Pediatric Respiratory Alkalosis

No Results

No Results

processing….

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]

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 image below).

See the list below:

Hypoxia

Metabolic acidosis

Direct CNS stimulation of respiration.

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

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].

Myrianthefs PM, Briva A, Lecuona E, et al. Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Am J Respir Crit Care Med. 2005 Jun 1. 171(11):1267-71. [Medline]. [Full Text].

[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].

Mary C Mancini, MD, PhD, MMM Surgeon-in-Chief and Director of Cardiothoracic Surgery, Christus Highland

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, Phi Beta Kappa, Society of Thoracic Surgeons

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.

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.

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.

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.

Pediatric Respiratory Alkalosis

Research & References of Pediatric Respiratory Alkalosis|A&C Accounting And Tax Services
Source

Share on Facebook

Tweet

Follow us