Her er en spennede studie som nevner at relasjonen mellom panikkanfall og hyperventillering kommer i utgangspunktet av metabolsk acidose, som er en kompensasjon for kronisk hyperventillering. Når CO2 synker øker nervesystemets sensitivitet til catacholaminer (stresshormoner som adrenalin og noradrenalin) og panikkanfallet kommer. I hyperkapnisk acidose (høy CO2) minker sensitiviteten til stresshormoner og kroppen beskyttes mot panikkanfall. Igjen en bekreftelse på at acidose fra CO2 er beskyttende, mens acidose fra andre ting er provoserende.

http://www.ncbi.nlm.nih.gov/pubmed/17713689

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462006005000048&lng=en&nrm=iso&tlng=en

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.

Chronic hyperventilation predisposes an individual to PD, since compensatory mechanisms (such as alterations in renal function and tissue buffer capacity) lead to chronic metabolic acidosis, which remains latent until it is activated by chronic hypocapnia.

Therefore, therapeutic approaches should address long-term regulation of respiratory patterns60 and elimination of metabolic acidosis.

Nevner at oksygenering av vev ikke er pga CO2 sin vasodilerende effekt, men fra økt pumping av blod og høyre-skift av oksygendissassosiasjonskurven. Denne studien ga ikke økt oksygenering av vev når hjertets pumpeevne ble holdt konstant. Den påpeker at blodtrykk og hjerterytme ikke ble endret ved hyperkapni, selv om hjertets pumpeevne øker.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464052/

It is well established that mild hypercapnia improves peripheral perfusion and increases tissue PO2. Our main question was whether peripheral vasodilation is a direct effect of the CO2 or a secondary result of increased cardiac output and related central autonomic homeostatic responses. We found that mild hypercapnia did not increase subcutaneous tissue oxygenation when systemic blood flow and mean arterial pressure remained constant during cardiopulmonary bypass. Increased tissue oxygenation during mild hypercapnia thus most likely results from a hyperdynamic circulatory response and shifting oxyhaemoglobin dissociation curve rather than direct peripheral vasodilation.

Hypercapnia increases both sympathetic and cardiac vagus nerve activity in anaesthetized dogs. Such co-activation of vagus and sympathetic systems, which can be initiated reflexively or by action on higher centres, has been shown to be of distinct physiological benefit in controlling reactions that relate cardiac function to body need. Since the sympathetic and parasympathetic systems are co-activated during systemic hypercapnia, blood pressure and heart rate response depends on the functional balance between these two systems. We were unable to evaluate heart rate during bypass, but have previously shown that both mean arterial blood pressure and heart rate remained essentially unchanged during hypercapnia even though cardiac output increases 25%.11

Thus, the vasodilator effect of CO2 is particularly marked in the cerebral circulation where a CO2 concentration of 7 to 10% nearly doubles cerebral blood flow (CBF) in humans,39 while mild hypercapnia (PaCO2 ~ 50 mmHg) impairs autoregulation of CBF and is associated with an overall increase in cerebral oxygenation.11, 40 A similar cerebrovascular response during cardiopulmonary bypass leads to an increase in CBF41 that is associated with a reduction in cerebral oxygen consumption.42 On the other hand, peripheral vasomotor tone during hypercapnia is essentially the result of a balance between the direct effects of CO2 and the level of sympathetic activity.38

The mechanism by which CO2 exerts its direct effects on the cerebral vasculature seems to involve nitric oxide (NO), ATP-sensitive potassium channels, and cyclooxygenase-dependent pathways. The CO2-NO axis is considered a cardinal pathway for CBF regulation in humans. Thus, although ATP-sensitive and Ca2+-activated potassium channels are also major systems that respond to hypercapnic acidosis, their response is incomplete in the absence of NO donors. In both animals43 and humans,44 hypercapnic vasodilatation is mediated by inhibition of nitric oxide synthase — the enzyme responsible for nitric oxide synthesis. It is probable that the vasodilation to hypercapnic acidosis is mediated either by increased synthesis of NO or increased sensitivity to NO.

However, 20 to 30 minutes is sufficient to obtain stable tissue oxygen values with tonometric systems that accommodate tissue oxygen probes.