hyperventilation

hyperventilation The ventilation of the lungs is the volume of air breathed in (and out) per minute. Hyperventilation means that this volume is excessive, such that carbon dioxide is lost from the lungs at a greater rate than it is being produced by metabolism in the body.

The term ‘hyperventilation’ does not apply to the increases in breathing that meet appropriately the varying demands of movement, work, and exercise. In the alveoli, in the depths of the lungs, when breathing changes involuntarily to meet these needs, there is very little change in the average concentrations of oxygen and of carbon dioxide. These concentrations are such that the blood, after exposure to them, leaves the lungs with its oxygen topped up to full saturation (however much has been removed during circulation around the body) and its carbon dioxide reduced to the concentration which is normal for arterial blood (however much has been added).

Now, deliberately, take a few extra deep breaths: in the lung alveoli the concentration of oxygen is immediately increased, and that of carbon dioxide decreased. This cannot load more oxygen into the blood, because the oxygen concentration in the lungs was already sufficient to saturate the oxygen-carrying capacity of its haemoglobin. However, what this over-breathing can and does do, very readily, is to remove more carbon dioxide. Then there is less of it in the blood leaving the lungs, and hence less in the arterial blood; and after a few more deep breaths, less everywhere in the body, because carbon dioxide diffuses readily in and out of body fluids and cells. But if attention is now diverted from breathing, any small decrease which has been imposed on the carbon dioxide level in the blood will have been detected by the chemoreceptors, leading to a reflex decrease in breathing which rapidly restores the blood carbon dioxide to its normal level.

What, then, happens if hyperventilation — deliberate over-breathing — is continued? The ‘wash-out’ of carbon dioxide progresses, from the lungs, and hence from the blood, and from the body tissues including, importantly, the brain. Carbon dioxide is a crucial variable in acid–base homeostasis; its reduction shifts the body fluids towards greater alkalinity (increased pH) and this has further knock-on effects. For one thing, it tends to cause constriction of some blood vessels, particularly those in the brain, reducing its blood supply and therefore its oxygen supply. So, in what might seem the midst of plenty when an excess of air is being shifted in and out of the lungs, the brain can actually be short of oxygen. It is for this reason that persistent, vigorous over-breathing soon makes us feel faint and dizzy. Another result of the alkalinization of the blood may be tetany: an uncontrollable twitching (caused by neuromuscular over-excitability consequent upon an increase in the binding of calcium ions to proteins in the plasma).

All of this implies that the measureable criterion of hyperventilation is lower-than-normal carbon dioxide in the blood. (This is usually expressed as the ‘PCO₂’, representing the partial pressure of carbon dioxide gas with which a sample of blood would be in equilibrium.) In most circumstances, in healthy people, the involuntary breathing control mechanisms keep the PCO₂ in arterial blood at the normal level, or bring it quickly back to that level following any disturbance.

There are, however, circumstances when other vital physiological adjustments take precedence over maintaining the normality of the arterial blood carbon dioxide. In these instances the body's reflex control of breathing itself results in hyperventilation. One of these circumstances is high-altitude hypoxia. When the pressure of oxygen in the inhaled air is too low to saturate the haemoglobin in the blood, an increase in breathing gains a little higher concentration of oxygen in the lungs, at the expense of decreasing the carbon dioxide. Some resulting disturbance of acid–base balance can be tolerated, and compensated for if exposure is prolonged. A second circumstance is an increase in blood acidity, such as occurs due to production of lactic acid in strenuous exercise, or of other acids in starvation. This disturbance is countered by reflex hyperventilation, causing a shift back in the alkaline direction by washing out carbon dioxide.

Short-term, minor degrees of hyperventilation can occur without conscious intention as an aspect of anxiety: adrenaline and other components of the stress response can also stimulate breathing. Airplane pilots, for example, have been reported to hyperventilate during landing procedure, and it is a common experience to be aware of overbreathing in some demanding situations. More seriously, full-blown ‘panic attacks’ are likely to be accompanied, and aggravated, and some would say caused, by hyperventilation.

There has been considerable medical interest, research, and some controversy in recent decades concerning the so-called hyperventilation syndrome(s). Certainly some people hyperventilate habitually, for reasons that are usually unclear, but that have been linked to psychological disorders. A wide variety of mental and physical symptoms have been attributed to such hyperventilation and its consequences, simulating other medical conditions, and even surgical emergencies. Improvement of health and well-being can follow a training regime to bring the breathing pattern back to normal.

Deliberate hyperventilation before breath-holding can extend the time before the breaking point at which the urge to breathe can be resisted no longer. It seems obvious that this is to be expected, simply because the more oxygen has been taken into the lungs the longer it will last. But it is not as simple as that, and the complexities are relevant to the potentially dangerous situation of over-breathing before diving or swimming underwater. The predominant factor that ends a breath-hold, by causing an overpowering drive to breathe, is a certain trigger level reached by the rising carbon dioxide; after overbreathing it takes longer to reach this trigger, because the starting level was lowered. But the overbreathing has not stored extra oxygen in the blood, so that it now has a longer time in which to go on being depleted. The result can be faintness or even unconsciousness, before the swimmer feels the need to surface. Although the progressive oxygen depletion itself also contributes to the drive to breathe in this situation, those individuals whose reflex response to oxygen lack is relatively insensitive may be at risk.

Sheila Jennett

See also breathing; carbon dioxide; chemoreceptors; diving; lungs; oxygen.