eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Alkalosis, Respiratory

Author: Mary C Mancini, MD, PhD, Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-Shreveport
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
Contributor Information and Disclosures

Updated: May 28, 2009

Introduction

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

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 Media file 2).
 

Schematic presentation of pathophysiology of hype...

Schematic presentation of pathophysiology of hyperventilation.

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Schematic presentation of pathophysiology of hype...

Schematic 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

Clinical

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.

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.

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

More on Alkalosis, Respiratory

Overview: Alkalosis, Respiratory
Differential Diagnoses & Workup: Alkalosis, Respiratory
Treatment & Medication: Alkalosis, Respiratory
Follow-up: Alkalosis, Respiratory
Multimedia: Alkalosis, Respiratory
References
Further Reading
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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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Keywords

respiratory alkalosis, alveolar hyperventilation, hyperventilation, acid-base disorders, increased blood pH, alkalemia, hypocapnia, urinary bicarbonate, plasma bicarbonate, acute alkalosis, chronic alkalosis, tetany, symptomatic hypocalcemia, dizziness, mental confusion, seizures, hypocarbia, excessive elimination of carbon dioxide, respiratory abnormality, hyperthermia, treatment, diagnosis

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Contributor Information and Disclosures

Author

Mary C Mancini, MD, PhD, Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-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.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
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: Merck Honoraria Speaking and teaching

 
 
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