This is a pathological syndrome that accompanies a number of diseases, which is based on a violation of gas exchange in the lungs. The clinical picture is based on signs of hypoxemia and hypercapnia (cyanosis, tachycardia, sleep and memory disorders), respiratory muscle fatigue syndrome and shortness of breath. DN is diagnosed on the basis of clinical data confirmed by indicators of blood gas composition, FVD. Treatment includes elimination of the cause of DN, oxygen support, and if necessary, mechanical ventilation.
ICD-10
J96 J96.0 J96.1 J96.9
General information
External respiration maintains continuous gas exchange in the body: the supply of atmospheric oxygen and the removal of carbon dioxide. Any violation of the function of external respiration leads to a violation of gas exchange between the alveolar air in the lungs and the gas composition of the blood. As a result of these disorders in the blood, the content of carbon dioxide increases and the oxygen content decreases, which leads to oxygen starvation, first of all, of the vital organs - the heart and brain.
In respiratory failure (DN), the necessary blood gas composition is not provided, or it is maintained due to overstrain of the compensatory capabilities of the external respiration system. A condition that is threatening to the body develops with respiratory failure, characterized by a decrease in the partial pressure of oxygen in the arterial blood of less than 60 mm Hg. Art., as well as an increase in the partial pressure of carbon dioxide more than 45 mm Hg. Art.
Causes
Respiratory failure can develop in various acute and chronic inflammatory diseases, injuries, tumor lesions of the respiratory system; with pathology from the respiratory muscles and heart; in conditions leading to restriction of chest mobility. Disruption of pulmonary ventilation and the development of respiratory failure can lead to:
- Obstructive disorders... Respiratory failure of the obstructive type is observed when it is difficult to pass air through the airways - trachea and bronchi due to bronchospasm, inflammation of the bronchi (bronchitis), ingress of foreign bodies, stricture (narrowing) of the trachea and bronchi, compression of the bronchi and trachea by a tumor, etc.
- Restrictive disorders... Respiratory failure of the restrictive (restrictive) type is characterized by a restriction of the ability of the lung tissue to expand and collapse and occurs in exudative pleurisy, pneumothorax, pneumosclerosis, adhesions in the pleural cavity, limited mobility of the rib cage, kyphoscoliosis, etc.
- Hemodynamic disorders... The cause of the development of hemodynamic respiratory failure can be circulatory disorders (for example, thromboembolism), leading to the inability to ventilate the blocked area of \u200b\u200bthe lung. The development of respiratory failure of the hemodynamic type also leads to the right-left shunting of blood through the open oval window with heart disease. In this case, a mixture of venous and oxygenated arterial blood occurs.
Classification
Respiratory failure is classified according to a number of characteristics:
1. By pathogenesis (mechanism of occurrence):
- parenchymal (hypoxemic, respiratory or pulmonary insufficiency of type I). Respiratory failure of the parenchymal type is characterized by a decrease in the content and partial pressure of oxygen in arterial blood (hypoxemia), which is difficult to correct with oxygen therapy. Most frequent reasons this type of respiratory failure is pneumonia, respiratory distress syndrome (shock lung), cardiogenic pulmonary edema.
- ventilation ("pumping", hypercapnic or type II respiratory failure). The leading manifestation of ventilation-type respiratory failure is an increase in the content and partial pressure of carbon dioxide in arterial blood (hypercapnia). Hypoxemia is also present in the blood, but it responds well to oxygen therapy. The development of ventilation respiratory failure is observed with weakness of the respiratory muscles, mechanical defects of the muscular and rib cage of the chest, and impaired regulatory functions of the respiratory center.
2. For etiology (reasons):
- obstructive. With this type, the functionality of the external respiration apparatus suffers: full inhalation and especially exhalation is difficult, and the respiratory rate is limited.
- restrictive (or restrictive). DN develops due to the limitation of the maximum possible inspiratory depth.
- combined (mixed). DN of the combined (mixed) type combines signs of obstructive and restrictive types with a predominance of one of them and develops with a long course of cardiopulmonary diseases.
- hemodynamic. DN develops against the background of a lack of blood flow or inadequate oxygenation of a part of the lung.
- diffuse. Respiratory failure of a diffuse type develops when the penetration of gases through the capillary-alveolar membrane of the lungs is impaired with its pathological thickening.
3. By the rate of increase of signs:
- Acute respiratory failure develops rapidly, in a few hours or minutes, as a rule, it is accompanied by hemodynamic disturbances and poses a danger to the life of patients (urgent resuscitation and intensive therapy are required). The development of acute respiratory failure can be observed in patients with chronic DN with its exacerbation or decompensation.
- Chronic respiratory failure can increase over several months and years, often gradually, with a gradual increase in symptoms, and may also be the result of incomplete recovery from acute DN.
4. According to indicators of blood gas composition:
- compensated (blood gas composition is normal);
- decompensated (presence of hypoxemia or hypercapnia of arterial blood).
5. By severity dN symptoms:
- DN I degree - characterized by shortness of breath with moderate or significant exertion;
- DN II degree - shortness of breath is observed with minor loads, the involvement of compensatory mechanisms at rest is noted;
- DN III degree - manifested by shortness of breath and cyanosis at rest, hypoxemia.
Respiratory Failure Symptoms
The signs of MD depend on the cause, type, and severity. The classic signs of respiratory failure are:
- manifestations of hypoxemia
Hypoxemia is clinically manifested by cyanosis (cyanosis), the degree of which expresses the severity of respiratory failure and is observed when the partial pressure of oxygen (PaO2) in arterial blood drops below 60 mm Hg. Art. For hypoxemia, hemodynamic disturbances are also characteristic, expressed in tachycardia and moderate arterial hypotension. With a decrease in PaO2 in arterial blood to 55 mm Hg. Art. memory impairments are observed for the events taking place, and with a decrease in PaO2 to 30 mm Hg. Art. the patient loses consciousness. Chronic hypoxemia is manifested by pulmonary hypertension.
- manifestations of hypercapnia
The manifestations of hypercapnia are tachycardia, sleep disturbances (insomnia at night and drowsiness during the day), nausea, and headaches. A rapid increase in the partial pressure of carbon dioxide (PaCO2) in arterial blood can lead to a state of hypercapnic coma associated with increased cerebral blood flow, increased intracranial pressure and the development of cerebral edema. The syndrome of weakness and fatigue of the respiratory muscles is characterized by an increase in the respiratory rate (RR) and the active involvement of the auxiliary muscles (muscles of the upper respiratory tract, neck muscles, abdominal muscles).
- syndrome of weakness and fatigue of the respiratory muscles
BH more than 25 per minute. can serve as an initial sign of fatigue of the respiratory muscles. BH reduction is less than 12 per minute. may portend respiratory arrest. An extreme variant of the syndrome of weakness and fatigue of the respiratory muscles is paradoxical breathing.
- dyspnea
Along with oxygen therapy, measures are taken to improve the drainage function of the bronchi: antibacterial drugs, bronchodilators, mucolytics, chest massage, ultrasonic inhalations, physiotherapy exercises, active aspiration of bronchial secretions is carried out through an endobronchoscope. With respiratory failure complicated by cor pulmonale, diuretics are prescribed. Further treatment of respiratory failure is aimed at eliminating the causes that caused it.
Forecast and prevention
Respiratory failure is a formidable complication of many diseases and is often fatal. In chronic obstructive pulmonary diseases, respiratory failure develops in 30% of patients. Prognostically, the manifestation of respiratory failure in patients with progressive neuromuscular diseases (ALS, myotonia, etc.) is unfavorable. Without appropriate therapy, death can occur within one year.
For all other pathologies leading to the development of respiratory failure, the prognosis is different, but it cannot be denied that DN is a factor that shortens the life expectancy of patients. The prevention of the development of respiratory failure provides for the exclusion of pathogenetic and etiological risk factors.
1. Decreased expiratory power.
2. Decrease in PSV.
3. Decreased FEV1.
4. Decrease in the Tiffno index (Tiffno index \u003d (FEV1 / VC) x 100%, the norm is 70-80%).
5. Decrease in MVL (due MVL \u003d VC X 35).
Restrictive type of DN
Causes of occurrence:
1) pulmonary fibrosis (pneumoconiosis, scleroderma);
2) pulmonary emphysema;
3) pleural adhesions;
4) exudative pleurisy, hydrothorax;
5) pneumothorax;
6) alveolitis, pneumonia, lung tumors;
7) removal of a portion of the lungs.
FVD changes in restrictive DN type
1. Decreased VC.
2. Decrease in MVL.
Mixed (obstructive-restrictive) type of DN
It is characterized by the presence in the patient of signs of obstructive and restrictive types in DN.
Acute DN
The term acute DN is understood.
1. Sudden occurrence of DN.
2. The gradual development of DN to a critical state requiring intensive therapy or resuscitation.
Stages of acute DN
Stage I - initial.
Characteristic:
Forced position of the patient - orthopnea;
Severe cyanosis of the skin and mucous membranes;
Agitation, anxiety, sometimes delirium, hallucinations;
Rapid breathing up to 40 in 1 minute;
Participation of auxiliary respiratory muscles in the act of breathing;
Tachycardia up to 120 in 1 minute;
Moderate arterial hypoxemia (Ra O 2 - 60-70 mm Hg) and normocapnia (Ra CO 2 - 35-45 mm Hg).
Stage II - deep hypoxia.
Characteristic:
The condition of the patients is extremely serious;
Shallow breathing, patients convulsively gasp for air;
Position - orthopnea;
Alternating periods of arousal with periods of sleepiness;
Respiratory rate exceeds 40 per minute;
Heart rate above 120 per minute;
Hypoxia (R a O 2 - 50-60 mm Hg) and hypercapnia (R a CO 2 - 50-70 mm Hg) are detected in the blood.
III stage - hypercapnic coma.
Characteristic:
Consciousness is absent;
Severe diffuse cyanosis;
Cold clammy sweat;
The pupils are dilated (mydriasis);
Breathing is shallow, rare, often arrhythmic - like Cheyne-Stokes;
In the blood, sharp hypoxia (R a O 2 - 40-55 mm Hg) and severe hypercapnia (R a CO 2 - 80-90 mm Hg) are detected.
Stages of chronic respiratory failure
| Stages | I (compensated) | II (pronounced subcompensated) | III (decompensated) |
| Dyspnea | Under prof. load | With daily stress | At rest |
| Cyanosis | No | Appears under load | Diffuse constant |
| Participation of accessory muscles in the act of breathing | Do not participate | Participation in the load is noticeable | Participate in peace |
| BH (in 1 min.) | mb norm | More than 20 alone | More than 20 alone |
| Heart rate (in 1 min.) | norm | Over 90 | Over 90 |
| Ventilation disorders | Decrease in performance up to 80-50% | Decrease in indicators up to 50-30% | Decrease in indicators below 30% |
LECTURE: Symptomatology and diagnosis of bronchitis and pulmonary emphysema
Acute bronchitis - this inflammatory process in the trachea, bronchi and (or) bronchioles, characterized by an acute course and diffuse reversible damage mainly to their mucous membrane.
Etiology of acute bronchitis
1. Infectious factors - influenza viruses, parainfluenza, adenoviruses, mycoplasmas (ie causative agents of acute respiratory diseases).
2. Physical factors - hot air and hypothermia, ionizing radiation.
3. Chemical factors - vapors of acids, alkalis, toxic substances (sulfur dioxide, nitrogen oxides).
4. Exposure to dust particles .
Predisposing factors:
Smoking;
Alcoholism;
Cardiovascular disease (left ventricular failure);
Nasal breathing disorders;
Focuses of chronic infection in the nasopharynx;
Severe diseases that reduce the body's immunological reactivity.
Phases of development of acute bronchitis
1. Reactive-hyperemic or neuro-reflex:
Hyperemia and edema of the mucous membrane;
Damage to the epithelium;
Suppression of mucociliary clearance;
Increased mucus production.
2. Infectious phase:
Fixation on the mucous membrane of a bacterial infection;
The development of purulent inflammation.
Classification of acute bronchitis
I. Etiological factor.
1. Acute infectious bronchitis.
2. Acute non-infectious bronchitis.
II. The nature of the inflammation.
1. Catarrhal.
2. Purulent.
3. Purulent-necrotic.
III. Localization of the lesion.
1. Proximal.
2. Distal.
3. Acute bronchiolitis.
IV. Functional features.
1. Non-obstructive.
2. Obstructive.
V. Current.
1. Acute - up to 2 weeks.
2. Protracted - up to 4 weeks.
3. Recurrent - occurs 3 or more times during the year.
Clinic of acute bronchitis
Complaints
1. Cough.
2. Separation of sputum.
3. Expiratory dyspnea (with bronchial obstruction syndrome).
4. Fever.
5. Signs of intoxication.
Inspection
1. Signs of fever: flushing of the face, glittering eyes, sweating.
2. Diffuse cyanosis (with broncho-obstructive syndrome).
3. The ribcage is not changed.
Percussion and palpation of the chest
Pathological changes are not detected.
Lung auscultation
1. Hard breathing.
2. Exhalation phase lengthening (with bronchial obstruction syndrome).
3. Dry wheezing.
Instrumental methods for the diagnosis of acute bronchitis
1. X-ray examination of the lungs: strengthening of the pulmonary pattern in the basal zones; expansion of the roots of the lungs.
2. Study of the function of external respiration.
The broncho-obstructive syndrome is characterized by:
Decrease in the value of the Tiffno index;
Decreased peak expiratory flow (PSV);
Moderate decrease in maximum ventilation (MVV).
Laboratory signs of acute bronchitis
1. General analysis blood:neutrophilic leukocytosis with a shift in the nuclear formula of neutrophils to the left; acceleration of ESR.
2. Biochemical blood test: increased levels of C-reactive protein, seromucoid, fibrinogen, glycoproteins, sialic acids.
3. Microscopic examination of sputum: a large number of leukocytes with a predominance of neutrophils; epithelium of the bronchi.
Chronic obstructive pulmonary disease (COPD)is a disease characterized by chronic diffuse inflammation of the bronchi, manifested by cough with sputum and shortness of breath, leading to a progressive impairment of pulmonary ventilation and obstructive gas exchange.
Epidemiological definition of COPD (WHO)
Patients with COPD should be considered those persons whose cough with sputum production lasts at least 3 months a year for 2 years in a row, provided that these patients have excluded other diseases that can cause the same symptoms (chronic pneumonia, bronchiectasis, tuberculosis, etc. others).
Etiology of COPD
COPD risk factors
Stages of COPD formation
Stage I - the threat of disease.
Exogenous and endogenous risk factors: smoking tobacco; long-term exposure to dust and other pollutants (irritants); frequent acute respiratory infections (more than 3 times a year); violation of nasal breathing; genetic predisposition, etc.
II stage - pre-illness.
Changes in the bronchial mucosa are characteristic:restructuring of the secretory apparatus; replacement of the ciliated epithelium with goblet cells; hyperplasia of the mucous glands; mucociliary insufficiency.
Clinical manifestations:smoker's cough; protracted and recurrent course of acute bronchitis.
Stage III - clinically established COPD.
Stage IV - complications: pulmonary emphysema; bronchiectasis; hemoptysis; respiratory failure; chronic cor pulmonale.
COPD pathogenesis
Respiratory function assessment (RPF) is the simplest test that characterizes functional capabilities and reserves respiratory system... A research method that allows you to assess the function of external respiration is called spirometry. This technique is currently widely used in medicine as a valuable method for diagnosing ventilation disorders, their nature, degree and level, which depend on the nature of the curve obtained in the study (spirogram).
Respiratory function assessment does not allow for a definitive diagnosis. However, spirometry greatly facilitates the task of making a diagnosis, differential diagnosis of various diseases, etc. Spirometry allows:
- to identify the nature of ventilation disorders that led to certain symptoms (shortness of breath, cough);
- to assess the severity of chronic obstructive pulmonary disease (COPD), bronchial asthma;
- conduct with specific tests differential diagnosis between bronchial asthma and COPD;
- monitor ventilation disorders and evaluate their dynamics, treatment effectiveness, assess the prognosis of the disease;
- to assess the risk of surgery in patients with ventilation disorders;
- to identify the presence of contraindications to certain physical activity in patients with ventilation disorders;
- check for ventilation disorders in patients at risk (smokers, occupational exposure to dust and irritants chemicals and others) who are not presenting complaints at the moment (screening).
The examination is carried out after half an hour's rest (for example, in bed or in a comfortable chair). The room must be well ventilated.
The survey does not require complex preparation. The day before spirometry, it is necessary to exclude smoking, drinking alcohol, and wearing tight clothing. Do not overeat before the test, do not eat less than a few hours before spirometry. It is advisable to exclude the use of short-acting bronchodilators 4-5 hours before the study. If this is not possible, it is necessary to inform the medical personnel conducting the analysis of the time of the last inhalation.
During the study, tidal volumes are assessed. Instructions on how to properly carry out breathing maneuvers are carried out nurse just before the study.
Contraindications
The technique has no clear contraindications, except for a general grave condition or impairment of consciousness, which does not allow spirometry to be performed. Since it is necessary to make certain, sometimes significant efforts to implement a forced respiratory maneuver, spirometry should not be performed in the first few weeks after myocardial infarction and operations on the thoracic and abdominal cavity, ophthalmic surgical interventions. The determination of the function of external respiration should also be delayed in case of pneumothorax, pulmonary hemorrhage.
If you suspect that the examined person has tuberculosis, all safety standards must be observed.
According to the research computer program a graph is automatically created - a spirogram.
The conclusion on the obtained spirogram may be as follows:
- norm;
- obstructive disorders;
- restrictive disorders;
- mixed ventilation disorders.
What verdict the doctor of functional diagnostics will make depends on the correspondence / inconsistency of the indicators obtained during the study with normal values. FVD indicators, their normal range, values \u200b\u200bof indicators by degrees of ventilation disorders are presented in the table ^
| Index | Rate,% | Conventionally norm,% | Mild violations,% | Moderate degree of violations,% | Severe degree of violations,% |
| Forced vital capacity (FVC) | ≥ 80 | - | 60-80 | 50-60 | < 50 |
| Forced expiratory volume in the first second (FEV1) | ≥ 80 | - | 60-80 | 50-60 | < 50 |
| Modified Tiffno index (FEV1 / FZHEL) | ≥ 70 (absolute value for this patient) | - | 55-70 (absolute value for a given patient) | 40-55 (absolute value for a given patient) | < 40 (абсолютная величина для данного пациента) |
| Average volumetric expiratory flow rate at the level of 25-75% of FVC (SOS25-75) | Over 80 | 70-80 | 60-70 | 40-60 | Less than 40 |
| Maximum volumetric flow rate at 25% of FVC (MOS25) | Over 80 | 70-80 | 60-70 | 40-60 | Less than 40 |
| Maximum volumetric flow rate at 50% of FVC (MOS50) | Over 80 | 70-80 | 60-70 | 40-60 | Less than 40 |
| Maximum volumetric flow rate at 75% of FVC (MOS75) | Over 80% | 70-80 | 60-70 | 40-60 | Less than 40 |
All data are presented as a percentage of the norm (the exception is the modified Tiffno index, which is an absolute value that is the same for all categories of citizens), determined depending on gender, age, weight and height. The most important is the percentage compliance with the standard indicators, and not their absolute values.
Despite the fact that in any study the program automatically calculates each of these indicators, the first 3 are the most informative: FVC, FEV 1 and the modified Tiffno index. Depending on the ratio of these indicators, the type of ventilation disturbances is determined.
FVC is the largest volume of air that can be inhaled after the maximum exhalation or exhaled after the largest inhalation. FEV1 is the part of FVC, which is determined in the first second of the breathing maneuver.
Determining the type of violation
With a decrease in FVC alone, restrictive disorders are determined, that is, disorders that limit the maximum mobility of the lungs during breathing. Restrictive ventilation disorders can be caused by both pulmonary diseases (sclerotic processes in the lung parenchyma of various etiologies, atelectasis, accumulation of gas or fluid in the pleural cavities, etc.), and chest pathology (ankylosing spondylitis, scoliosis), leading to restriction of its mobility.
With a decrease in FEV1 below normal values \u200b\u200band the ratio of FEV1 / FVC< 70% определяют обструктивные нарушения - патологические состояния, приводящие к сужению просвета дыхательных путей (бронхиальная астма, ХОБЛ, сдавление бронха опухолью или увеличенным лимфатическим узлом, облитерирующий бронхиолит и др.).
With a joint decrease in FVC and FEV1, a mixed type of ventilation disorders is determined. In this case, the Tiffno index can correspond to normal values.
Based on the results of spirometry, it is impossible to give an unambiguous conclusion. Deciphering the results obtained should be carried out by a specialist, be sure to correlate them with the clinical picture of the disease.
Pharmacological tests
In some cases, the clinical picture of the disease does not allow to unambiguously determine what the patient has: COPD or bronchial asthma. Both of these diseases are characterized by the presence of bronchial obstruction, but narrowing of the bronchi in bronchial asthma is reversible (except for advanced cases in patients who have not received treatment for a long time), and in COPD it is only partially reversible. The reversibility test with a bronchodilator is based on this principle.
The study of FVD is carried out before and after inhalation of 400 μg of salbutamol (Salomol, Ventolin). An increase in FEV1 by 12% of the initial values \u200b\u200b(about 200 ml in absolute terms) indicates a good reversibility of the narrowing of the lumen of the bronchial tree and indicates in favor of bronchial asthma. An increase of less than 12% is more typical for COPD.
Less widespread was the test with inhaled glucocorticosteroids (ICS), prescribed as a trial therapy for an average of 1.5-2 months. Respiratory function is assessed before and after the appointment of ICS. An increase in FEV1 by 12% compared with the baseline indicates the reversibility of bronchial narrowing and a greater likelihood in a patient with bronchial asthma.
With a combination of complaints characteristic of bronchial asthma, with normal spirometry indicators, tests are performed to detect bronchial hyperreactivity (provocative tests). During them, the initial values \u200b\u200bof FEV1 are determined, then inhalation of substances that provoke bronchospasm (methacholine, histamine) or an exercise test is carried out. The decrease in FEV1 by 20% from the initial values \u200b\u200bis evidence in favor of bronchial asthma.
Diffusion respiratory failure occurs when:
- thickening of the alveolar-capillary membrane (edema);
- decrease in the area of \u200b\u200bthe alveolar membrane;
- reducing the time of blood contact with alveolar air;
- an increase in the layer of fluid on the surface of the alveoli.
Types of respiratory rhythm disorders
The most common form of breathing disorders is shortness of breath. Distinguish between inspiratory dyspnea, characterized by difficulty breathing, and expiratory dyspnea with difficulty exhaling. A mixed form of shortness of breath is also known. It can also be constant or paroxysmal. In the origin of shortness of breath, not only diseases of the respiratory organs E, but also the heart, kidneys, and the hematopoietic system often play a role.
The second group of respiratory rhythm disorders is periodic breathing, i.e. group rhythm, often alternating with stops or with intercalated deep breaths. Periodic breathing is divided into basic types and variations.
The main types of periodic breathing:
- Wave-like.
- Incomplete Cheyne-Stokes rhythm.
- Cheyne-Stokes rhythm.
- Biota rhythm.
Options:
- Tonus fluctuations.
- Deep intercalated breaths.
- Alternating.
- Complex allorhythmias.
The following groups of terminal types of periodic respiration are distinguished.
- Big breath of Kussmaul.
- Apneastic breathing.
- Gasping breath.
There is one more group of respiratory rhythm disturbances - dissociated breathing.
These include:
- paradoxical movements of the diaphragm;
- asymmetry of the right and left half of the chest;
- peyner respiratory center block.
Dyspnea
Shortness of breath is understood as a violation of the frequency and depth of breathing, accompanied by a feeling of lack of air.
Dyspnea is a reaction of the external respiration system, which provides an increased supply of oxygen to the body and the removal of excess carbon dioxide (considered as protective and adaptive). The most effective shortness of breath in the form of an increase in the depth of breathing in combination with its rapidity. Subjective sensations do not always accompany shortness of breath, so one should focus on objective indicators.
(module direct4)
There are three degrees of deficiency:
- I degree - occurs only with physical stress;
- II degree - at rest, deviations of pulmonary volumes are found;
- III degree - characterized by dyspnea at rest and is combined with excessive ventilation, arterial hypoxemia and the accumulation of under-oxidized metabolic products.
Respiratory failure and shortness of breath as its manifestation is a consequence of impaired ventilation and the corresponding insufficient oxygenation of blood in the lungs (with limited alveolar ventilation, airway stenosis, circulatory disorders in the lungs).
Perfusion disorders occur with abnormal vascular and intracardiac shunts, vascular diseases.
Other factors also cause shortness of breath - a decrease in cerebral blood flow, general anemia, toxic and mental influences.
One of the conditions for the formation of shortness of breath is the preservation of a sufficiently high reflex excitability of the respiratory center. The absence of shortness of breath during deep anesthesia is considered as a manifestation of inhibition created in the respiratory center in connection with a decrease in lability.
The leading links in the pathogenesis of shortness of breath: arterial hypoxemia, metabolic acidosis, functional and organic lesions of the central nervous system, increased metabolism, impaired blood transport, difficulty and restriction of chest movements.
Non-respiratory lung function
The basis of non-respiratory functions of the lungs are metabolic processes specific to respiratory organs. The metabolic functions of the lungs consist in their participation in the synthesis, deposition, activation and destruction of various biologically active substances (BAS). The ability of the lung tissue to regulate the level of a number of biologically active substances in the blood is called the “endogenous pulmonary filter” or “pulmonary barrier”.
Compared to the liver, the lungs are more active in relation to the metabolism of biologically active substances, since:
- their volumetric blood flow is 4 times greater than hepatic;
- only through the lungs (with the exception of the heart) all blood passes, which facilitates the metabolism of biologically active substances;
- in pathology with redistribution of blood flow ("centralization of blood circulation"), for example, in shock, the lungs can play a decisive role in the exchange of biologically active substances.
Up to 40 types of cells have been found in the lung tissue, of which the most attention are attracted by cells with endocrine activity. They are called Feiter and Kulchitsky cells, neuroendocrine cells or APUD-system cells (apudocytes). The metabolic function of the lungs is closely related to the gas transport.
Thus, with impaired pulmonary ventilation (more often hypoventilation), impaired systemic hemodynamics and blood circulation in the lungs, an increased metabolic load is noted.
The study of the metabolic function of the lungs with their various pathologies made it possible to distinguish three types of metabolic changes:
- Type 1 is characterized by an increase in the level of biologically active substances in the tissue, accompanied by an increase in the activity of enzymes of their catabolism (in acute stress situations - the initial stage of hypoxic hypoxia, the early phase acute inflammation and etc.);
- Type 2 is characterized by an increase in the content of biologically active substances, combined with a decrease in the activity of catabolic enzymes in the tissue (with repeated exposure to hypoxic hypoxia, a prolonged inflammatory bronchopulmonary process);
- Type 3 (less common) is characterized by a deficiency of biologically active substances in the lungs, combined with suppression of the activity of catabolic enzymes (in pathologically altered lung tissue with long periods of bronchiectasis).
The metabolic function of the lungs has a significant effect on the hemostatic system, which, as you know, takes part not only in maintaining the liquid state of the blood in the vessels and in the process of thrombus formation, but also affects the hemorheological parameters (viscosity, aggregation ability of blood cells, fluidity), hemodynamics, etc. vascular permeability.
The most typical form of pathology that occurs with the activation of the coagulation system is the so-called shock lung syndrome, characterized by disseminated intravascular coagulation of blood. The "shock lung" syndrome is basically modeled by the administration of adrenaline to animals, which ensures pulmonary tissue edema, the formation of hemorrhagic foci, as well as activation of the kallikrein-kinin blood system.
Respiratory failure. Clinical and expert characteristics. Respiratory failure is a condition of the body in which the normal function of the respiratory system is insufficient to provide the body with the required amount of oxygen and remove the required amount of carbon dioxide. The correspondence of the lung volumes and the amount of absorbed oxygen at rest to their proper value and the normal use of ventilated air, i.e., the normal value of the O2 utilization factor (CI), indicate normal diffusion of oxygen, and, consequently, the normal amount of blood flowing per unit time through lungs. These conditions ensure normal uniform pulmonary gas exchange, normal blood gas composition and oxygen saturation of arterial blood, normal pulmonary circulation. When one of these links that ensure the normal function of the respiratory system is disrupted, respiratory failure develops.
There are three degrees of respiratory failure.
Respiratory failure of the I degree is characterized by shortness of breath that occurs with significant and even moderate physical exertion. The indicators that determine the function of external respiration at rest are moderately deviated from the proper values \u200b\u200band indicate a violation of the biomechanics of respiration. At the same time, the following decrease: the rate of forced expiration in the first second (Tiffno's test) to 72-75%, vital capacity of the lungs (VC) - up to 62-65%, maximum ventilation of the lungs (MVL) - up to 55-60%; increase: respiratory rate (RR) - up to 20-22 per minute, respiratory minute volume (RV) up to 132-135%, residual volume (RO) - up to 48%; functional residual capacity (FRC) is 60% of the total lung capacity (OEL). The partial pressure of oxygen (РO2) and carbon dioxide (РCO2) is slightly reduced: РO2 -97 mm Hg. Art., PСO2 -36 mm. Oxygen uptake is slightly increased: at rest 117-120%.
Arterial blood oxygen saturation is slightly reduced - 92-93%, venous blood saturation -40-45%. When breathing with oxygen, the saturation of arterial blood rises to normal (96-99%), with physical activity it decreases by 3-4%. The time of desaturation from oxygen is normal for most (3-4 minutes), and sometimes it is increased (5-6 minutes). The width of the right branch of the pulmonary artery on the central tomogram is slightly increased - 15.6 mm.
In electrokymographic study, there is a tendency to increase the speed of propagation of the pulse wave to the right branch of the pulmonary artery (Hd) - 185-210 cm / sec, to the peripheral pulmonary pulse (Pd) - 150-155 cm / sec. The phase of isometric contraction of the right ventricle is increased (0.05 seconds). After a pharmacological test (1 ml of a 0.1% solution of atropine or adrenaline), the speed of propagation of the pulse wave with the same number of heartbeats is normalized, and the phase of isometric contraction of the right ventricle does not change.
In patients with grade I respiratory failure with a radiocardiological study using I131, hemodynamic parameters are within normal limits. The volume of circulating blood (BCC) is 71 ml / kg, the minute volume of blood (MCV) is 5! l, systolic index (SI) -3 l / m 2, stroke index (SI) -41.5 ml / m 2, external work of the heart (W) - 9.8 kg / m / min, peripheral vascular resistance (N) - 1630 dynes / cm / sec-5.
The etheric time of blood flow is 10-12 seconds, the magnesian time is 18-20 seconds, the venous pressure is 95 mm of water. Art.
Respiratory failure of the II degree is characterized by shortness of breath, which occurs with little physical exertion. The indicators of the function of external respiration at rest are significantly deviated from the proper values. At the same time, the following decrease: Tiffno test - up to 60-65%, VC - up to 52-55%, MVL - up to 48-50%; increase: BH - up to 23-25 \u200b\u200bper minutes, MOU - up to 150-155%, GS - up to 52-55%, FRU - up to 65-70%; РO2 is lowered and amounts to 85-90 mm Hg. Art., and PСO2 - increased to 42-45 mm. Oxygen uptake increased to 127%. Decreased oxygen saturation of arterial (85-89%) and venous (35-40%) blood. When breathing oxygen, it rises to 96%, with physical activity it decreases by 5%. The desaturation time from oxygen is increased from 6 to 8 minutes and indicates uneven pulmonary ventilation.
The width of the right branch of the pulmonary artery increases to 22 mm.
The speed of propagation of the pulse wave up to W - 195-246 cm / sec, up to Pd-160-175 cm / sec. After a pharmacological test, it slightly decreased, which indicates sclerotic changes in the pulmonary artery system. The phase of isometric contraction of the right ventricle is significantly increased (0.06 seconds). This is confirmed by the data of electrocardiographic studies and hemodynamic parameters, indicating the plus-decompensation of chronic pulmonary heart, as indicated by an increase in BCC -88 ml / kg, IOC -6.1 L, SI -3.65 L / m2, SI -48 ml / m2, W - 11.3 kg / m / min and a relative decrease N - up to 1370 dynes / cm / sec-6. The etheric time of blood flow is 14 seconds, the magnesian time is 22-24 seconds, and the venous pressure is 105 mm of water. Art. With respiratory failure of the II degree, there are signs of decompensation of chronic cor pulmonale of I, I-II degree.
Respiratory failure of the III degree is characterized by shortness of breath, expressed at rest; the indicators characterizing the function of external respiration and its biomechanics are sharply deviated from the proper values. At the same time, the following decrease: Tiffno's test - up to 50-55%; VC - up to 50%, MVL - up to 45-47%; increase: BH - up to 28 per minute, MO - up to 163%, RO - up to 56%, FRU - up to 70%; not only the reserve, but also the additional and tidal volume decreases sharply. PO2-81 mm Hg. Art., PСO2 - 45.6 mm. Oxygen absorption and CI in patients of this group decrease and indicate shallow and ineffective breathing. The saturation of arterial blood with oxygen is reduced to 85%, venous - to 35%. When breathing with oxygen, saturation increases to 96%, with incomplete physical activity - decreases by 6%. The time for desaturation from oxygen increases from 8 to 12 minutes.
The width of the right branch of the pulmonary artery is sharply increased (24 mm). The speed of propagation of the pulse wave is significantly increased to Hd (226-264 cm / sec) and Pd (165-180 cm / sec). After a pharmacological test, the spreading rate remained almost unchanged and indicates severe pulmonary hypertension. The phase of isometric contraction of the right ventricle is significantly increased (0.065 seconds) and indicates a significant violation of the contractile function of the myocardium, which is confirmed by an ECG: deviation of the electrical axis of the heart to the right, high, pointed P wave in II, III of standard and right chest leads, decrease in T wave and displacement segment RS-T down in the same leads and increased heart rate (90-95 per minute).
In patients during this period, pronounced phenomena of right ventricular failure are observed, which is confirmed by hemodynamic shifts, indicating minus decompensation (according to Wollheim, 1931): BCC - 87 ml / kg, IOC - 4.5 L, SI - 2.7 L / m 2, SI - 31 ml / m 2, W - 8.2 kg / m / min, and an increase in N - 1970 dyne / cm / sec-5. The air time of blood flow is 15 seconds, the magnesian time is 24 seconds, venous pressure is more often within the normal range (94 mm of water column).
With respiratory failure of the III degree, there are signs of circulatory disorders in the right ventricular type (I-II, II or III degrees).
Methods for detecting morphological changes and functional disorders. To identify respiratory failure, it is important to ask questions, which allows you to determine the degree of physical stress at which shortness of breath appears in patients with chronic lung diseases. On examination, the severity of cyanosis, the nature of respiratory movements, participation in the act of breathing of the auxiliary muscles, the presence of pulsation in the epigastric region due to hypertrophy of the right ventricle are established. When percussion and auscultation of the chest determine the nature and severity of the lesion of the respiratory system.
Fluoroscopy (radiography) allows you to establish the nature, localization and severity of morphological changes in the lungs, as well as pulmonary circulation and heart. The samples of Sokolov and Sadofiev make it possible to judge the severity of emphysema of the lungs. With bronchography, the nature of the morphological changes in the tracheobronchial tree is determined.
It is very important to determine the indicators of the function of external respiration, namely; determination of volumes and capacities - total lung capacity (OEL), vital capacity of the lungs (VC), respiratory, additional, reserve and residual volumes; respiratory minute volume (RV), respiratory rate, respiratory equivalent (DE), maximum ventilation (MVV), forced expiratory flow rate (Tiffno's test), bioelectrical activity of the respiratory muscles, intrathoracic and intraalveolar pressure, which allow to judge the state of respiratory biomechanics.
Along with this, the study of pulmonary gas exchange is of great importance: oxygen absorption, partial pressure of oxygen and carbon dioxide in the alveolar air, oxygen utilization factor (OI); the gas composition of the blood and the saturation of arterial blood with oxygen, allowing to establish the effectiveness of pulmonary ventilation.
Recently, electrokymography (ECI) has been used to study pulmonary ventilation, pulmonary circulation and myocardial contractile function of the right and left ventricles.
Of the hemodynamic parameters for determining the functional state, radioisotope cardiography is important, with the help of which the volume of circulating blood and plasma, minute volume of blood, stroke and cardiac indices, blood volume in the lungs (Q), peripheral vascular resistance, external work of the heart and coronary blood flow ( E. Korkus). The available methods of hemodynamic research are determination of ether and magnesian time of blood flow and venous pressure.
Of the methods of biochemical research for characterizing the degree of respiratory failure, it is important to determine the oxygen vacate before and after physical exercise, the activity of carbonic anhydrase, and protein fractions of the blood.
When deciding on surgical treatment, catheterization of the heart and pulmonary artery is often used with the use of pharmacological tests to clarify the nature of changes in the vessels of the pulmonary circulation.
Clinical and labor prognosis, indicated and contraindicated types and working conditions. Clinical and labor prognosis, shown and contraindicated types and working conditions for respiratory failure depend on the nature of the disease, the course of the pathological process, the degree of respiratory failure, the nature of the main profession and working conditions.
In most patients with chronic nonspecific lung diseases with respiratory failure of the 1st degree, the clinical prognosis is favorable. Along with the treatment of the underlying disease, a rational work arrangement is essential. Patients are shown work that is not associated with significant physical stress, most of the professions of intellectual labor are available in favorable meteorological and sanitary and hygienic conditions. Contraindicated work associated with significant, even episodic, physical stress and strain of the respiratory system, in unfavorable meteorological and sanitary and hygienic conditions, in contact with allergic substances, broncho- and pulmotropic poisons.
With respiratory failure of the II degree, the clinical and work prognosis is less favorable due to insignificant compensatory possibilities. Patients have access to work associated with minor physical and moderate neuropsychic stress, near their place of residence, in favorable meteorological and sanitary and hygienic conditions. Work that requires significant and even moderate physical stress is contraindicated; some types of intellectual work associated with significant neuropsychic stress are inaccessible.
In case of respiratory failure of the III degree, the clinical and labor prognosis is unfavorable. Any work in production conditions is contraindicated for these patients. Sometimes they can be recommended light types of work at home, provided that the raw materials are delivered to them and the finished product is received from them.
Criteria for determining the disability group. The criteria for determining disability groups in case of respiratory failure in patients with chronic lung diseases is the confidence that the recommended work in certain working conditions cannot worsen the patient's condition. Therefore, even with respiratory failure of the 1st degree, when there are contraindicated production factors in the main profession, patients are of limited working ability (disabled III group).
In case of respiratory failure of the II degree due to severe functional impairments, patients are more often disabled (disabled people of group II), only a part of young patients with education, qualifications and a positive attitude to work can be considered to be of limited working capacity (disabled people of group III). They can be advised to work close to their place of residence, associated with moderate neuropsychic or minor physical stress in a dry, warm and dust-free environment.
With respiratory failure of the III degree, the clinical and labor prognosis is unfavorable; most of the patients are disabled (disabled people of group II), and sometimes they need long-term outside care (disabled people of group I). They can be encouraged to work from home.
Rehabilitation paths. In patients with respiratory failure due to chronic nonspecific lung diseases, especially in grade I, the possibilities of medical and professional rehabilitation are significant. For this purpose, it is necessary to carry out dispensary observation of all patients with chronic obstructive bronchitis, emphysema of the lungs, pneumosclerosis, bronchiectasis, bronchial asthma and other diseases of the respiratory system, and to prescribe medication and spa treatment. In case of flu and other diseases, the duration of temporary disability should be longer than that of healthy people who fell ill with the same viral diseases.
The possibilities of social and labor rehabilitation are especially great in this period: employment of patients at the conclusion of a medical institution (providing them with the types of work shown, retraining and retraining of patients under the age of 40-45). Older patients who were in contraindicated work should be recognized as disabled for the purpose of rational employment, so that the nature of work and working conditions do not have a negative impact on the patient's health. The latter is an important factor in the prevention of disease progression.
With respiratory failure of the II degree, the possibilities of medical and social rehabilitation are reduced mainly to the prevention of more pronounced functional disorders. A rational work arrangement is of great importance in order to prevent the I group of disability.
With respiratory failure of the III degree, medical rehabilitation by treatment should be carried out, and professional rehabilitation is often impossible due to the age of the patients.