Alt om hva som gjør at vi ikke greier å holde pusten lenge.
This article reviews the basic properties of breath-holding in humans and the possible causes of the breath at breakpoint. The simplest objective measure of breath-holding is its duration, but even this is highly variable. Breath-holding is a voluntary act, but normal subjects appear unable to breath-hold to unconsciousness. A powerful involuntary mechanism normally overrides voluntary breath-holding and causes the breath that defines the breakpoint. The occurrence of the breakpoint breath does not appear to be caused solely by a mechanism involving lung or chest shrinkage, partial pressures of blood gases or the carotid arterial chemoreceptors. This is despite the well-known properties of breath-hold duration being prolonged by large lung inflations, hyperoxia and hypocapnia and being shortened by the converse manoeuvres and by increased metabolic rate.
Breath-holding has, however, two much less well-known but important properties. First, the central respiratory rhythm appears to continue throughout breath-holding. Humans cannot therefore stop their central respiratory rhythm voluntarily. Instead, they merely suppress expression of their central respiratory rhythm and voluntarily ‘hold’ the chest at a chosen volume, possibly assisted by some tonic diaphragm activity. Second, breath-hold duration is prolonged by bilateral paralysis of the phrenic or vagus nerves. Possibly the contribution to the breakpoint from stimulation of diaphragm muscle chemoreceptors is greater than has previously been considered. At present there is no simple explanation for the breakpoint that encompasses all these properties.
At breakpoint from maximum inflation in air, the Pa/etO2 is typically 62 ± 4 mmHg and the PetCO2 is typically 54 ± 2 mmHg (n = 5; Lin et al. 1974), and the longer the breath-hold the more they change.
Nunn (1987) estimates that consciousness in normal adults is lost at PaO2 levels below ∼27 mmHg and PaCO2 levels between 90 and 120 mmHg.
This is because the rhythmic EMG and negative pressure waves occur simultaneously, because their frequency and amplitude are within the respiratory range and because they increase as CO2 levels rise towards the end of the breath-hold. This CO2 rise would stimulate the central respiratory rhythm.
Endelig en studie som viser direkte hva som skjer med CO2 når vi holder pusten etter utpust. Her kaller de det etter «functional residual capacity» (wikipedia), altså etter en normal og passiv utpust. Denne studien viser først og fremst hva som skjer i løpet av én enkelt pustehold. De nevner også at det tar 5-10 sekunder etter innpust igjen før CO2 nivet begynner å synke. Så i metablsk pust (RecoveryBreathing) hvor vi puster 10sek inn/ut og har 10 sek pause bør CO2 lett kunne stabiliseres på et høyere nivå enn normalt.
Hele Studien: http://journal.publications.chestnet.org/data/Journals/CHEST/21737/958.pdf
Breath-holding serves as a model for studying gas exchange during clinical situations in which cessation of ventilation occurs. We chose to examine the arterial blood gas changes that occurred during breath-holding, when breath-holding was initiated from functional residual capacity (FRC) while breathing room air. Eight normal subjects who had a radial artery catheter placed for another study were taught to breath-hold on command from FRC. FRC was determined using respiratory inductance plethysmography. Arterial blood gas specimens were obtained at 5-s intervals until the termination of breath-holding. The average breath-holding time (+/-SD) was 35 (+/-10 s). The PaO2, PaCO2, and pH values were plotted against time and individually fit to logistic equations for each subject. The arterial PaO2 fell by a mean of 50 mm Hg during the first 35 s of breath-holding under these conditions, while the arterial PCO2 rose by a mean of 10.2 mm Hg during the first 35 s and the pH fell by a mean of 0.07 in the first 35 s. The rapid decline in PaO2 is greater than that previously reported using different methods and should be considered in clinical situations in which there is an interruption of oxygenation and ventilation at FRC while breathing room air. The changes in PaCO2 and pH are similar to those previously reported in paralyzed apneic patients.
We demonstrated during 5 breath-holding runs in which additional arterial specimens were obtained at 5 and 10 s after breath-hold (Fig 6) that the elevated arterial PCO2 did not begin to fall until at least 5 s after breaking from the breath-hold in 1 run and greater than 10 s in 3 other runs. This implies that the removal of the remaining arterial PCO2 by the lungs took longer than 5 s before recirculation from pulmonary capillary blood could lower the arterial PCO2 in the radial artery. The second less significant factor that explains the persistent elevation of arterial PCO2 is the concentrating effect caused by the decreasing LV. The concentrating effect occurs with breath-holding, as more oxygen is removed from the lungs than carbon dioxide is added. As carbon dioxide production continues to occur, the capillary