Overview.
Alveolar hypoventilation syndrome is a syndrome of inadequate ventilation in which the volume of ventilation of the alveoli cannot be adapted to the level of tissue metabolism, resulting in a decrease in the partial pressure of oxygen in the alveoli and the partial pressure of oxygen in the arterial blood and an increase in the partial pressure of carbon dioxide in the arterial blood, but is clinically significant, and in which the PaCO2 is usually higher than 6.67 kPa (50 mmHg).
Etiology
Many clinical conditions can lead to chronic alveolar hypoventilation, commonly:
1. Diseases of the respiratory receptors
Carotid body dysfunction and trauma, metabolic acidosis.
2. Brainstem diseases
Medullary poliomyelitis, cerebral infarction, demyelinating diseases, long-term application of certain drugs (e.g. sedatives, anesthetics), primary alveolar hypoventilation syndrome.
3. Diseases of the spinal cord and peripheral nerves and respiratory muscles
Poliomyelitis, motor neuron disease, peripheral neuropathy, myasthenia gravis, muscular dystrophy, chronic myopathy.
4.Thoracic diseases
Obesity-hypoventilation syndrome, posterior scoliosis deformity, etc.
5.Lung and airway diseases
Chronic obstructive pulmonary disease, cystic fibrosis, pharyngeal and airway obstruction, obstructive sleep apnea syndrome, etc.
Pathogenesis
Hypoventilation syndromes, although the underlying etiology is inconsistent, have similar underlying clinical features, i.e., elevated alveolar and arterial blood PCO2 due to alveolar hypoventilation. There is a sort of inverse correlation between alveolar PCO2 and PaO2, and an increase in alveolar PCO2 inevitably leads to a decrease in alveolar PO2, thus producing arterial hypoxemia. This typical pathophysiologic change occurs during nocturnal sleep and is more pronounced when respiratory drive is further reduced.
Symptoms
Symptoms vary according to the degree of ventilation impairment and may include apathy, dizziness, headache, fatigue, lethargy, excessive sweating, and in severe cases optic disc edema, increased blood pressure, stress ulcers, cyanosis, pulmonary hypertension, and cor pulmonale.
Examination
1. Blood gas analysis
Blood gas analysis measures arterial oxygen saturation, arterial partial pressure of oxygen decreases, while arterial partial pressure of carbon dioxide, hydrogen ion concentration, bicarbonate concentration, carbon dioxide binding capacity are increased, and hematocrit increases.
2. Lung function test
Pulmonary function tests show restrictive or obstructive ventilatory dysfunction.
Diagnosis
Diagnosis can be made on the basis of clinical manifestations, physical signs and laboratory tests. Differential diagnosis should be made with pulmonary heart disease.
Treatment
1. Treatment of primary disease
The main measures for the treatment of this syndrome.
2. Respiratory stimulants
Suitable for those who have been induced by sedation or oxygenation.
3. Keep the airway open
Bronchodilators, hormones, expectorants can be used.
4. Oxygen therapy
Nasal tube oxygen or ventilator positive pressure ventilation.
5. Correct acidosis
For those with respiratory acidosis, especially mixed acidosis, aminotriol can be used to correct.
6. Carbonic anhydrase inhibitors
Such as acetazolamide (acetazolamide), can be used in chronic cases, but in the acute phase of carbon dioxide paralysis is prohibited.
7. Symptomatic management
If it is not caused by diaphragm or phrenic nerve pathology, diaphragm pacing can be used; obese people should lose weight.