The lungs and the chest wall are elastic structures. When the diaphragm lowers,
the lungs find themselves in a cavity where the intrapleural pressure is lowered,
because the diaphragm, like a sort of syringe plunger, going down, creates
depression, a sort of "suction".
Therefore the lungs are also obliged to
follow the diaphragm and expand, allowing the entry of air into them. After
inhalation, the lungs return to the initial position, essentially "deflate" and
the air escapes along with the waste gases. This obviously happens in a healthy
lung, because in chronic bronchial pneumopathies obstructive, this process is
prevented, up to the established pictures of fibrothorax or interstitiopathy
It consists in the exchange of gas (O2 and CO2) between blood and tissues.
This is the most important stage of breathing, as it allows the life of cells.
Oxygen diffusion occurs passively in relation to the pressure gradient (65 mmHg)
existing between blood and tissues, even if several investigations suggest the
existence of particular carrier molecules (carriers of oxygen) and that
transport is also regulated by metabolic needs of cells. Also for the CO2 that
is produced following the decarboxylation of carboxylic acids, together with the
presence of a pressure gradient (7-8 mmHg) the hypothesis of an active mechanism
is invoked.
The respiratory failure are divided into:
- Pure hypoxemic respiratory insufficiency (type I): corresponds only to
the lack of oxygen in the arterial blood (partial pressure of O 2 in the
arterial blood of less than 60 mmHg) with normal carbon dioxide (CO2)
- Hypoxemic-hypercapnic respiratory insufficiency (type II): corresponds
to the simultaneous presence of O2 deficiency associated with excess of CO2 in
the arterial blood (partial pressure of CO2 in the arterial blood above 45 mmHg)
Once the oxygen has penetrated into the cell, it then participates
in all its oxidative mechanisms, reacting with different enzymes. The condition
is therefore defined that a deficiency of oxygen (hypoxaemia) occurs in the
blood, accompanied or not to increase the carbon dioxide (hypercapnia), due to
alterations of one or more phases of respiration. In practice we talk about
respiratory failure when the Pao2 is less than 60 mmHg and the Pa CO2 exceeds 49
mmHg.
When there is only hypoxemia, one speaks of partial respiratory
insufficiency, if hypercapnia is also present, one speaks of I.R. total. The
inadequacy will be established when it is already evident in conditions of rest
and latent if it appears after a light physical exercise. Moreover, in relation
to the duration and the modalities of onset, it will be acute or chronic and
chronic flare-ups due to complications. The I.R.. acute and chronic exacerbation
can be partial or global and in the latter eventuality, since the mechanisms of
renal compensation (reabsorption of bicarbonates) are slow, the resulting
acidosis is decompensated, whereas in I.R. Chronic acid usually has compensated
respiratory acidosis.
In relation to the pathogenesis, I.R. It can be caused by:
a) Ventilatory insufficiency, ie the lung is unable to expand due to mechanical
ventilation problems, e.g. in multiple rib fractures;
b) altered ventilatory system we can have in the following conditions:
1) rib cage: Cifoscoliosis, fibrothorax, thoracoplasty, ankylosing spondylitis,
obesity hypoventilation
2) Airways and lungs: laryngeal and tracheal stenosis, obstructive sleep apnea (OSAS),
chronic obstructive pulmonary disease
b) Alveolar-capillary insufficiency, ie the blood does not oxygenate due to
thickening of the alveolar-capillary membrane;
c) Circulatory insufficiency, e.g. the heart is not able to pump the mass of the
circulating blood and, therefore, the pulmonary circulation is prevented and the
oxygenation is insufficient.
d) alterations in the composition of the air, e.g. a subject is at high altitude
or restricted in an environment with stale air (closets, submarines, pressurized
cabins, etc.)
There are also some diseases in which respiratory failure manifests with
hypoxemia and / or hypercapnia:
Chronic obstructive pulmonary disease, respiratory distress syndrome, asthma,
hemothorax, as a complication during treatment, head trauma, acute pulmonary
edema, massive pulmonary embolism, hypertensive pneumothorax
Often multiple mechanisms contribute, to varying degrees, to determining the
I.R.
In relation to the magnitude of the metabolic alterations caused by the I.R.
different degrees are distinguished:
In the first degree of I.R. latent or (compensated) hypoxemia has occurred only
after light exercise.
In the second degree, or manifest, hypoxemia is also at rest.
In the third degree, hypercapnia is added to hypoxemia.
In the fourth degree there is also respiratory acidosis.
In the fifth degree there is a hypercapnic coma.
We can distinguish various degrees of hypoxemia:
- mild: arterial saturation in O2 above 90% (normally about 97.5%);
- of slight gravity: arterial saturation in O2 between 80 and 90%;
- severe: arterial saturation in O2 between 70 and 80%;
- very serious: arterial saturation in O2 less than 70%.
For hypercapnia there are various degrees:
- mild: CO2 Pa between 45 and 49 mmHg;
- of slight severity: PaCO2 between 50 and 59 mmHg;
- severe: PaCO2 between 60 and 70 mmHg;
- very severe: PaCO2 higher than 70 mmHg.
Exacerbation of chronic obstructive bronchitis Difficult treatment of acute
exacerbation of chronic bronchitis, introduction Mechanical ventilator
The objectives are to correct hypoxia, possibly by administering oxygen, and at
the same time to treat the respiratory acidosis that may arise. The oxygen mask
(see oxygen therapy) is used in 70% of cases, alternatively mechanical
ventilation or nasal cannulae, in any case the amount of oxygen in the air that
is breathed must never exceed 50% because of the high toxicity.
The treatment changes depending on the related disease: as well as pharmacological (antibiotics, bronchodilators) may also include lifestyle correction (abstention from smoking or alcohol, follow a balanced diet to reduce weight, etc.)