The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder

Abstract

The role of hyperventilation -hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação -a hipocapnia no patomecanismo do distúrbio de pânico A b s t r a c t 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 (pCO 2 ) 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.Descriptors: Acidosis; Catecholamines; Hyperventilation; Hypocapnia; Panic disorder Resumo Objetivo: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventilação crônica representa um mecanismo protetor contra os ataques de pânico. Método: Revisão seletiva da literatura a partir da base de dados Medline. Foram selecionados relatos referentes à inter-relação entre transtorno do pânico, hiperventilação, acidose, alcalose, liberação de catecolaminas e sensibilidade a catecolaminas, sendo os achados estruturados de modo a formar um modelo integrado. Discussão: Os ataques de pânico do transtorno do pânico desenvolvem-se com base numa acidose metabólica, que é uma resposta compensatória à hiperventilação crônica. Os ataques são desencadeados por um súbito aumento da pressão parcial de dióxido de carbono (pCO 2 ), quando a acidose (metabólica) latente se manifesta pela acidose hipercápnica. A condição acidótica induz liberação de catecolaminas. A simpaticotonia não pode manifestar-se durante...

Acid–base dysregulation and chemosensory mechanisms in panic disorder: a translational update

“…20 Thus, it is intriguing that despite their disparate effects, respiratory acidosis and metabolic alkalosis, both CO 2 inhalation and sodium lactate administration lead to extracellular and intracellular acidosis in the brain. 16, 21 In addition, neuroimaging studies also raise the possibility of dysregulated acid–base buffering and increased plasma and brain lactate responses to metabolic challenges in PD. 22, 23, 24 There is also a high prevalence of hyperventilation and other respiratory abnormalities among patients with PD.…”

“…22, 23, 24 There is also a high prevalence of hyperventilation and other respiratory abnormalities among patients with PD. 21, 25, 26 The link between panic attacks and pH disturbances also forms the basis of the false suffocation alarm theory of spontaneous panic, where CO 2 hypersensitivity may exist due to a malfunctioning suffocation alarm monitor. 27 Below we discuss specific areas of investigation that support the panic-pH link.…”

“…27 However, this is a faulty response because the respiratory alkalosis caused by hyperventilation is always associated with a compensatory metabolic acidosis produced by tissue buffering systems that release H + ions. 21 Panic challenge studies with acetazolamide shed light on the role of protons as effector molecules for generating panic responses; acetazolamide, a carbonic anhydrase inhibitor, blocks the facilitated conversion of CO 2 to bicarbonate and H + , leading to increases in CO 2 concentrations. Interestingly, administration of intravenous acetazolamide fails to induce panic attacks in patients with PD 53, 54 suggesting that H + ions, rather than CO 2 per se may facilitate panicogenesis.…”

Management of altered mental status — Hyperventilation due to panic in a child with juvenile diabetes — A case report

“…There are different opinions about the role of hyperventilation in panic disorders. The most widely accepted is the theory put forward by Klein 15) which states that hyperventilation is protective against panic reactions 16) . While this view explains the taking of "deep breaths" by people who are feeling anxious it does not take into account the effect that the hypocapnia induced by this voluntary hyperventilation has on the sympathetic nervous system.…”

Effect of End Tidal Carbondioxide concentration on different phases of menstrual cycle in subjects suffering with Premenstrual syndrome

“…These changes in catecholamine level and sensitivity affect heart . Lower intracellular pH is the trigger for noradrenaline release from the locus coeruleus during panic attacks (20).The changes in sympathetic activity during premenstrual phase are associated with tension and anxiety (21).…”