Pediatric Respiratory Alkalosis Workup
- Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Michael R Bye, MD more...
A simple step-wise approach proves useful for further workup in patients with respiratory alkalosis, such as the following:
Step 1: Prove the presence of respiratory alkalosis by an ABG. A PCO 2 less than 35 indicates alveolar hyperventilation. A pH greater than 7.4 is highly suggestive of alkalosis. When both are found, respiratory alkalosis is likely.
Step 2: Assess the chronicity of hyperventilation. Reference range HCO 3 - with a pH greater than 7.45 suggests acute hyperventilation, whereas low HCO 3 - with a pH of 7.4-7.45 suggests a chronic partially compensated process.
Step 3: An arterial-alveolar oxygen gradient within the reference range and a pH greater than 7.4 is consistent with hyperventilation secondary to direct CNS stimulation, with normal lung function.
Step 4: Arterial pH less than 7.4 is usually observed with alveolar hyperventilation as compensation for metabolic acidosis (overcompensation for metabolic acidosis is very rare).
Step 5: Respiratory alkalosis is likely with hypoxemia with alveolar hyperventilation. However, determining if the alkalosis is caused by the hypoxia or if the hypoxia and the alkalosis are caused by the underlying pulmonary disease is difficult.
Measurement of arterial pH, HCO3-, and PCO2 are crucial. Transcutaneous or end-tidal PCO2 may be used in place of arterial PCO2; however, transcutaneous PCO2 requires normal skin perfusion, and end-tidal pCO2 is useful only in the presence of normal lung function and when no other acid-base disturbance is suspected. Furthermore, the noninvasive tests do not measure the pH.
A detailed history and careful physical examination should indicate an underlying disorder.
Standard nomograms (see image below) help diagnose simple acid-base disorders, despite the following limitations:
See the list below:
They describe acid-base status in children with a steady-state condition. Hence, nomograms are not helpful for patients with rapidly changing status.
Nomograms lose precision at extremes.
Values falling in respiratory alkalosis may overlap with other mixed disorders and ultimately require clinical judgment.
Hyperventilation syndrome is often considered a diagnosis of exclusion. Physicians must consider other causes before making the diagnosis. However, in the typical patient with a normal alveolar-arterial oxygen gradient with an acute stress, the diagnosis can be made with confidence.
Drug screening may be helpful.
Chest radiography may be indicated.
Ventilation/perfusion imaging, helical chest CT imaging, or CT angiography may be performed if pulmonary embolism is suspected.
CT imaging or MRI of the brain may be indicated if CNS pathology is suspected.
Johnson RA. Respiratory alkalosis: a quick reference. Vet Clin North Am Small Anim Pract. 2008 May. 38(3):427-30, vii. [Medline].
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. 2009 Mar. 24(3):825-8. [Medline].
Yang XF, Shi XY, Ju J, Zhang WN, Liu YJ, Li XY, et al. 5% CO2 inhalation suppresses hyperventilation-induced absence seizures in children. Epilepsy Res. 2014 Feb. 108(2):345-8. [Medline].
Basu S, Barman S, Shukla R, Kumar A. Effect of oxygen inhalation on cerebral blood flow velocity in premature neonates. Pediatr Res. 2014 Feb. 75(2):328-35. [Medline].
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. 2008 Oct. 69(10):1262-7. [Medline].
[Guideline] Lee WM, Stravitz RT, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases Position Paper on acute liver failure 2011. Hepatology. 2012 Mar. 55(3):965-7. [Medline]. [Full Text].
Bhutani VK, Chima R, Sivieri EM. Innovative neonatal ventilation and meconium aspiration syndrome. Indian J Pediatr. 2003 May. 70(5):421-7. [Medline].
Biçakçi Z, Olcay L. Citrate metabolism and its complications in non-massive blood transfusions: association with decompensated metabolic alkalosis+respiratory acidosis and serum electrolyte levels. Transfus Apher Sci. 2014 Jun. 50(3):418-26. [Medline].
Blüher S, Schulz M, Bierbach U, Meixensberger J, Tröbs RB, Hirsch W, et al. Central lactic acidosis, hyperventilation, and respiratory alkalosis: leading clinical features in a 3-year-old boy with malignant meningeal melanoma. Eur J Pediatr. 2008 Apr. 167(4):483-5. [Medline].
Datta BN, Stone MD. Hyperventilation and hypophosphataemia. Ann Clin Biochem. 2009 Mar. 46:170-1. [Medline].
Frangiosa A, De Santo LS, Anastasio P, De Santo NG. Acid-base balance in heart failure. J Nephrol. 2006 Mar-Apr. 19 Suppl 9:S115-20. [Medline].
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. 2006 May. 13(5):539-43. [Medline].
Jaing TH, Lin JL, Lin YP, Yang SH, Lin JJ, Hsia SH. Hyperammonemic encephalopathy after induction chemotherapy for acute lymphoblastic leukemia. J Pediatr Hematol Oncol. 2009 Dec. 31(12):955-6. [Medline].
[Guideline] Polson J, Lee WM. AASLD position paper: the management of acute liver failure. Hepatology. 2005 May. 41(5):1179-97. [Medline].
Schwaderer AL, Schwartz GJ. Back to basics: acidosis and alkalosis. Pediatr Rev. 2004 Oct. 25(10):350-7. [Medline].
Weissbach A, Tirosh I, Scheuerman O, Hoffer V, Garty BZ. Respiratory alkalosis and metabolic acidosis in a child treated with sulthiame. Pediatr Emerg Care. 2010 Oct. 26(10):752-3. [Medline].