Hyperventilation causes dilation of arteries?

Veronique sunshyne at austin.rr.com
Wed Jan 12 16:00:14 EST 2000


> Hi,
>
> I understand that upon hyperventilation, the amount of CO2 in the
> blood goes down and as a result the pH goes up. And then, supposedly
> as a consequence, the arteries dilate, blood streams in and is not
> available for the brain anymore and you get dizzy.
>
> Why does the high pH cause the arteries to dilate? What are they
> thinking? Does this mechanism have any physiological usefulness?
>
> Thanks,
>   Axel

This has been taken from http://www.umds.ac.uk/physiology/BDS1B/1B33.htm

The effects of hyperventilation

Hyperventilation is an increase in the breathing above the level needed to
keep the PACO2 constant; in hyperventilation the PACO2 falls.
Hyperventilation should be distinguished from hyperpnoea, which occurs in
exercise when the carbon dioxide production is increased, and is an increase
in ventilation that stops the PACO2 from rising. Pain and anxiety cause
hyperventilation so it is important for dentists to understand and recognise
the effects of hyperventilation. As well as reducing the PACO2,
hyperventilation makes the PAO2 rise but subjects who hyperventilate from a
Douglas bag containing 5% CO2 in air, which will prevent the PACO2 falling
during the hyperventilation, will show few of the effects of
hyperventilation. Therefore most of the effects of hyperventilation are due
to the fall in PACO2; however the dry mouth and coughing seen during and
after hyperventilation persist when hyperventilating with 5% CO2 in air so
they are not due to a fall in the PACO2. The dry mouth is produced by the
high flow of air over the mucosa making saliva evaporate, and a similar
effect will occur throughout the respiratory tract. The drying of the mucous
membranes will stimulate irritant receptors that reflexly induce coughing.

Effects on the breathing

The normal stimulus for breathing is the partial pressure of carbon dioxide
which will fall during hyperventilation. Therefore it becomes increasingly
difficult to hyperventilate as time goes by; muscle fatigue may also
contribute to this. After hyperventilation, breathing may slow down or even
stop because of the low partial pressure of carbon dioxide.

After prolonged hyperventilation, breathing may be intermittent
(Cheyne-Stokes breathing), because of the differences in the way oxygen and
carbon dioxide are carried in the body fluids. There are approximately 500
ml/l of carbon dioxide in blood, and most of it is in the form of hydrogen
carbonate ions (HCO3-). These ions are able to cross the capillary
endothelium so they will be found throughout the extracellular fluid with
little in intracellular fluid because of the negative potential inside
cells. The volume of extracellular fluid (plasma plus interstitial fluid) is
approximately 16 l, so there are at least 8 l of carbon dioxide in the body
(16 l x 500 ml/l). If prolonged hyperventilation reduced the amount of
carbon dioxide by, for example, half, there would be 4 l left in the body
and 4 l more would have to be produced before the amount of carbon dioxide
in the body returned to normal. The body produces 200 ml/min of carbon
dioxide at rest so it would take 20 minutes for the amount of carbon dioxide
to return to normal after such a severe degree of hyperventilation.

The solubility of oxygen in the body fluids is low, so there will be only
small amounts of oxygen in the cells and interstitial fluid, compared to the
amount bound to haemoglobin in the blood. The concentration of oxygen in
arterial blood is approximately 200 ml/l and it will be lower in venous
blood; the blood volume is approximately 5 l so the amount of oxygen in the
blood will be no more than 1 l (5 l x 200 ml/l). There will be some oxygen
also in the lungs; the volume of the functional residual capacity is around
2.5 l and the air within it, even though it will have a higher than normal
concentration of oxygen after hyperventilation, can be no more than 20%
oxygen. Therefore, there will be approximately 0.5 l of oxygen in the lungs
(2.5 l x 20/100), giving a total amount of oxygen in the body of 1.5 l. The
oxygen will be consumed at 250 ml/min at rest so would last for 6 minutes;
in practice, hypoxia will stimulate the breathing long before the oxygen is
used up when the partial pressure of carbon dioxide is still very low. The
hypoxia will stimulate a few breaths which will reduce the hypoxic
stimulation and, because the carbon dioxide is still low, the breathing will
stop again. The amount of oxygen in the body will fall again until the
hypoxia stimulates breathing once more, giving intermittent breathing which
will continue until the partial pressure of carbon dioxide has returned to
normal.

The change in pH and its effects

The blood pH will rise during hyperventilation because the reaction:

CO2 + H2O ----> H+ + HCO3-

will move to the left as the hyperventilation reduces the concentration of
carbon dioxide. The plasma proteins contain some carboxyl and amino groups
that will lose hydrogen ions as the pH rises.

R-COOH ----> R-COO- + H+         R-NH3+ ----> R-NH2 + H+

Consequently, the plasma proteins will become more negatively and less
positively charged during hyperventilation. Approximately half the calcium
ions in the plasma are carried bound to proteins and the increasing
negativity of the proteins will make more calcium bind to them during
hyperventilation, so the concentration of free calcium will now fall.

The reduced free calcium concentration will have an effect on the threshold
of nerve fibres. When a nerve fibre is depolarised, the membrane becomes
more permeable to sodium ions which rush in making the inside more positive.
At the same time as the sodium ions go in, potassium ions will leave the
cell because the depolarisation means that the electrical potential which
holds the potassium inside the cell has reduced. For small depolarisations
that do not reach the threshold, the number of potassium ions going out is
greater than the number of sodium ions going in, so the cell becomes more
negative and returns to the resting membrane potential: the threshold has
not been reached. As the depolarisations get larger, the inward current of
sodium increases faster than the outward current of potassium ions and
eventually a potential is reached where there are more sodium ions coming in
than potassium going out, so the cell becomes more positive and an action
potential is produced: the cell has been depolarised beyond its threshold.
At rest and for small depolarisations, the current of sodium ions is
inhibited by calcium ions so that during hyperventilation, when the free
calcium concentration falls, the inward current of sodium ions increases.
Therefore, the threshold will be reached more easily and eventually action
potentials will occur spontaneously.

Spontaneous action potentials in afferent fibres produce tingling, pins and
needles or other strange sensations in the hands, feet and other
extremities; normal sensations are not produced because the pattern of
action potentials in the nerve fibres are unusual. If the optic nerve is
affected, flashes of light will be seen and ringing in the ears may arise
from spontaneous action potentials in the auditory nerve.

If efferent nerve fibres are involved, the muscles they supply will contract
involuntarily, explaining the difficulty in writing. The contraction is due
to action potentials arising in the nerves, not in the muscle fibres
themselves: if the facial nerve is tapped where it emerges from the parotid
gland in someone who is hyperventilating, the muscles of the face will
contract, giving a marked grimace (Chvostek's sign) even though the muscles
themselves were not tapped. In hyperventilation the hands and feet are
particularly affected and become flexed because there are larger amounts of
flexor than of extensor muscles; these contractions are referred to as
carpo-pedal spasm. Muscle contractions due to a low calcium concentration
are generally known as tetany, which can be confused in speech with the
plural of tetanus. Severe tetany can be fatal because the muscle adducting
the vocal cords, the lateral crico-arytenoid, may be affected, closing the
airway.

The cardiovascular changes

Carbon dioxide is a vasodilator, so the low level of carbon dioxide in the
body will have a direct effect on arterioles, constricting them and reducing
the blood flow to the organs they supply. Carbon dioxide also stimulates the
vasomotor centre so the low level of carbon dioxide will produce less
activity in sympathetic constrictor fibres, making arterioles dilate. Organs
which normally have a high level of sympathetic activity, such as the skin,
will show the vasodilatation and the faces of subjects who are
hyperventilating may be red; organs like the brain in which the arterioles
have very little sympathetic activity to be inhibited, will obviously show
the vasoconstriction, because of the direct effect of the low carbon
dioxide. The brain becomes hypoxic but this has less effect on the cerebral
arterioles than the low partial pressure of carbon dioxide, so the blood
flow remains low despite the hypoxia, producing dizziness and tunnel vision.
In the brain there may be a reactive hyperaemia when the hyperventilation is
stopped and the dilatation of the meningeal arterioles can allow the
arterial pulsations to reach the meninges causing the pulsing headache which
may occur after the hyperventilation.

There is also a marked tachycardia (acceleration of the heart rate) during
hyperventilation. Part of this may arise from the exertion involved in
hyperventilation, but the tachycardia is less marked after hyperventilating
with 5% CO2, suggesting it is related to the low levels of carbon dioxide.
There are stretch receptors in the lung which can affect the heart rate and
they will be stimulated more intensely and more often during
hyperventilation, but if they were the sole cause of the tachycardia, the
heart rate would be the same after hyperventilating with 5% CO2 as after
hyperventilating with air. If vasodilatation occurred in many organs, there
might be a drop in arterial pressure which could produce a tachycardia
through the baroreceptor reflex but measurements of arterial blood pressure
during voluntary hyperventilation suggest that the arterial pressure does
not fall. If the hyperventilation is due to an incorrect setting of an
artificial ventilator that works by positive pressure, there will be a low
arterial pressure because the positive pressure artificial ventilation
impedes the venous return. In other cases, it appears most likely that the
tachycardia arises from either a change in nervous activity going to the
sino-atrial node (inhibition of the vagus or stimulation of the sympathetic
fibres) or from effects of the low free calcium ion concentration on the
membrane potentials of sino-atrial node cells, similar to the effects on
nerve fibres.

Hope it helped!
PS: Took me 30 seconds to find that....

Veronique







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