Pediatric Respiratory Alkalosis Clinical Presentation

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

History

  • Patients primarily have clinical manifestations of the disorder causing the respiratory alkalosis; the effects of respiratory alkalosis per se are fewer.
  • Acute respiratory alkalosis has more intense features than chronic respiratory alkalosis because later renal compensation and cellular adaptation minimize the pH change.
  • Alkalosis, by promoting the binding of calcium to albumin, can reduce the fraction of ionized calcium in blood, causing tetany. Symptomatic hypocalcemia is more common with respiratory alkalosis than with metabolic alkalosis.
  • Patients have symptoms of underlying disorders.
  • Rapid decrease in PCO2 can result in dizziness, mental confusion, and (rarely) seizures, even with a PO2 that is within the reference range. This is probably due to the cerebral vasoconstriction caused by the hypocarbia.
  • Patients may have tetany due to reduced ionized calcium in blood.
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Physical

  • Vital signs
    • Patients have fever if respiratory alkalosis is the result of an infectious disorder.
    • Hyperthermia of any origin may, in turn, result in respiratory alkalosis.
    • Acute respiratory alkalosis may cause mild tachycardia.
    • Respiratory rate is usually high. In some cases, the hyperventilation is primarily a manifestation of increased tidal volume and the respiratory rate may not be markedly elevated. This is often observed in the respiratory alkalosis compensating diabetic ketoacidosis.
    • Blood pressure is usually maintained, except when respiratory alkalosis is caused by massive pulmonary embolism or sepsis.
  • CNS
    • Effects are secondary to the reduction in cerebral blood flow (CBF) caused by reduction in PCO2. CBF may decrease by 1-2 mL/100 g/min for each 1 mm Hg fall in PCO2, with maximum reduction in CBF of 40-50% achieved with a PCO2 of 20-25 mm Hg.
    • Reduced CBF may cause altered mentation, dizziness, and sometimes seizures.
  • Cardiovascular system
    • Cardiovascular effects of acute hypocapnia are minimal in patients who are awake. Tachycardia may be the only observable manifestation.
    • Electrolyte imbalance resulting from respiratory alkalosis may very rarely induce dysrhythmias, although only in patients with underlying heart disease.
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Causes

  • Hypoxia and hypoxemia: Any condition associated with a fall in the PaO2 below 55 mm Hg or with decreased oxygen delivery to the tissues increases minute ventilation, causing respiratory alkalosis. Causes include the following:
    • Altitude/low fraction of inspired oxygen (FIO2)
    • Anemia
    • Hypotension
    • Lung disease
  • Pulmonary disorders: Interstitial, airway, and parenchymal pulmonary diseases affect PO2 more prominently than PCO2, and hyperventilation usually results in hypocapnia.[3] Inflammation of the irritant receptors in the airways and parenchyma also causes hyperventilation, resulting in respiratory alkalosis. Causes include the following:
    • Edema (hydrostatic or permeability)
    • Embolism
    • Airway obstruction/inflammation
    • Pneumonia: A classic presentation of Pneumocystis pneumonia is hypoxemia with respiratory alkalosis.
    • Interstitial lung disease
  • Mechanical ventilation: Respiratory alkalosis could result from a ventilatory rate or tidal volume that is too high or from the patient triggering excessive additional breaths.
  • Extrapulmonary disorders: In these cases, the child has normal lung function with an overriding ventilatory stimulus. These disorders usually result in the most severe respiratory alkalosis. Causes include the following:
    • Anxiety, stress
    • Neurologic disease (eg, stroke, infection, trauma, tumor)
    • Hormones/drugs (eg, catecholamines, progesterone, methylxanthines, salicylates/doxapram, nicotine)
    • Pregnancy
    • Hyperthermia
    • Liver failure, especially with hepatic encephalopathy: Guidelines have been established for the management of acute liver failure.[4]
    • Sepsis
    • Recovery from metabolic acidosis
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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].

 
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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.
 
 
 
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