Arterial carbon dioxide tension represents the balance betweenthe production and elimination of carbon dioxide, and in healthypersons, it is maintained within narrow physiologic limits.Hypocapnia, even when marked, is normally well tolerated, oftenwith few apparent effects. Transient induction of hypocapniacan lead to lifesaving physiological changes in patients withsevere intracranial hypertension or neonatal pulmonary-arteryhypertension, but hypocapnia of longer duration in criticallyill patients may adversely affect outcomes.1,2 Despite concernabout adverse effects, the induction of hypocapnia has commonlybeen recommended for diverse disease states.3,4,5 Thus, hypocapnia,whether produced deliberately3,4,5 or accidentally,6,7 remainsprevalent in clinical . . . [Full Text of this Article]
Development of Arterial Hypocapnia
Therapeutic Induction of Hypocapnia
Head Injury
Other Forms of Coma
Neonatal Care
Anesthesia and Surgery
Accidental Induction of Hypocapnia
Hypocapnia as a Common Component of Disease
Pathobiology of Hypocapnia
Hypocapnia, Hypocapnic Alkalosis, and Acid–Base Status
Respiratory versus Metabolic Alkalosis
Hypocapnia, Cellular Metabolism, and Oxygenation
Dose–Response Relation and Duration of Hypocapnia
Hypocapnia and the Brain
Intracranial Hypertension
Mechanisms of Deleterious Central Nervous System Effects
Deleterious Central Nervous System Effects in Clinical Context
Neonatal Brain Injury
Traumatic Brain Injury
Acute Stroke
Postoperative Psychomotor Dysfunction
Panic Disorder
Altitude Sickness
Hypocapnia and the Lung
Hypocapnia and the Tracheobronchial Tree
Acute Lung Injury
Pathophysiology
Clinical Consequences
Neonatal Lung Dysfunction
Hypocapnia and the Cardiovascular System
Myocardial Ischemia
Cardiac Dysrhythmias
Hypocapnia and Heart–Lung Interactions
Hypocapnia and Human Development
Summary
Source Information
From the Department of Physiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, and the Department of Anaesthesia and Intensive Care, St. Vincent's University Hospital, Dublin, Ireland (J.G.L.); and the Department of Critical Care Medicine and the Lung Biology Program, the Research Institute, the Hospital for Sick Children, and the Program in Critical Care Medicine, University of Toronto, Toronto (B.P.K.).
Address reprint requests to Dr. Kavanagh at the Department of Critical Care Medicine, the Hospital for Sick Children, 555 University Ave., Toronto, ON M5G 1X8, Canada, or at bpk@sickkids.ca.
Related Letters:
Hypocapnia
Carey B. J., Brusilow S. W., Laffey J., Kavanagh B. P.
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N Engl J Med 2002;
347:1533, Nov 7, 2002.
Correspondence
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