] After 2-6 hours, respiratory alkalosis is renal compensation begins by decreasing bicarbonate reabsorption. The kidneys respond more to the decreased PaCO2 rather than the increased pH. Complete kidney compensation may take several days and requires normal kidney function and intravascular volume status.[3] The expected change in serum bicarbonate concentration can be estimated as follows:

  • Acute - Bicarbonate (HCO 3 -) falls 2 mEq/L for each decrease of 10 mm Hg in the PCO 2; that is, ΔHCO 3 = 0.2(ΔPCO 2); maximum compensation: HCO 3 - = 12-20 mEq/L
  • Chronic - Bicarbonate (HCO 3 -) falls 5 mEq/L for each decrease of 10 mm Hg in the PCO 2; that is, ΔHCO 3 = 0.5(ΔPCO 2); maximum compensation: HCO 3 - = 12-20 mEq/L

Note that a plasma bicarbonate concentration of less than 12 mmol/L is unusual in pure respiratory alkalosis alone and should prompt the consideration of a metabolic acidosis as well.[2]

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 – PCO 2)
  • Chronic respiratory alkalosis: Change in pH = 0.017 X (40 – PCO 2)
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Epidemiology

Frequency

United States

The frequency of respiratory alkalosis varies depending on the etiology. The most common acid-base abnormality observed in critically ill patients is respiratory alkalosis.[3]

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.

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Prognosis

The prognosis of respiratory alkalosis is variable and depends on the underlying cause and the severity of the underlying illness.

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Patient Education

Patients with hyperventilation syndrome as the etiology of their respiratory alkalosis may particularly benefit from patient education. The underlying pathophysiology should be explained in simple terms, and patients should be instructed in breathing techniques that may be used to relieve the hyperventilation. Reassurance is key for these patients.

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Contributor Information and Disclosures
Author

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Gregg T Anders, DO Medical Director, Great Plains Regional Medical Command , Brooke Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

Jackie A Hayes, MD, FCCP Clinical Assistant Professor of Medicine, University of Texas Health Science Center at San Antonio; Chief, Pulmonary and Critical Care Medicine, Department of Medicine, Brooke Army Medical Center

Jackie A Hayes is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

April Lambert-Drwiega, DO Fellow, Department of Pulmonology and Critical Care Medicine, East Tennessee State University

April Lambert-Drwiega is a member of the following medical societies: American College of Physicians, American Medical Association, American Osteopathic Association, and Southern Medical Association

Disclosure: Nothing to disclose.

References
  1. Kazmaier S, Weyland A, Buhre W, et al. Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease. Anesthesiology. 1998 Oct. 89(4):831-7. [Medline].

  2. Effros RM, Wesson JA. Acid-Base Balance. Mason RJ, Broaddus VC, Murray JF, Nadel JA, eds. Murray and Nadel's Textbook of Respiratory Medicine. 4th ed. Philadelphia, PA: Elsevier Saunders; 2005. Vol 1: 192-93.

  3. DuBose TD, Jr. Acidosis and Alkalosis. Kasper DL, Braunwald E, Fauci AS, Hauser Sl, Longo DL, Jameson JL,eds. Harrison's Principles of Internal Medicine. 16th. New York, NY: McGraw-Hill; 2005. 270-1.

  4. Phillipson EA, Duffin J. Hypoventilation and Hyperventilation Syndromes. Mason RJ, Broaddus VC, Murray JF, Nadel JA, eds. Murray and Nadel's Textbook of Respiratory Medicine. 4th ed. Philadelphia, PA: Elsevier Saunders; 2005. Vol 2: 2069-70, 2080-84.

  5. Goldman A. Clinical tetany by forced respiration. JAMA. 1922. 78:1193-95.

  6. Haldane JS, Poulton EP. The effects of want of oxygen on respiration. J Physiol. 1908. 37:390-407.

  7. Kirsch DB, Jozefowicz RF. Neurologic complications of respiratory disease. Neurol Clin. 2002 Feb. 20(1):247-64, viii. [Medline].

  8. Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996 Feb. 109(2):516-34. [Medline].

 
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