Respiratory acidosis

Respiratory acidosis is characterized by a primary increase in PSR ₂ with or without a compensatory increase in HCO ³ ~; The pH level is usually low, but may be close to normal. Diagnosis is based on clinical data and the determination of the gas composition of arterial blood and plasma electrolyte levels. Treatment of the underlying cause is necessary: O ₂ and artificial ventilation are often required .

[1], [2],

Causes of the respiratory acidosis

The reason is a decrease in the respiratory rate and / or tidal volume (hypoventilation) due to disorders of the central nervous system, respiratory system or iatrogenic causes.

Respiratory acidosis is the accumulation of CO ₂  (hypercapnia) due to a decrease in respiratory rate and / or respiratory volume (hypoventilation). The causes of hypoventilation include conditions that disrupt the function of the respiratory center of the central nervous system; violation of the neuromuscular transmission and other causes of muscle weakness, obstructive, restrictive and parenchymal lung diseases. Hypoxia  usually accompanies hypoventilation.

[3], [4], [5], [6], [7], [8], [9], [10]

Symptoms of the respiratory acidosis

Symptoms of respiratory acidosis depend on the speed and degree of increase in PSR ₂. CO ₂  rapidly penetrates the blood-brain barrier; symptoms and signs are the result of high concentrations of CO ₂  in the central nervous system (low pH of the central nervous system) and any concomitant hypoxia.

Acute (or acutely progressive chronic) respiratory acidosis causes headache, impaired consciousness, anxiety, drowsiness, stupor (CO ₂  anesthesia). Slowly developing, stable respiratory acidosis (as in COPD) can normally be tolerated, but patients may experience memory loss, sleep disturbance, excessive daytime drowsiness, personality change. Signs include abnormalities of gait, tremor, decrease of deep tendon reflexes, myoclonic cramps, "fluttering tremor", edema of the optic nerve.

Forms

Respiratory acidosis can be acute or chronic: the chronic form is asymptomatic, but acute or progressive forms are characterized by headache, impaired consciousness and drowsiness. Symptoms include tremor, myoclonic cramps, "fluttering tremor".

The difference in forms is based on the degree of metabolic compensation: initially, CO _{2 is}  ineffective, but 3-5 days later the kidneys significantly increase the reabsorption of HCO ³.

[11], [12]

Diagnostics of the respiratory acidosis

It is necessary to determine the gas composition of arterial blood and plasma electrolyte levels. Anamnesis and examination data usually help to guess the cause. Calculation of the alveolar  arterial gradient O ₂  [PO ₂ on inhalation (arterial PO ₂  + 5/4 arterial POP ₂ )] can help differentiate lung diseases from extrapulmonary pathology; the normal gradient practically excludes pulmonary diseases.

[13], [14], [15], [16], [17]

Treatment of the respiratory acidosis

Treatment consists in providing adequate ventilation by intubation of the trachea or the use of non-invasive ventilation with positive pressure. To correct respiratory acidosis sufficiently adequate ventilation but chronic hypercapnia should be corrected slowly (e.g., over several hours or longer), since too rapid decrease in PCO ₂  can cause alkalosis postgiperkapnichesky when seen starting compensatory giperbikarbonatemiya; the observed sharp increase in the pH level in the central nervous system can lead to convulsions and death. If necessary, correction of deficiency of K and CI is carried out.

The introduction of NaHCO ^{3 is}  usually contraindicated, since HCO ³ can be converted to PCO ₂  plasma, but it slowly penetrates the blood-brain barrier, increasing the pH of the plasma and not affecting the pH in the CNS. Exceptions are cases of severe bronchospasm, when HCO ³  increases the sensitivity of the smooth muscles of the bronchi to beta -agonists.