Disturbance of ventilation

Violation of ventilation - is to increase PaCO ₂ (hypercapnia), where respiratory function can be more assured of the body forces.

The most common causes are exacerbation of asthma and COPD. It manifests as shortness of breath, tachypnea and anxiety. May be the cause of death. Diagnosis is based on clinical data and studies of arterial blood gases; X-ray examination of the chest and a clinical study allow us to clarify the causes of this condition. Treatment depends on the specific clinical situation and often requires ventilation.

[1], [2], [3], [4], [5], [6], [7]

What causes disturbed ventilation?

Hypercapnia occurs when a decrease in alveolar ventilation or inability to ventilate compensate for increased production of CO2.

Reduction of alveolar ventilation is the result of reduced minute ventilation or increased ventilation of dead space.

Minute ventilation decreases when the load does not match the respiratory system and the body's ability to provide adequate ventilation.

Physiological dead space is part of the airway, which does not participate in gas exchange. It includes anatomical dead space (oropharynx, trachea) and alveolar dead space (the volume of the alveoli that are ventilated, but not perfused). Physiological dead space is normally 30-40% of the total tidal volume, but it can be increased to 50% with endotracheal intubation and more than 70% with massive pulmonary embolism, severe emphysema and asthmatic status. With constant minute ventilation, increasing the dead space reduces CO2 emissions.

Hypercapnia is the result of a violation of ventilation. The increase in CO2 production can be observed with fever, sepsis, trauma, hyperthyroidism, malignant hyperthermia and an increase in the burden on the respiratory system.

Hypercapnia leads to a decrease in the pH of the arterial blood (respiratory acidosis). Severe acidosis (pH <7.2) causes a narrowing of the pulmonary arterioles, systemic vasodilation, decreased myocardial contractility, hyperkalemia, hypotension and increased myocardial excitability, increasing the likelihood of severe arrhythmia. Acute hypercapnia causes cerebral vasodilation and increased intracranial pressure. Correction of acidosis is due to the buffer systems of the blood and the urinary system. However, Ra-CO2 increase occurs faster than the reaction of compensatory mechanisms (in apnea, PaCO2 increases at a rate of 3-6 mm Hg).

Symptoms of ventilation disorders

The main symptom of the violation of ventilation is shortness of breath. There may be tachypnea, tachycardia, the inclusion of additional muscles in the breath, increased sweating, agitation, a decrease in the total respiratory volume, irregular surface breathing, paradoxical movements of the abdominal wall.

CNS disorders can be from mild to severe with depression and coma. Chronic hypercapnia is better tolerated than acute hypercapnia.

Diagnosis of ventilation disorders

Disturbance of ventilation can be suspected in patients with respiratory distress syndrome, weakening of breathing, cyanosis, impaired consciousness and pathology, which leads to neuromuscular weakness. Tachypnea (respiratory rate> 28-30 per minute) can not last long, especially in the elderly.

In this case, it is necessary to carry out an emergency study of arterial blood gases, continue pulsoximetry and perform an X-ray examination of the lungs. The presence of respiratory acidosis (eg, pH <7.35 and PCO2> 50) confirms the diagnosis. In patients with chronic ventilation impairment there is an increase in PCO2 (60-90 mm Hg), and the pH compensates moderately; so in such patients the level of pH reduction is not an important sign of acute hypoventilation.

The study of functional tests allows early diagnosis to diagnose a beginning impairment of ventilation, especially in patients with neuromuscular weakness, in whom it can develop without any precursors. The vital capacity is from 10 to 15 ml / kg and the maximum inspiratory pressure is 15 cm of water. Art. Suggest a threatening state.

After identifying this condition, it is necessary to establish its cause. Sometimes the cause is obvious and is associated with a certain disease (eg, asthma, myasthenia gravis, etc.). However, other reasons are possible, for example, PE after surgery, neurological or neuromuscular disorders, etc. Neuromuscular status can be assessed by functional tests (inspiratory and exhalation strength), neuromuscular conduction (electromyography and nerve conduction studies), and the reasons for the weakening of the pattern toxicology studies, sleep studies, thyroid function, etc.).

[8], [9], [10], [11], [12]

Treatment of ventilation disorders

Treatment of ventilation disorders should be aimed at eliminating the imbalance between the load and the reserves of the respiratory system. Obvious causes (such as bronchospasm, foreign body, obturation with mucus of the airways) should be eliminated.

The other two most common causes are exacerbation of asthma (asthmatic status (AS) and COPD.) Respiratory failure in COPD is expressed by the term "acute" against the background of chronic acute respiratory failure (ACHR).

Treatment of asthmatic status

Patients should be treated in the intensive care unit.

NIPPV allows you to quickly reduce the work of the respiratory muscles and in some patients to avoid intubation or have a time reserve for the realization of the effect of drug therapy. Unlike patients with COPD, where the facial mask is very effective, in patients with bronchial asthma, the mask is aggravated by a feeling of lack of air, so getting used to the mask should be gradual. After explaining the benefits of the mask, it is applied to the face and a slight pressure is applied - CPAP 3-5 cm of water. Art. After habituation, the mask is tightly applied to the face, the pressure increases until the comfortable state of the patient appears and the work of the respiratory musculature decreases. The final settings are usually the following: IPAP 10-15 cm of water. Art. And EPAP 5-8 cm of water. Art.

Endotracheal intubation is indicated with aggravation of respiratory failure, which is clinically manifested by a violation of consciousness, monosyllabic speech and shallow breathing. The level of arterial blood gases, indicating an increase in hypercapnia, is also an indication for intubation of the trachea. Nevertheless, the study of blood gases is not considered mandatory and should not replace the medical solution. Orotracheal intubation is preferable to nasal intubation, since it allows the use of tubes of larger diameter, reducing the resistance to gas flow.

After intubation, patients with asthmatic status may develop hypotension and pneumothorax. The number of these complications and the associated lethality were significantly reduced by the introduction of a method that aims to limit the dynamic overgrowth of the lungs, rather than to achieve a normal voltage of P2O2. With asthmatic status, ventilation, which contributes to the achievement of normal pH, usually results in a significant overexpiration of the lungs. To avoid this, the initial fan settings are made as follows: a tidal volume of 5-7 ml / kg and a respiratory rate of 10-18 per minute. The flow of gases can be quite high (120 l / min) with a square wave shape. This method allows you to reduce the minute ventilation and increase the expiration time. Dangerous dynamic over-inflation of lungs is unlikely if the plateau pressure is below 30-35 cm of water. Art. And an internal PEEP below 15 cm of water. Art. Plateau pressure is above 35 cm of water. Art. Can be corrected by reducing the tidal volume (assuming that high blood pressure is not the result of low chest or abdominal wall stretch) or respiratory rate.

In principle, the peak pressure can be reduced by reducing the flow rate or changing the respiratory curve to the downward, but this can not be done. A low air flow shortens the exhalation time, increases the residual volume of the lungs at the end of the exhalation, resulting in a high internal PEEP.

With the use of low respiratory volumes, hypercapnia may develop, but it is considered a lesser evil compared to over-inflation of the lungs. Usually, the arterial blood pH above 7.15 is normally tolerated, but in some cases it may be necessary to use high doses of sedatives and opioids. After intubation, the use of muscle relaxants in the peri-indubation period should be avoided, as in combination with glucocorticoids this can lead to severe and sometimes irreversible myopathy, especially when used for more than 24 hours. For sedation, sedatives, rather than muscle relaxants, should be administered.

In most patients, on the 2nd-5th day, the condition improves, which allows us to begin excommunication from the ventilator. Approaches to Exemption from Ventilation on page 456.

OCDD treatment

In patients with OCHD, the cost of breathing is several times higher than in patients without concomitant lung disease, the respiratory system is rapidly decompensated. In such patients, it is necessary to timely identify and eliminate the prerequisites for the development of such a condition. To restore the balance between the neuromuscular status and the load on the respiratory system, bronchodilators and glucocorticoids are used to eliminate obstruction and dynamic overemployment of the lungs, antibiotics - to treat the infection. Hypokalemia, hypophosphatemia and hypomagnesemia can exacerbate muscle weakness and slow the recovery process.

NIPPV is preferred for many patients with OCDN. Probably about 75% of those receiving NIPPV do not require tracheal intubation. Advantages of such ventilation are ease of use, the possibility of a temporary cessation while improving the patient's condition, expanding the possibilities of independent breathing. If necessary, NIPPV is easy to restart again.

Typically, the following parameters are set: IPAP10-15 cm of water. Art. And EPAP 5-8 cm of water. Art. Then, depending on the clinical situation, the parameters are corrected. The relationship to the potential effect of high IPAP on the lungs is the same as previously reported.

Deterioration of the condition (the need for intubation) is assessed by clinical data; assessment of the gas composition of blood can be misleading. So some patients are good at tolerating high values of hypercapnia, while others at lower values need intubation of the trachea.

The goal of mechanical ventilation with OCDD is to minimize dynamic over-inflation of the lungs and relieve the load from overworked respiratory muscles. Initially, the use of A / C with a respiratory volume of 5-7 ml / kg and a breathing rate of 20-24 per minute is recommended, in order to limit the occurrence of high internal PEEP, some patients need to reduce the respiratory rate. In contrast to the internal PEEP, the device sets the value of PEEP, which makes up PEEP <85% of the internal PEEP (usually 5-10 cm H2O). This reduces the work done on breathing, and rarely contributes to dynamic over-breathing of the lungs.

In most patients, A / C should be discontinued 24-48 hours before being transferred to spontaneous breathing. With asthmatic status, patients are usually heavily loaded in contrast to SA, which requires mild sedation. Nevertheless, it is often impossible to achieve adequate relaxation. At the same time, it is necessary to constantly monitor the patient, as he can make attempts to activate the respiratory muscles, which will lead to low airway pressure at the beginning or at the inspiration, the inability to trigger the ventilator trigger and indicate high internal PEEP and / or weakness of the respiratory muscles. The settings of the ventilator should be such as to minimize this phenomenon by prolonging the exhalation time; unsuccessful attempts of excommunication from a respirator are often associated with fatigue of the respiratory muscles. At the same time, it is impossible to distinguish the weakness of the respiratory muscles as a result of fatigue and reduced strength.