An abnormal type of breath is known as "periodic breathing", which occurs in various morbid conditions. The patient breathes deeply for a short period of time and then breathes superficially, or does not breathe at all for another short period, so on, cyclically. The most common type of periodic breath is the one known as Cheyne-Stokes breathing. It is characterized by a breathing of increasing depth and then decreasing until it fades, with cycles that repeat indefinitely at intervals ranging from 45 seconds to 3 minutes.
Another type is the so-called Biot breath, characterized by normal breathing cycles - 1, 2, 3, 4 or more acts per cycle - each followed by a period of complete apnea. The cycles are repeated indefinitely and have a very variable duration, sometimes just 10 seconds, other times even 1 minute. For Cheyne-Stokes breath or periodic breathing in the medical field, we mean a pathological breath. In this state the person alternates between apnea and even long periods (it can even reach 20 seconds) in phases in which one passes gradually from deep breathing to an increasingly shallow one (short and frequent breathing cycles) which ends again in the apnea phase. This loop can be prolonged for several days but is usually transitory. Usually when this state occurs, there is not much left to do and the patient is destined for exitus within a few hours.
We admit that breathing becomes much more frequent and deeper than usual. In this case the PCO2 of the pulmonary blood is lowered and, a few seconds later, this blood reaches the brain and inhibits breathing. Consequently, in the pulmonary blood the Pco2 progressively increases. After a few seconds the blood with a high content of C02 reaches the respiratory center and the respiration is activated again, so that, once again, the subject goes into hyperpnea, starting a new cycle and so on, causing the periodic breathing of Cheyne-Stokes. It is obvious that the periodic feedback required for the perpetuation of Cheyne-Stokes breath could be attributed to the oscillations in more and less of the blood concentration of the oxygen. However, Cheyne-Stokes's breathing may also occur after denervation of the chemoreceptors, which shows that the stimulus constituted by the lack of oxygen does not represent a necessary component. Since the feedback mechanism at the base of Cheyne-Stokes's breathing is operative in any subject, the question to be answered does not concern the reason for its occurrence in certain pathological conditions, but rather the reason why it does not always occur and in every individual.
The fact is that the feedback under discussion is strongly dampened. Damping of the normal respiratory control mechanism. In order for the Cheyne-Stokes oscillation to occur, some time must pass in the hyperpnoemic phase before the PCO2 of body fluids falls to a level below normal. Then this decrease in PCO2 starts the apnoic phase, which also has to last long enough for the tissue PCO2 to increase well above the normal average level. In other words, body fluids as a whole contain a huge amount of respiratory gases, so it takes long periods of apnea or hyperventilation, before significant changes in the concentration of these gases can be produced. In normal subjects, before these changes can be made, usually the respiratory center re-adjusts the respiratory rhythm so as to avoid, in the body fluids, those wide excursions of the PCO2 that are responsible for Cheyne-Stokes breathing. Thus, the enormous capacity that tissues have to store carbon dioxide acts as a "damping" factor that prevents the formation of Cheyne-Stokes breathing in normal subjects. However, even in normal people, feedback is not completely muted. Therefore, if an individual voluntarily puts himself into hyperpnea for a minute or more and then re-affirms his own breathing to involuntary control, he first presents a period of apnea and then one or two very muted breath cycles of Cheyne-Stokes. There are several conditions in which the damping of the feedback mechanism can be overwhelmed and then spontaneous oscillation may occur.
Two of these conditions are:
1) the longer duration of blood flow from the lungs to the brain and
2) a greater gain
of the respiratory control feedback mechanisms by the respiratory center. Breath of Cheyne-Stokes from increase of time of circulation from the lungs to the
brain.
If the transmission of blood from the lungs to the brain undergoes a strong delay, the damping factor described above can not operate satisfactorily,
so as to block the feed-back, since the gases of the body fluids can now vary drastically before the center respiratory system may experience the modification
of blood gas concentration.
Consequently, the amplification or "gain" of the feedback circuit is strongly enhanced and then the system spontaneously oscillates. It has been
experimentally established that 1 or 2 minutes of delay in the passage of blood from the lungs to the brain causes in almost all experimental animals the
spontaneous onset of the Chyene-Stokes breath. Breath of Cheyne-Stokes from increase of the "gain" of the feedback system in the respiratory center.
Sometimes, injuries in the brain trunk increase the feedback gain of the respiratory center, in response to changes in PCO2 and blood pH. This does not
mean that the sensitivity of the centers to these two humoral factors is necessarily increased, but rather that minimal variations in the concentration
of one of the two factors cause drastic variations in ventilation. In fact, the respiratory center is often strongly depressed even if the "gain" of the control
system is high. By way of example, there may be complete shutdown of the ventilation to a 30 mm Hg Pco2 and, however, at 40 mm Hg of Pco2 there will be
half-normal ventilation. In this case the variation of the ventilation is infinite - from infinity to a determined value -. Therefore, the "gain" is
infinite even if the ventilation is only reduced to half the normal. Consequently, the respiratory control system can oscillate, up and down, between
breathing and apnea, as characteristically occurs in the Cheyne-Stokes breath. This is probably due to the fact that Cheyne-Stokes breathing occurs in many
patients with brain injuries.
Heart failure is the most common cause of Cheyne-Stokes breathing, which can sometimes occur continuously and each time for several months. In these cases, many factors seem to participate in determining Cheyne-Stokes's breathing. In the first place, in slowing down the circulation, in the insufficiency of the heart, the time of transmission of the blood from the lungs to the brain increases, thus reducing the efficiency of the damping system mentioned above. Secondly, the volume of the left heart is sometimes greatly increased. This also increases the circulation time from the lungs to the brain. Combining this factor with the slowing of blood flow, the time required for the passage of blood from the lungs to the brain - which is usually 5-10 seconds - can increase by as much as 6 times, ie up to 30-60 seconds, radius in the as from experiments in the dog there are spontaneous oscillations. Thirdly, there is another factor that perhaps comes into play in determining a Cheyne-Stokes breath of the same kind as one in heart failure. It consists of the difficulty of taking oxygen in case of pulmonary edema. In this case, the oxygen saturation of the arterial blood takes place at a level so low as to significantly effect the feedback mechanism, consisting of the hypoxia-chemoreceptor system, which greatly increases the feedback gain in the oscillatory system of Cheyne-Stokes. A particular reason in favor of the validity of this factor lies in the fact that oxygen therapy often succeeds in eliminating Cheyne-Stokes's breathing in cardiopaths.
In many patients with very high cerebrospinal fluid pressure, in people suffering from cerebral contusion, by direct compression on the brain tissues, or from destructive brain disease, a periodic breathing often takes place which usually lasts for a short time, after which death intervenes. This is a breath like the Biot type, but sometimes it can be of the Cheyne-Stokes type. That is, the respiratory acts occur in groups of 2, 3 or 4 and so on, instead of at increasing depth and then degrading until apnea. The mechanism of Biot's breathing is not known, but it is to be considered that it depends on a direct anomaly of the mechanism of the fundamental rhythm of the same respiratory center. The short periodicity of Biot's breath means that almost certainly it is not supported by the same feedback mechanism that underlies Cheyne-Stokes's breathing.
It's a deep and labored breathing pattern often associated with severe
metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney
failure. It is a form of hyperventilation, which is any breathing pattern that
reduces carbon dioxide in the blood due to increased rate or depth of
respiration.
In metabolic acidosis, breathing is first rapid and shallowbut as acidosis
worsens, breathing gradually becomes deep, labored and gasping. It is this
latter type of breathing pattern that is referred to as Kussmaul breathing.
Kussmaul breathing is respiratory compensation for a metabolic acidosis,
most commonly occurring in diabetics in diabetic ketoacidosis. Blood gases of a
patient with Kussmaul breathing will show a low partial pressure of CO2
in conjunction with low bicarbonate because of a forced increased respiration (blowing
off the carbon dioxide). Base excess is severely negative. The patient feels
an urge to breathe deeply, an "air hunger", and it appears almost involuntary.
A metabolic acidosis soon produces hyperventilation, but at first it will tend
to be rapid and relatively shallow. Kussmaul breathing develops as the acidosis
grows more severe. Indeed, Kussmaul originally identified this type of breathing
as a sign of coma and imminent death in diabetic patients.