Hyperventilation occurs when the rate and quantity of alveolar ventilation of carbon
dioxide exceeds body's production of carbon dioxide. Hyperventilation can be voluntary
or involuntary. When alveolar ventilation is excessive, more
carbon dioxide will be removed from the blood stream than the body can produce. This causes
the concentration of carbon dioxide in the blood stream to fall and produces a state
known as hypocapnia. The body normally attempts to compensate for this metabolically. If excess
ventilation cannot be compensated metabolically, it will lead to a rise in blood pH. This rise
in blood pH is known as respiratory alkalosis. When hyperventilation leads to respiratory
alkalosis, it may cause a number of physical symptoms: dizziness, tingling in the lips,
hands or feet, headache, weakness, fainting and seizures. In extreme cases it can cause
carpopedal spasms.
Distinction from other breathing terms In very general terms, hyperventilation is
an increased alveolar ventilation. This is not to be confused with the term hyperpnea
which pertains to an increased minute ventilation. In hyperpnea, increased ventilation is appropriate
for a metabolic acidotic state whereas in hyperventilation, increased ventilation is
inappropriate for the metabolic state of blood plasma.
Hyperventilation should not be confused with tachypnea or hyperpnea. Both these terms neutrally
describe the manner of breathing rather than the impact that breathing has on carbon dioxide
levels. Exercise, fever, shivering, and other disorders can cause the body to produce more
carbon dioxide than normal. The body attempts to correct for this by breathing more rapidly
and deeply. This corrective behavior does not lead to excess ventilation. Rather it
brings the body into balance by compensating for excess CO2 production. Thus hyperpnea
in this context is not hyperventilation. In fact, if the excess CO2 production cannot
be completely cast off via hyperpnea, then a person will in fact be hypoventilating even
though they are breathing faster or more deeply than normal. For example, in certain respiratory
disorders, the transfer of carbon dioxide from the blood to the alveoli may be blocked.
No matter how deep or fast the person tries to breathe, they cannot expel enough carbon
dioxide. Causes
Hyperventilation can be voluntary or involuntary. Swimmers sometimes voluntarily hyperventilate
in hopes of extending dive time or extending the length of time they can swim underwater
without rising to take a breath, though this puts them at risk for shallow water blackout.
Anesthesiologists sometimes recommend that their patients hyperventilate prior to putting
them under general anesthesia. Certain kinds of Yoga, for example, Bhastrika yoga also
employ voluntary hyperventilation. Involuntary hyperventilation can occur in
response to both physical and emotional stimuli. These include reduced air pressure at high
altitudes, raised progesterone levels in pregnancy, head injury, stroke, respiratory disorders
such as asthma and pneumonia, cardiovascular problems such as pulmonary embolisms, anemia,
adverse reactions to certain drugs, physical or emotional stress, fear, pain, and anxiety.
Hyperventilation can also be mechanically produced in people on respirators.
Stress or anxiety commonly are causes of hyperventilation; this is known as hyperventilation syndrome.
Hyperventilation can also be brought about voluntarily, by taking many deep breaths in
rapid succession. Hyperventilation can also occur as a consequence of various lung diseases,
head injury, or stroke and various lifestyle causes. In the case of metabolic acidosis,
the body uses hyperventilation as a compensatory mechanism to decrease acidity of the blood.
In the setting of diabetic ketoacidosis, this is known as Kussmaul breathing – characterized
by long, deep breaths. Hyperventilation can also occur when someone
exercises over their VO2 max, when they're unable to generate sufficient energy through
purely aerobic respiration, but hyperventilate in an effort to do so. The VO2 max is a representation
of an individual's aerobic capacity during exercise of large duration and low intensity,
for example the marathon. It is the highest rate of oxygen consumption reached during
maximum exertion in long duration exercises. If the intensity of exercise increases past
an individual's VO2 max the consumption of oxygen will be relatively stabilized and the
body will utilize anaerobic energy substrates, e.g. hepatic glycogen through glycolysis,
also known as passing the anaerobic threshold. As the result of the above-mentioned process
there is an increase of lactic acid and carbon dioxide in the blood and therefore a decrease
of the pH of the blood. Carbon dioxide is transported as bicarbonate ion through the
blood during the gaseous exchange of oxygen and carbon dioxide between alveoli and blood
capillaries through the respiratory membrane. The increase of the level of carbon dioxide
in the blood reflects the more anaerobic metabolism past the anaerobic threshold by and hence
provokes the hyperventilation. Mechanism
In normal breathing, both the depth and frequency of breaths are varied by the neural system,
primarily in order to maintain normal amounts of carbon dioxide but also to supply appropriate
levels of oxygen to the body's tissues. This is mainly achieved by measuring the carbon
dioxide content of the blood; normally, a high carbon dioxide concentration signals
a low oxygen concentration, as we breathe in oxygen and breathe out carbon dioxide at
the same time, and the body's cells use oxygen to burn fuel molecules, making carbon dioxide
as a by-product. Normal minute ventilation is generally 5–8 liters of air per minute
at rest for a 70 kg man. If carbon dioxide levels are high, the body
assumes that oxygen levels are low, and accordingly, the brain's blood vessels dilate to assure
sufficient blood flow and supply of oxygen. Conversely, low carbon dioxide levels cause
the brain's blood vessels to constrict, resulting in reduced blood flow to the brain and lightheadedness.
The gases in the alveoli of the lungs are nearly in equilibrium with the gases in the
blood. Normally, less than 10% of the gas in the alveoli is replaced with each breath
taken. Deeper or quicker breaths as in hyperventilation exchange more of the alveolar gas with ambient
air and have the net effect of expelling more carbon dioxide from the body, since the carbon
dioxide concentration in normal air is very low.The resulting low concentration of carbon
dioxide in the blood is known as hypocapnia. Since carbon dioxide is carried as bicarbonate
in the blood, the loss of carbon dioxide will drive bicarbonate to combine with hydrogen
ions to form more carbon dioxide. The loss of hydrogen ions results in the blood becoming
alkaline, i.e. the blood pH value rises. This is known as a respiratory alkalosis.
This alkalization of the blood causes vessels to constrict. The high pH value resulting
from hyperventilation also reduces the level of available calcium, which affects the nerves
and muscles, causing constriction of blood vessels and tingling. This occurs because
alkalization of the plasma proteins increases their calcium binding affinity, thereby reducing
free ionized calcium levels in the blood. Therefore, low levels of carbon dioxide can
cause tetany by altering the albumin binding of calcium such that the ionised fraction
of calcium is reduced. Therefore, there are two main mechanisms that
contribute to the cerebral vasoconstriction that is responsible for the lightheadedness,
paresthesia, and fainting often seen with hyperventilation. One mechanism is that low
carbon dioxide causes increased blood pH level, causing blood vessels to constrict. The other
mechanism is that the alkalosis causes decreased freely ionized blood calcium, thereby causing
cell membrane instability and subsequent vasoconstriction and paresthesia.
Hyperventilation can be useful in the management of head trauma. After head injuries, fluids
can leak into the cranial vault, thus elevating intracranial pressure. Since the total cranial
volume is relatively fixed, and the brain is much more compressible than the skull,
in settings of increased intracranial pressure, the brain is preferentially compressed and
damaged. Hyperventilation, and the resultant cerebral vasoconstriction, is useful in this
situation, since it decreases the volume of blood in the brain. Less blood volume in the
cranial cavity results in less pressure compressing the brain. However, this vasoconstriction
comes at the cost of reducing blood flow to the brain, which can potentially result in
ischemic damage. Treatment
The first step that should be taken is to treat the underlying cause. If hypoxia is
present supplemental oxygen may be useful. If it is due to anxiety as the cause of hyperventilation
syndrome, counseling to identify and address triggers may be useful, possibly supported
by a few days of benzodiazepines. References
See also List of terms of lung size and activity
Control of respiration Respiratory alkalosis
Shallow water blackout, the role of hyperventilation in some drowning incidents