Ventilation disturbance

Ventilation impairment is an increase in PaCO2 ₍ hypercapnia), when the respiratory function can no longer be provided by the body's forces.

The most common causes are exacerbation of asthma and COPD. It manifests itself as dyspnea, tachypnea and anxiety. It can be the cause of death. The diagnosis is based on clinical data and arterial blood gas analysis; chest X-ray and clinical examination help clarify the causes of this condition. Treatment depends on the specific clinical situation and often requires mechanical ventilation.

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What causes ventilation problems?

Hypercapnia occurs when alveolar ventilation is reduced or ventilation is unable to compensate for increased CO2 production.

A decrease in alveolar ventilation is the result of a decrease in minute ventilation or an increase in dead space ventilation.

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

Physiologic dead space is the part of the respiratory tract that does not participate in gas exchange. It includes anatomical dead space (oropharynx, trachea) and alveolar dead space (volume of alveoli that are ventilated but not perfused). Physiologic dead space normally accounts for 30-40% of the total tidal volume, but can increase to 50% with endotracheal intubation and more than 70% with massive pulmonary embolism, severe emphysema, and asthmatic status. With constant minute ventilation, an increase in dead space reduces CO2 release.

Hypercapnia is the result of impaired ventilation. Increased CO2 production may occur with fever, sepsis, trauma, hyperthyroidism, malignant hyperthermia, and increased respiratory stress.

Hypercapnia leads to a decrease in arterial blood pH (respiratory acidosis). Severe acidosis (pH < 7.2) causes pulmonary arteriole constriction, 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. Acidosis is corrected by the blood and urinary buffer systems. However, the increase in Pa-CO2 occurs faster than the reaction of compensatory mechanisms (in apnea, PaCO2 increases at a rate of 3-6 mm Hg).

Symptoms of ventilation problems

The main symptom of ventilation disorder is dyspnea. Tachypnea, tachycardia, involvement of additional muscles in breathing, increased sweating, agitation, decreased total respiratory volume, irregular shallow breathing, paradoxical movements of the abdominal wall may be observed.

CNS disorders can range from minor to severe with depression of consciousness and coma. Chronic hypercapnia is better tolerated than acute hypercapnia.

Diagnosis of ventilation disorders

Ventilation dysfunction may be suspected in patients with respiratory distress syndrome, decreased breathing, cyanosis, impaired consciousness, and pathology that leads to neuromuscular weakness. Tachypnea (respiratory rate > 28-30 per minute) may not persist for long, especially in the elderly.

In this case, it is necessary to conduct an urgent study of arterial blood gases, continue pulse oximetry, and perform a chest X-ray. The presence of respiratory acidosis (e.g., pH < 7.35 and PCO2 > 50) confirms the diagnosis. In patients with chronic ventilation problems, PCO2 increases (60-90 mm Hg), and pH compensatorily decreases moderately; therefore, in such patients, the degree of pH decrease is not an important sign of acute hypoventilation.

The study of functional tests allows early diagnosis of the beginning of ventilation disorder, especially in patients with neuromuscular weakness, in whom it can develop without any precursors. Vital capacity from 10 to 15 ml/kg and maximum inspiratory vacuum of 15 cm H2O give grounds to assume a threatening condition.

Once this condition has been identified, its cause must be determined. Sometimes the cause is obvious and is related to a specific disease (e.g. asthma, myasthenia, etc.). However, other causes are also possible, such as postoperative pulmonary embolism, neurological or neuromuscular disorders, etc. Neuromuscular status can be assessed by functional tests (inspiratory and expiratory strength), neuromuscular conductivity (electromyography and nerve conduction studies), and causes of pattern weakening (toxicological studies, sleep studies, thyroid function, etc.).

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Treatment of ventilation disorders

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

The other two most common causes are asthma exacerbation (status asthmaticus (AS)) and COPD. Respiratory failure in COPD is termed acute-on-chronic respiratory failure (ACRF).

Treatment of status asthmaticus

Patients should be treated in an intensive care unit.

NIPPV allows to quickly reduce the work of the respiratory muscles and in some patients to avoid intubation or have some time to implement the effect of drug therapy. Unlike patients with COPD, for whom the face mask is very effective, in patients with bronchial asthma the mask aggravates the 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 small pressure is applied - CPAP 3-5 cm H2O. After getting used to it, the mask is tightly applied to the face, the pressure is increased until the patient feels comfortable and the work of the respiratory muscles decreases. The final settings are usually the following: IPAP 10-15 cm H2O and EPAP 5-8 cm H2O.

Endotracheal intubation is indicated when respiratory failure worsens, which is clinically manifested by impaired consciousness, monosyllabic speech, and shallow breathing. Arterial blood gas levels indicating increasing hypercapnia are also an indication for tracheal intubation. However, blood gas testing is not considered mandatory and should not replace medical judgment. Orotracheal intubation is preferable to nasal intubation because it allows the use of larger-diameter tubes, reducing resistance to gas flow.

Hypotension and pneumothorax may develop after intubation in patients with status asthmaticus. The incidence of these complications and their associated mortality have been significantly reduced by the introduction of a technique that aims to limit dynamic lung overinflation rather than to achieve normal PCO2 tension. In status asthmaticus, ventilation that promotes normal pH usually results in significant lung overinflation. To avoid this, initial ventilator settings are made as follows: tidal volume 5-7 ml/kg and respiratory rate 10-18 breaths per minute. Gas flows can be quite high (120 L/min) with a square waveform. This technique allows a decrease in minute ventilation and an increase in expiratory time. Dangerous dynamic lung overinflation is unlikely if plateau pressure is below 30-35 cm H2O and intrinsic PEEP is below 15 cm H2O. Plateau pressure is above 35 cm H2O. can be corrected by decreasing the tidal volume (assuming that the high pressure is not the result of low compliance of the chest or abdominal walls) or the respiratory rate.

In principle, peak pressure can be reduced by decreasing the flow rate or changing the respiratory curve to a downward one, but this should not be done. Low air flow reduces the expiratory time, increases the residual volume of the lungs at the end of expiration, resulting in high internal PEEP.

Hypercapnia may develop with low tidal volumes, but is considered the lesser evil compared to overinflation of the lungs. Arterial blood pH above 7.15 is usually well tolerated, but high doses of sedatives and opioids may be required in some cases. After intubation, the use of muscle relaxants in the peri-intubation 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. Sedatives, not muscle relaxants, should be used to control agitation.

Most patients experience an improvement in their condition within 2–5 days, which allows us to begin weaning from mechanical ventilation. Approaches to weaning from mechanical ventilation are on page 456.

Treatment of acute respiratory distress syndrome

In patients with acute respiratory failure, the cost of breathing is several times higher than in patients without concomitant lung disease, the respiratory system quickly decompensates. In such patients, it is necessary to promptly 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 overinflation of the lungs, antibiotics are used to treat infection. Hypokalemia, hypophosphatemia and hypomagnesemia can increase muscle weakness and slow down the recovery process.

NIPPV is preferred for many patients with ACF. Probably about 75% of those receiving NIPPV do not require tracheal intubation. The advantages of this type of ventilation are ease of use, the ability to temporarily stop when the patient's condition improves, and the ability to breathe spontaneously. NIPPV can be easily restarted if necessary.

The following parameters are usually set: IPAP10-15 cm H2O and EPAP 5-8 cm H2O. Then, depending on the clinical situation, the parameters are adjusted. The attitude towards the potential effect of high IPAP on the lungs is the same as presented earlier.

Deterioration (need for intubation) is assessed clinically; blood gas measurements can be misleading. Some patients tolerate high levels of hypercapnia well, while others require tracheal intubation at lower levels.

The goal of mechanical ventilation in acute respiratory failure is to minimize dynamic overinflation of the lungs and relieve the strain on the overtired respiratory muscles. Initially, the use of A/C with a tidal volume of 5-7 ml/kg and a respiratory rate of 20-24 per minute is recommended; to limit the occurrence of high intrinsic PEEP in some patients, a decrease in the respiratory rate is required. In contrast to the intrinsic PEEP, the ventilator is set to a PEEP value of PEEP < 85% of the intrinsic PEEP (usually 5-10 cm H2O). This reduces the work of breathing and rarely contributes to dynamic overinflation of the lungs.

In most patients, ventilator weaning should be stopped 24-48 hours before transition to spontaneous breathing. Patients with status asthmaticus are usually deeply mobilized, unlike SA, which requires light sedation. However, adequate relaxation is often not achieved. The patient must be closely monitored for respiratory muscle attempts, which will result in low airway pressures at the start or during inspiration, failure to trigger the ventilator, and indicate high intrinsic PEEP and/or respiratory muscle weakness. Ventilator settings should be such as to minimize this phenomenon by prolonging expiratory time; unsuccessful weaning attempts are often associated with respiratory muscle fatigue. It is impossible to differentiate between respiratory muscle weakness due to fatigue and decreased strength.