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Respiratory Alkalosis Differential Diagnoses

  • Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Aug 04, 2016
 
 

Diagnostic Considerations

Hyperthyroidism: Hyperthyroidism increases the ventilation chemoreflexes, thereby causing hyperventilation. These chemoreflexes return to normal with treatment of the hyperthyroidism.

Pregnancy: Progesterone levels are increased during pregnancy. Progesterone causes stimulation of the respiratory center, which can lead to respiratory alkalosis. Chronic respiratory alkalosis is a common finding in pregnant women.[3]

Congestive heart failure: Patients with congestive heart failure (and other low cardiac-output states) hyperventilate at rest, during exercise, and during sleep. Owing to pulmonary congestion, pulmonary vascular and interstitial receptors are stimulated. Additionally, the low cardiac-output state and hypotension stimulate breathing via the arterial baroreceptors.

Chronic/severe liver disease: Several mechanisms have been hypothesized to explain the hyperventilation associated with liver disease. Increased levels of progesterone, ammonia, vasoactive intestinal peptide, and glutamine can stimulate respiration. Patients with severe disease or portal hypertension may have small pulmonary arteriovenous anastomoses in the lungs or portal-pulmonary shunts, which result in hypoxemia. This stimulates the peripheral chemoreceptors and leads to hyperventilation. The degree of respiratory alkalosis correlates with the severity of hepatic insufficiency.[3]

Salicylate overdose: Initially, a respiratory alkalosis occurs, which is followed by a metabolic acidosis that induces secondary hyperventilation.

Fever and sepsis: Fever and sepsis may manifest as hyperventilation, even before hypotension develops. The exact mechanism is not known but is thought to be due to carotid body or hypothalamic stimulation by the increased temperature.

Gram-negative sepsis: Before fever, hypoxemia, or hypotension develops, acute respiratory alkalosis may be the only early finding.[3]

Pain: Hyperventilation may be due to stimulation of the peripheral and central chemoreceptors, as well as the behavioral control system.

Hyperventilation syndrome: This is also known as psychogenic hyperventilation and was first described in 1935.[10] It is due to stress and anxiety, both of which act on the behavioral respiratory control system. The hyperventilation ceases during sleep, when the behavioral control system is inactive and only the metabolic system is controlling breathing. The diagnosis of hyperventilation syndrome should be a diagnosis of exclusion.[2] Rule out all organic medical conditions, including pulmonary embolism, cardiac ischemia, and hyperthyroidism, before establishing a diagnosis of hyperventilation syndrome.

Differential Diagnoses

 
 
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. Park JJ, Choi DJ, Yoon CH, et al. The prognostic value of arterial blood gas analysis in high-risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry. Eur J Heart Fail. 2015 Jun. 17 (6):601-11. [Medline].

  5. Raphael KL, Murphy RA, Shlipak MG, et al. Bicarbonate Concentration, Acid-Base Status, and Mortality in the Health, Aging, and Body Composition Study. Clin J Am Soc Nephrol. 2016 Feb 5. 11 (2):308-16. [Medline].

  6. 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.

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

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

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

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

 
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