Pediatric Respiratory Alkalosis 

  • Author: Mary C Mancini, MD, PhD; Chief Editor: Michael R Bye, MD   more...
 
Updated: May 28, 2009
 

Background

Respiratory alkalosis is one of many acid-base disorders found among critically ill patients. It is detected by ABG and electrolyte levels. To diagnose respiratory alkalosis or assess the severity of the condition, the physician must understand clinical acid-base balance. Alkalosis, by definition, is a pathologic state that causes or tends to cause an increase in blood pH. Hence, one can have an alkalosis with normal pH if compensation has occurred; alkalemia is defined as a blood pH above 7.44. The term respiratory in respiratory alkalosis refers to the primary respiratory mechanism responsible for the change.[1]

Next

Pathophysiology

Hypocapnia (low PCO2) develops whenever CO2 elimination by the lungs exceeds tissue production. One or more of 3 basic mechanisms usually underlie respiratory alkalosis (see image below).

Schematic presentation of pathophysiology of hyperSchematic presentation of pathophysiology of hyperventilation.
  • Hypoxia
  • Metabolic acidosis
  • Direct CNS stimulation of respiration.

Compensation

In respiratory acid-base disturbances, changes in ventilation, and hence PCO2, represent the primary disturbance, and compensation occurs by alterations in plasma bicarbonate.

In chronic respiratory alkalosis, increased urinary bicarbonate excretion resists the pH change caused by hypocapnia. This renal compensation begins within several hours and takes several days for the maximal response.

In acute respiratory alkalosis, an initial small decrease may occur in plasma bicarbonate concentration because of chemical mass action. Hypocapnia leads to increased formation of carbonic acid, to lowered plasma hydrogen ion concentration (alkalemia), and to concomitant reduced plasma bicarbonate concentration. This is quantitatively less profound than renal compensation and is not related to change in bicarbonate excretion.[2]

Formulas for estimating appropriate compensation in simple respiratory alkalosis (limit of compensation is [HCO3-] of approximately 15) include the following:

  • Acute alkalosis - Change in pH = (change in PCO2) X 0.08
  • Chronic alkalosis - Change in pH = (change in PCO2) X 0.003
Previous
Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Mary C Mancini, MD, PhD  Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana State University School of Medicine in Shreveport

Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons, and Southern Surgical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Girish G Deshpande, MD, MBBS, FAAP  Assistant Professor, Department of Pediatrics, Division of Critical Care Medicine, Children's Hospital of Illinois at OSF St Francis Medical Center

Girish G Deshpande, MD, MBBS, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

G Patricia Cantwell, MD, FCCM  Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Barry J Evans, MD  Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center, Mineola, NY; Professor of Clinical Pediatrics, State University of New York at Stony Brook, Stony Brook, NY

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD  Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

References

  1. Johnson RA. Respiratory alkalosis: a quick reference. Vet Clin North Am Small Anim Pract. May 2008;38(3):427-30, vii. [Medline].

  2. Ueda Y, Aizawa M, Takahashi A, Fujii M, Isaka Y. Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production. Nephrol Dial Transplant. Mar 2009;24(3):825-8. [Medline].

  3. Steiss JE, Wright JC. Respiratory alkalosis and primary hypocapnia in Labrador Retrievers participating in field trials in high-ambient-temperature conditions. Am J Vet Res. Oct 2008;69(10):1262-7. [Medline].

  4. [Guideline] Polson J, Lee WM. AASLD position paper: the management of acute liver failure. Hepatology. May 2005;41(5):1179-97. [Medline].

  5. Datta BN, Stone MD. Hyperventilation and hypophosphataemia. Ann Clin Biochem. Mar 2009;46:170-1. [Medline].

  6. Frangiosa A, De Santo LS, Anastasio P, De Santo NG. Acid-base balance in heart failure. J Nephrol. Mar-Apr 2006;19 Suppl 9:S115-20. [Medline].

  7. Hagiwara N, Ooboshi H, Ishibashi M, et al. Elevated cerebrospinal fluid lactate levels and the pathomechanism of calcification in Fahr's disease. Eur J Neurol. May 2006;13(5):539-43. [Medline].

  8. Myrianthefs PM, Briva A, Lecuona E, et al. Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Am J Respir Crit Care Med. Jun 1 2005;171(11):1267-71. [Medline]. [Full Text].

 
Previous
Next
 
Acid-base nomogram shows confidence bands for simple acid-base disturbances. Conversion factor is 1 torr = 0.13 kPa.
Schematic presentation of pathophysiology of hyperventilation.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.