By definition of alveolar hypoventilation we mean the condition in which the
emogas is performed, when the PCO2, arterial (Pa CO2) increases above the normal
level of 37-43 mmHg, but is generally found at levels greater than 50 and 80
mmHg. Hypoventilation disorders can be acute or chronic. Chronic hypoventilation
can be the result of numerous diseases, although in many cases the defect is
simply in the respiratory metabolic control system or in the neuromuscular
respiratory system or in the respiratory apparatus itself, intended as a
ventilation system, and therefore respiratory bellows. The disturbances
associated with a damaged respiratory impulse include a series of infirmities,
both of the center and the breathing, that are the peripheral and central
chemoreceptors and of the brain trunk neurons, and of the respiratory system
disorders understood as muscles that contract and motor neurons that innervate
them; finally, the ventilatory system can also be damaged, for example in
subjects with severe skeletal changes or in bronchopathic patients (see bpco and
smoke).
Below are listed the conditions of conical hypoventilation.
- Impaired respiratory mechanism:
a) Peripheral and central chemoreceptors: dysfunction and trauma of the carotid
body, prolonged hypoxia, metabolic alkalosis
b) Respiratory neurons of the encephalic trunk: bulbar polio, encephalitis,
encephalic trunk infarction, trauma, demyelinating diseases of the encephalic
trunk, chronic administration of drugs, alveolar hypoventilation syndrome
- Defective neuromuscular respiratory system:
a) Spinal cord and peripheral nerves: severe brain trauma, prolonged hypoxia,
polimielitis, motor neuron disease, peripheral neuropathy
b) Respiratory muscles: myasthenia gravis, muscular dystrophy, chronic myopathy
- Altered ventilatory system:
a) thoracic cage: Cifoscoliosis, Fibrothorax, Thoracoplasty, Ankylosing
spondylitis, Obesity hypoventilation
b) Pulmonary and airway laryngeal and tracheal stenosis, obstructive sleep apnea
(OSAS), Cystic fibrosis, Chronic obstructive pulmonary disease
Regardless of the cause, the hallmark of all alveolar hypoventilation syndromes is an increase in alveolar PCO2 (Pa CO2), thus resulting in respiratory acidosis and an increase in the plasma concentration of HC03- , in addition to a decrease in the concentration of Cl-. The increase in PaCO2 produces a mandatory decrease in PAO, resulting in hypoxemia. If severe, hypoxemia manifests clinically in the form of cyanosis and can stimulate erythropoiesis and induce a secondary polycythemia. Furthermore, the combination of chronic hypoxemia and hypercapnia can induce pulmonary vasoconstriction and eventually lead to pulmonary hypertension, right ventricular hypertrophy and congestive heart failure. Arterial blood gas disorders appear increased especially during sleep due to further reduction of respiratory stimulation. The resulting increased nocturnal hypercapnia can cause cerebral vasodilation and lead to morning migraine; even the quality of sleep can be severely damaged, resulting in tiredness in the morning, associated with somnolence during the day, mental confusion and intellectual deficit.
To understand if a patient has hypercapnia the diagnosis is always difficult, because
it is necessary to analyze various aspects and make a correct diagnosis. First
of all, the patient must be considered for the analysis of respiratory gases, to
understand if hypoxemia is severe or if there is hypercapnia, identifying the
disorder in the metabolic respiratory control system. A good chest X-ray is
always the starting point for excluding or confirming respiratory diseases,
acute or chronic, accompanied by a CT scan, if appropriate, and a spirometry
survey, to evaluate the gas exchange. There are two possible occurrences:
patients who ventilate poorly, with FEV1, reduced, for example in respiratory
obstructive forms, or with reduced vital pulmonary capacity, ie with a lung that
can not accumulate air in ventilation (see bpco). Most often it is the classic
chronic bronchopathic patient with emphysema or the OSAS patient for obstruction
of the upper respiratory tract, especially if obese. In other cases, if it is a
patient with neuromuscular system disorders, it is necessary to diagnose
pathologies affecting the respiratory motoneurons and to think of outcomes of
poliomyelitis, myasthenia gravis, demyelinating diseases, etc. Defects in the
neuromuscular respiratory system damage the muscle strength, then all the exams
dependent on muscle activity (voluntary or in response to metabolic stimuli) are
abnormal, but the resistance and pulmonary distensibility and gas exchange are
normal. Defects in the ventilatory system generally damage the gaseous exchange;
on the contrary, the examinations on the activity or the muscular force, which
do not influence the air flow of the behavioral respiratory control system (anatomically
distinct from the metabolic control system), the neuromuscular system and the
ventilatory system are intact, these patients can normally initiate voluntary
hyperventilation, generate normal inspiratory and expiratory muscle pressures to
counter an airway occlusion, generate normal lung volumes and flows to a routine
spirometry, possess normal pulmonary resistance and distensibility, and a
difference in PO, alveolar arterial normal. Patients with defects in the
neuromuscular respiratory system show altered responses to chemical stimuli;
moreover, they fail to generate voluntary hyperventilation or normal static
respiratory muscle pressure, or normal lung volumes or flows. However, at least
in the early stages of the disease, the resistance and distensibility of the
respiratory system and the difference in alveolar arterial oxygen are normal.
Treatment of chronic hypoventilation should be set individually according to the patient's particular disorder, circumstances and needs and should include measures to counter the underlying disease. A simultaneous metabolic alkalosis should be corrected, including too high HC03 levels, given the degree of chronic hypercapnia. Oxygen suppression is useful for attenuating hypoxemia, polycythemia and pulmonary hypertension, but it can exacerbate C02 retention and associated neurological symptoms. For this reason, oxygen should be prescribed with great caution and the results carefully monitored. Pharmacological agents able to stimulate respiration (in particular progesterone) benefit some patients, although they generally give disappointing results. In most patients with chronic hypoventilation related to impaired respiratory stimulation or neuromuscular disease, effective treatment of the disorder requires mechanical ventilatory assistance. In case of severe hypoventilation, continuous 24-hour treatment may be necessary, although in many patients ventilatory assistance exclusively during sleep produces noticeable clinical improvements together with a lowering of daytime CO2. For patients suffering from a reduced respiratory impulse but with lower respiratory motor neurons, phrenic nerve and intact respiratory muscles, a diaphragmatic regulation by means of a phrenic electrode implant can be very effective. However, electrophrenic regulation is contraindicated for patients with defects to the nerves and respiratory muscles. Such patients can generally be successfully treated by either intermittent negative pressure ventilation within an armor or intermittent positive pressure ventilation via tracheostomy or nasal mask. Positive pressure ventilation using a nasal mask is the best method for patients who need ventilatory assistance only during sleep, as it eliminates the need for a tracheostomy and avoids the problem of an upper airway occlusion that could arise with a negative pressure fan. Hypoventilation related to restrictive chest wall disorders can also be successfully treated by means of positive pressure intermittent night-time ventilation using a nasal mask or tracheostomy. In addition, a nocturnal ventilatory system has been suggested for patients with chronic hypercapnic obstructive pulmonary disease, as a way to alleviate a possible chronic exhaustion of the respiratory muscles, but the validity of a similar approach has yet to be demonstrated.
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