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New Findings: What is the central question of this study? What are the independent effects of hypoxia and hypocapnia on cerebral haemodynamics and cognitive function? What is the main finding and its importance? Exposure to hyperventilation-induced hypocapnia causes cognitive impairment in both normoxia and hypoxia. In addition, supplementation of carbon dioxide during hypoxia alleviates the cognitive impairment and reverses hypocapnia-induced vasoconstriction of the cerebrovasculature. These data provide new evidence for the independent effect of hypocapnia on the cognitive impairment associated with hypoxia., Abstract: Hypoxia, which is accompanied by hypocapnia at altitude, is associated with cognitive impairment. This study examined the independent effects of hypoxia and hypocapnia on cognitive function and assessed how changes in cerebral haemodynamics may underpin cognitive performance outcomes. Single reaction time (SRT), five-choice reaction time (CRT) and spatial working memory (SWM) tasks were completed in 20 participants at rest and after 1 h of isocapnic hypoxia (IH, end-tidal oxygen partial pressure ( P ET O 2 ) = 45 mmHg, end-tidal carbon dioxide partial pressure ( P ETC O 2 ) clamped at normal) and poikilocapnic hypoxia (PH, P ET O 2  = 45 mmHg, P ETC O 2 not clamped). A subgroup of 10 participants were also exposed to euoxic hypocapnia (EH, P ET O 2  = 100 mmHg, P ETC O 2 clamped 8 mmHg below normal). Middle cerebral artery velocity (MCAv) and prefrontal cerebral haemodynamics were measured with transcranial Doppler and near infrared spectroscopy, respectively. IH did not affect SRT and CRT performance from rest (566 ± 50 and 594 ± 70 ms), whereas PH (721 ± 51 and 765 ± 48 ms) and EH (718 ± 55 and 755 ± 34 ms) slowed response times (P < 0.001 vs. IH). Performance on the SWM task was not altered by condition. MCAv increased during IH compared to PH (P < 0.05), which was unchanged from rest. EH caused a significant fall in MCAv and prefrontal cerebral oxygenation (P < 0.05 vs. baseline). MCAv was moderately correlated to cognitive performance (R 2  = 0.266-0.289), whereas prefrontal cerebral tissue perfusion and saturation were not (P > 0.05). These findings reveal a role of hyperventilation-induced hypocapnia per se on the development of cognitive impairment during normoxic and hypoxic exposures., (© 2019 The Authors. Experimental Physiology © 2019 The Physiological Society.)

Recent clinical trial research suggests that baseline low end-tidal CO 2 (ETCO 2 , the biological marker of hyperventilation) may predict poorer response to cognitive-behavioral therapy (CBT) for anxiety-related disorders. The present study examined the predictive value of baseline ETCO 2 among patients treated for such disorders in a naturalistic clinical setting. Sixty-nine adults with a primary diagnosis of a DSM-5 anxiety disorder, obsessive-compulsive disorder, or posttraumatic stress disorder completed a 4-min assessment of resting ETCO 2 , and respiration rate (the first minute was analyzed). Lower ETCO 2 was not associated with a diagnosis of panic disorder, and was associated with lower subjective distress ratings on certain measures. Baseline ETCO 2 significantly predicted treatment dropout: those meeting cutoff criteria for hypocapnia were more than twice as likely to drop out of treatment, and ETCO 2 significantly predicted dropout beyond other pre-treatment variables. Weekly measurement suggested that the lower-ETCO 2 patients who dropped out were not responding well to treatment prior to dropout. The present results, along with previous clinical trial data, suggest that lower pre-treatment ETCO 2 is a negative prognostic indicator for CBT for anxiety-related disorders. It is suggested that patients with lower ETCO 2 might benefit from additional intervention that targets respiratory abnormality., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Sustained or spontaneous hyperventilation has been associated with a variety of physical symptoms and has been linked to a number of organic illnesses and mental disorders. Theories of panic disorder hold that hyperventilation either produces feared symptoms of hypocapnia or protects against feared suffocation symptoms of hypercapnia. Although the evidence for both theories is inconclusive, findings from observational, experimental, and therapeutic studies suggest an important role of low carbon dioxide (CO2) levels in this disorder. Similarly, hypocapnia and associated hyperpnia are linked to bronchoconstriction, symptom exacerbation, and lower quality of life in patients with asthma. Raising CO2 levels by means of therapeutic capnometry has proven beneficial effects in both disorders, and the reversing of hyperventilation has emerged as a potent mediator for reductions in panic symptom severity and treatment success., (2010 Elsevier B.V. All rights reserved.)

Objective: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks., Method: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model., Discussion: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase., Conclusion: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.

Hyperventilation has numerous theoretical and empirical links to anxiety and panic. Voluntary hyperventilation (VH) tests have been applied experimentally to understand psychological and physiological mechanisms that produce and maintain anxiety, and therapeutically in the treatment of anxiety disorders. From the theoretical perspective of hyperventilation theories of anxiety, VH is useful diagnostically to the clinician and educationally to the patient. From the theoretical perspective of cognitive-behavior therapy, VH is a way to expose patients with panic disorder to sensations associated with panic and to activate catastrophic cognitions that need restructuring. Here we review panic disorder treatment studies using breathing training that have included VH. We differentiate the roles of VH in diagnosis, education about symptoms, training of breathing strategies, interoceptive exposure, and outcome measurement--discussing methodological issues specific to these roles and VH test reliability and validity. We propose how VH procedures might be standardized in future studies.