Pediatric Respiratory Alkalosis Clinical Presentation
- Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Michael R Bye, MD more...
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.
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.
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)
Interstitial, airway, and parenchymal pulmonary diseases affect PO2 more prominently than PCO2, and hyperventilation usually results in hypocapnia. 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)
Pneumonia: A classic presentation of Pneumocystis pneumonia is hypoxemia with respiratory alkalosis.
Interstitial lung disease
Respiratory alkalosis could result from a ventilatory rate or tidal volume that is too high or from the patient triggering excessive additional breaths.
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:
Neurologic disease (eg, stroke, infection, trauma, tumor)
Hormones/drugs (eg, catecholamines, progesterone, methylxanthines, salicylates/doxapram, nicotine)
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. 
Recovery from metabolic acidosis
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].