Overview

The symptoms of hyperventilation vary according to the extent that blood gases are altered and the duration of the problem. Tingly fingers and lips, or "pins and needles" (paraesthesia) is very common, although there can be neurological and other symptoms as well. All of these symptoms have one underlying cause: respiratory alkalosis from blowing off too much CO₂.

Paraesthesia

This common symptom of hyperventilation is caused by imbalances in ion transport in sensory nerve terminals, due to the alkalosis. All of the ion channels and transporters in sensory (and other nerves) are sensitive to changes in extracellular pH, and their activities are out of balance in different ways in alkalaemia. Mogyoros et al.(2000) discuss the details of these alterations in ion fluxes in various paraesthesias. In short, persistent sodium channel activation leads to hyperreactivity of sensory nerves, producing the strange sensations.

Dizziness and fainting

Most arteries in the body constrict in response to increased pH in the surrounding environment. This make good physiological sense on a local, microscale since a tissue that is not producing CO₂ (and hence H⁺) probably does not require urgent perfusion. Because neurons have no anaerobic metabolism rapid changes in blood flow can be required and the cerebral arteries are quite sensitive to changes in local pH in order to divert blood to those regions requiring O₂. However, when all of the blood perfusing the brain is alkaline, this leads to constriction of all cerebral blood vessels, producing back pressure and throbbing in the larger vessels. This produces the headache in hyperventilation, and can lead to fainting if brain perfusion is too low.

Tetany and convulsions

The mechanism underlying these symptoms is complex. Firstly, recall that H⁺ bind to blood proteins such as haemoglobin (see here). Calcium also binds to blood proteins, so the two ions compete. In the respiratory alkalosis that results from hyperventilation, there are fewer H⁺ present in plasma, so more free ionised calcium binds to plasma protein. The result is hypocalcaemia, which produces the symptoms of tetany and colvulsions.

You'd think that lower blood calcium would lead to less activity in excitable cells, since the driving force for calcium entry into muscles and nerves would be decreased. However, early experiments in animals show that the tetany seen in hypocalcaemia can be blocked with antagonists of nicotinic acetylcholine receptors, implicating motor neuron hyperexcitablity, much like the effect on sensory nerves. The opening of neuronal sodium channels is affected by local calcium ion concentration, so hypocalcaemia increases the firing of neurons in the periphery (leading to tetany) and central nervous system (leading to convulsions).