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Pediatric Respiratory Alkalosis Clinical Presentation

  • Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Michael R Bye, MD  more...
Updated: Jan 16, 2015


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,[3] 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.



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.

The 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.

The effects of hperoxemia and hypoxemia on CBF velocity in premature neonates appear to depend on gestational age.[4]

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.



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 (FIO 2)
  • Anemia
  • Hypotension
  • Lung disease

Pulmonary disorders

Interstitial, airway, and parenchymal pulmonary diseases affect PO2 more prominently than PCO2, and hyperventilation usually results in hypocapnia.[5] 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, although these are primarily focused on adult patients with hepatic failure. [6]
  • Sepsis
  • Recovery from metabolic acidosis
Contributor Information and Disclosures

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

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

Disclosure: Nothing to disclose.


Girish G Deshpande, MD, MBBS, FAAP Associate Professor of Pediatrics, Interim Director and Division Chief of Critical Care Medicine, Department of Pediatrics, University of Illinois College of Medicine at Peoria; Consulting Staff, 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

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo

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

Disclosure: Nothing to disclose.

Additional Contributors

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/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

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, Wilderness Medical Society

Disclosure: Nothing to disclose.

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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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