Violations of FVD i degree III. What is the function of external respiration and why is it determined? How is the study

1. Decreased expiratory power.

2. Decrease in PSV.

3. Decrease in FEV1.

4. Decrease in the Tiffno index (Tiffno index \u003d (FEV1 / VC) x 100%, normal - 70-80%).

5. Decrease in MVL (due to MVL \u003d VC X 35).

Restrictive type of DN

Causes of occurrence:

1) pulmonary fibrosis (pneumoconiosis, scleroderma);

2) emphysema;

3) pleural adhesions;

4) exudative pleurisy, hydrothorax;

5) pneumothorax;

6) alveolitis, pneumonia, lung tumors;

7) removal of the area of \u200b\u200bthe lungs.

Changes in HPF with the restrictive type of DN

1. Decrease in VC.

2. The decrease in MVL.

Mixed (obstructive-restrictive) type of DN

It is characterized by the presence of signs of obstructive and restrictive types in the patient.

Acute day

The term acute DN is understood.

1. The sudden occurrence of DN.

2. The gradual development of DN to a critical state requiring intensive care or resuscitation.

Stages of acute NAM

I stage - initial.

Characteristic:

Forced position of the patient - orthopnea;

Severe cyanosis of the skin and mucous membranes;

Arousal, anxiety, sometimes delirium, hallucinations;

Rapid breathing up to 40 in 1 minute;

The 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).

II stage - deep hypoxia.

Characteristic:

The condition of patients is extremely serious;

Superficial breathing, patients frantically gasp for air;

Position - orthopnea;

The alternation of periods of excitement with periods of drowsiness;

Respiratory rate exceeds 40 in 1 minute;

Heart rate per minute above 120;

Hypoxia (P a O 2 - 50-60 mm Hg) and hypercapnia (P a CO 2 - 50-70 mm Hg) are detected in the blood.

III stage - hypercapnic coma.

Characteristic:

Consciousness is absent;

Pronounced diffuse cyanosis;

Cold sticky sweat;

Pupils dilated (mydriasis);

Breathing shallow, rare, often arrhythmic - like Chain-Stokes;

Sharp hypoxia (P a O 2 - 40-55 mm Hg) and pronounced hypercapnia (P a CO 2 - 80-90. Mm Hg) are detected in the blood.

Stages of chronic respiratory failure

Stages	I (compensated)	II (expressed subcompensated)	III (decompensated)
Dyspnea	When prof. load	Under daily stress	At rest
Cyanosis	Not	Appears under load	Diffuse constant
The participation of auxiliary muscles in the act of breathing	Not involved	Visibly involved in exercise	Participate alone
BH (in 1 min.)	mb norm	Over 20 alone	Over 20 alone
Heart rate (in 1 min.)	norm	More than 90	More than 90
Ventilation disturbances	Decrease in indicators to 80-50%	Decrease in indicators to 50-30%	Decrease in indicators below 30%

LECTURE: Symptomatology and diagnosis of bronchitis and emphysema

Acute bronchitis - This is an inflammatory process in the trachea, bronchi and (or) bronchioles, characterized by an acute course and diffuse reversible lesion mainly of their mucous membrane.

Etiology of acute bronchitis

1. Infectious factors - influenza viruses, parainfluenza, adenoviruses, mycoplasmas (ie, causative agents of acute respiratory infections).

2. Physical factors - hot air and hypothermia, ionizing radiation.

3. Chemical factors - pairs of acids, alkalis, toxic substances (sulfur dioxide, nitrogen oxides).

4. Exposure to dust particles .

Predisposing factors:

Smoking;

Alcoholism;

Cardiovascular disease (left ventricular failure);

Impaired nasal breathing;

Foci of chronic infection in the nasopharynx;

Severe diseases that reduce the immunological reactivity of the body.

The phases of the development of acute bronchitis

1. Reactive-hyperemic or neuro-reflex:

Hyperemia and swelling of the mucous membrane;

Damage to the epithelium;

Inhibition 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. Unobstructive.

2. Obstructive.

V. The course.

1. Acute - up to 2 weeks.

2. Long - 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, eye gloss, sweating.

2. Diffuse cyanosis (with bronchial obstructive syndrome).

3. The chest is not changed.

Percussion and palpation of the chest

Pathological changes are not detected.

Auscultation of the lungs

1. Hard breathing.

2. Lengthening of the expiratory phase (with bronchial obstruction syndrome).

3. Dry rales.

Instrumental methods for the diagnosis of acute bronchitis

1. X-ray examination of the lungs: increased pulmonary pattern in the basal zones; expansion of the roots of the lungs.

2. Functional research external respiration.

For bronchial obstructive syndrome are characteristic:

Decrease in the Tiffno index value;

Decreased peak expiratory flow rate (PSV);

Moderate decrease in maximum lung ventilation (MVL).

Laboratory signs of acute bronchitis

1. General analysis blood:neutrophilic leukocytosis with a shift in the nuclear formula of neutrophils to the left; ESR acceleration.

2. Biochemical blood test: levels of C-reactive protein, seromucoid, fibrinogen, glycoproteins, sialic acids increase.

3. Microscopic examination of sputum: a large number of leukocytes with a predominance of neutrophils; epithelium of the bronchi.

Chronic Obstructive Pulmonary Disease (COPD)- This is a disease characterized by chronic diffuse inflammation of the bronchi, manifested by cough with sputum and shortness of breath, leading to progressive impairment of pulmonary ventilation and obstructive gas exchange.

Epidemiological Definition of COPD (WHO)

Patients with COPD should be considered those who have a cough with sputum lasting at least 3 months a year for 2 consecutive years, provided that these patients exclude other diseases that can cause the same symptoms (chronic pneumonia, bronchiectasis, tuberculosis and others).

Etiology of COPD

Risk Factors for COPD

Stages of COPD

Stage I - threats of disease.

The presence of exogenous and endogenous risk factors: tobacco smoking; prolonged 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.

Characteristic changes in the mucous membrane of the bronchi:restructuring of the secretory apparatus; replacement of ciliated epithelium with goblet cells; mucosal hyperplasia; mucociliary insufficiency.

Clinical manifestations:smoker's cough; protracted and relapsing course of acute bronchitis.

Stage III - Clinically formed COPD.

Stage IV - complications: emphysema; bronchiectasis; hemoptysis; respiratory failure; chronic pulmonary heart.

COPD pathogenesis

Diffuse respiratory failure occurs with:

1. thickening of the alveolar-capillary membrane (swelling);
2. decrease in the area of \u200b\u200bthe alveolar membrane;
3. reducing the time of contact of blood with alveolar air;
4. an increase in the fluid layer on the surface of the alveoli.

Types of respiratory rhythm disorders
The most common form of respiratory distress is shortness of breath. Distinguished inspiratory dyspnea, characterized by difficulty in inhaling, and expiratory shortness of breath with difficulty exhaling. A mixed form of dyspnea is also known. It can also be permanent or paroxysmal. In the origin of shortness of breath often play a role not only diseases of the respiratory system E, but also the heart, kidneys, hematopoiesis system.
The second group of respiratory rhythm disorders is periodic breathing, i.e. group rhythm, often alternating with stops or with deep insertion of deep breaths. Periodic breathing is divided into main types and variations.

The main types of periodic breathing:

1. Wavy.
2. Incomplete chain of chain stokes.
3. Chain Stokes rhythm.
4. The rhythm of Biota.

Options:

1. Tonic vibrations.
2. Deep insertion breaths.
3. Alternating.
4. Complicated allorhythmias.

The following groups of terminal types of periodic breathing are distinguished.

1. Kussmaul's big breath.
2. Apneystic breathing.
3. Gasping breath.

There is another group of respiratory rhythm disturbances - dissociated breathing.

These include:

1. paradoxical movements of the diaphragm;
2. asymmetry of the right and left half of the chest;
3. peyner breathing center unit.

Dyspnea
Dyspnea refers to 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, providing an increased supply of oxygen to the body and elimination of excess carbon dioxide (considered as protective and adaptive). The most effective is 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 you should focus on objective indicators.

(module direct4)

There are three degrees of failure:

• I degree - occurs only during physical exertion;
• II degree - at rest deviations of pulmonary volumes are found;
• Grade III - characterized by shortness of breath at rest and combined with excessive ventilation, arterial hypoxemia and the accumulation of under-oxidized metabolic products.

Respiratory failure and shortness of breath as its manifestation are a consequence of a violation of ventilation and corresponding insufficient oxygenation of the blood in the lungs (with restriction of alveolar ventilation, stenosis of the respiratory tract, circulatory disorders in the lungs).
Perfusion disorders occur with abnormal vascular and intracardial shunts, vascular diseases.
Other factors cause shortness of breath - a decrease in cerebral blood flow, general anemia, toxic and mental effects.
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 dyspnea during deep anesthesia is considered as a manifestation of inhibition created in the respiratory center due to 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 system. The metabolic functions of the lungs are their participation in the synthesis, deposition, activation and destruction of various biologically active substances (BAS). The ability of 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 with the liver, the lungs are more active in relation to the metabolism of biologically active substances, since:

1. their volumetric blood flow is 4 times greater than hepatic;
2. only blood passes through the lungs (with the exception of the heart), which facilitates the metabolism of biologically active substances;
3. in pathology with redistribution of blood flow ("centralization of blood circulation"), for example, in shock, the lungs can be crucial in the exchange of biologically active substances.

Up to 40 cell types were found in lung tissue, of which the cells with endocrine activity attracted the most attention. They are called Feiter and Kulchitsky cells, neuroendocrine cells or APUD system cells (apudocytes). The metabolic function of the lungs is closely related to gas transport.
So, with impaired pulmonary ventilation (often hypoventilation), impaired systemic hemodynamics and blood circulation in the lungs, an increased metabolic load is noted.

Study of the metabolic function of the lungs during their diverse pathology allowed to distinguish three types of metabolic shifts:

• 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 their catabolism enzymes (in acute stressful situations - the initial stage of hypoxic hypoxia, the early phase of acute inflammation, 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 protracted inflammatory bronchopulmonary process);
• Type 3 (less commonly detected) 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 bronchiectatic disease).

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 blood in the vessels and in the process of thrombosis, but also affects hemorheological parameters (viscosity, aggregation ability of blood cells, fluidity), hemodynamics and vascular permeability.
The most typical form of pathology associated with the activation of the coagulation system is the so-called “shock lung” syndrome, which is characterized by disseminated intravascular coagulation of blood. The “shock lung” syndrome is basically modeled by the introduction of adrenaline to the animals, which provides pulmonary edema, the formation of hemorrhagic foci, and the activation of the kallikrein-kinin blood system.

Poor respiratory function.

Classification of respiratory failure, types of ventilation disorders.

The concept of pulmonary heart failure.

Under breathing It is understood as a complex continuous biological process, as a result of which a living organism consumes oxygen from the external environment, and emits carbon dioxide and water into it.

Breathing as a process involves three phases:

1) external respiration;

2) blood gas transport;

3) tissue, internal respiration, i.e. consumer

tissue oxygenation and secretion by them

carbon dioxide - actually breathing.

External respiration is provided by the following mechanisms:

lung ventilation, as a result of which

the outside air enters the alveoli, and is removed from the alveoli;

2) gas diffusion, i.e. the penetration of O2 from the gas mixture into the blood of the pulmonary capillaries and CO2 from the latter into the alveoli (due to the difference between the partial pressure of the gases in the alveolar air and their voltage in the blood);

3) perfusion, i.e. blood flow through the pulmonary capillaries, providing capture from the alveoli with O2 blood and the release of CO2 from it into the alveoli.

Types of external respiration disorders:

I. ventilation;

II. diffusion;

III. perfusion (circulatory).

The main pulmonary volumes and capacities

	tidal volume	0.25 - 0.5 L (15% VEL)
WFMP	functional dead air	0.15 L from
RO vyd	expiratory reserve	1,5 - 2,0l (42% YEL)
Ro vd	reserve inspiratory volume	1,5 - 2,0l (42% YEL)
	Lung capacity YEL \u003d DO + Rovyd + Rovd	3.5-5.0 liters in men, in women, 0.5-1.0 liters less.
	residual volume	1.0 - 1.5 L (33% VEL)
	total lung capacity OEL \u003d DO + ROYVD + ROVD + OO	5.0 - 6.0 L

Dynamic parameters of the respiratory aspect:

	resting breathing rate	14-18 in 1min
	minute volume of breath
	MOD \u003d TO * BH	6 - 8 l / min
	when walking	up to 20 l / min
	up to 50 - 60 l / min
FZHEL	forced vital capacity of the lungs of the exhalation - the difference in lung volumes between the beginning and end of the forced expiration	3,5 - 5,0l
	maximum lung ventilation. MVL is the “limit of breath”, among athletes it reaches	120 - 200 l / min

	forced expiratory volume - an indicator of bronchial patency, equal to the volume of air exhaled in 1 sec at the maximum expiratory flow; test Votchala –Tiffno	70 - 85% of VC. for men 20-60 years old
Tiff-no Index	ratio FEV1 / VC; expressed as a percentage and is a sensitive indicator of bronchial patency	the norm is > 70% (82,7)
	Peak volume expiratory flow - maximum flow during exhalation of the first 20% FVC	4-15 l / s

PNEUMOTACHOMETRY

used to determine the maximum volumetric speed (power) of the exhalation and inhalation (MVD and MVD)

Mvyd - 5 l / s, MIA - 4.5 - 5 l / s

Analyzing the value of the actual VC and Mvid and MIA, one can judge the nature of the violations of the FVD:

Restrictive type: VC - significantly reduced; Mvyd - N

Obstructive type: VC - N, Mvid significantly reduced

Mixed type: ↓ YELLOW, ↓ Mvyd.

I. Pathogenesis of ventilation disorders.

The hypoventilation of the alveoli is of primary importance. The reason for it may be:

1. Day centrogenic:

Oppression of the respiratory center (anesthesia, brain injury, cerebral ischemia with sclerosis of cerebral vessels, prolonged hypoxia, high hypercapnia, taking morphine, barbiturates, etc.)

2. DN neuromuscular:

1) Violations of the nerve conduction or neuromuscular transmission of an impulse to the respiratory muscles (spinal cord injury, polio, nicotine poisoning, botulism).

2) Diseases of the respiratory muscles (myasthenia gravis, myositis).

3. Thoracodiaphragmatic:

1) Restriction of the movement of the chest (pronounced kyphoscoliosis, ossification of the costal cartilage, ankylosing spondylitis, congenital or traumatic deformation of the ribs, fracture of the ribs, arthrosis and arthritis of the rib-vertebral joints).

2) Restriction of the movement of the lungs by extrapulmonary causes (pleural adhesions, pleural effusions, pneumothorax, ascites, flatulence, restriction of the movement of the diaphragm, a high degree of obesity, Pickwick syndrome).

4. DN Bronchopulmonary (with pathological processes in the lungs and respiratory tract)

Ventilation disorders in the lungs can occur as a result of the following reasons:

decrease in functioning lung tissue (pneumonia, lung tumor,

atelectasis) - restrictive type of DN

reduction of lung tissue extensibility (fibrosis, pneumocaniosis, congestion in the pulmonary circulation) - restrictive type

impaired patency of the upper and lower respiratory tract (stenosis, laryngeal paralysis, gorian, trachea and bronchial tumors) - obstructive type

II. Diffusion deficiency

The most common cause of diffusion insufficiency is swelling of the alveolar-capillary wall, an increase in the fluid layer on the surface of the alveoli and interstitial fluid between the alveolar epithelium and the capillary wall (with left ventricular failure, with toxic pulmonary edema).

Diffusion is also impaired in diseases leading to compaction, coarsening of collagen and the development of connective tissue in the interstitium of the lung:

hammen Rich interstitial fibrosis.

berylliosis;

productive hypertrophic alveolitis.

III. Perfusion disorders

Normally, there is a correlation between the volume of ventilation and pulmonary blood flow and each section of the lung. These values \u200b\u200bare clearly related to each other by a certain ratio, normally amounting to 0.8 - 1 for the lung as a whole.

Va /Q = 4/5 =0.8

Respiratory failure (NAM) -this is a state of the body in which the normal gas composition of the blood is not maintained, or it is achieved due to more intensive work of the external respiration apparatus and heart, which leads to a decrease in the functional capabilities of the body

Bronchopulmonary DN can be obstructive, restrictive and mixed, which is manifested by corresponding changes in the parameters of the high pressure

Obstructive type characterized by difficulty in passing air through the bronchi:

foreign body

swelling of the mucosa

bronchospasm

narrowing or compression of the trachea or large bronchi with a tumor

obstruction by the secretion of bronchial glands.

Restrictive type violation of ventilation is observed when the ability of the lungs to expand and fall is limited:

pneumonia

emphysema

pneumosclerosis

resection of the lung or its lobe

hydro- or pneumothorax;

massive pleural adhesions;

kyphoscoliosis;

ossification of costal cartilage.

Mixed type(combined) occurs with prolonged pulmonary and heart disease.

Allocate acute and chronic DN.

There are three degrees of severity of respiratory failure according to Dembo:

1. Latent (asymptomatic) DN

2. Compensated Nam

Pulmonary heart disease.

It includes respiratory failure and circulatory failure of the right ventricular type, which arise as a result of diseases that primarily affect the bronchopulmonary system (COPD, pulmonary emphysema, bronchial asthma, tuberculosis, pulmonary fibrosis and granulomatosis, etc.), which disrupt chest mobility (kyphoscoliosis, pleural fibrosis, ossification of the costal joints, obesity), or primarily affecting the vascular system of the lungs (primary pulmonary hypertension, thrombosis and pulmonary embolism, arteritis).

Pulmonary heart failure as a dynamic syndrome, it has the following phases of development.

1. respiratory failure;

2. a combination of respiratory failure with

hyperfunction and hypertrophy of the right heart, i.e. compensated pulmonary heart;

3. a combination of respiratory failure with

circulatory failure in the right ventricular type, i.e. decompensated pulmonary heart, or pulmonary heart failure proper.

Obstructive ventilation disorders occur due to: 1. narrowing of the lumen of the small bronchi, especially bronchioles due to spasm (bronchial asthma; asthmatic bronchitis); 2. narrowing of the lumen due to thickening of the walls of the bronchi (inflammatory, allergic, bacterial edema, edema with hyperemia, heart failure); 3. presence of viscous mucus on the bronchial cover with an increase in its secretion by goblet cells of bronchial epithelium, or mucopurulent sputum; 4. narrowing due to cicatricial deformity of the bronchus; 5. development of an endobronchial tumor (malignant, benign); 6. compression of the bronchi from the outside; 7. the presence of bronchiolitis.

Restrictive ventilation disorders have the following causes:

1. pulmonary fibrosis (interstitial fibrosis, scleroderma, berylliosis, pneumoconiosis, etc.);

2. large pleural and pleurodiaphragmatic adhesions;

3. exudative pleurisy, hydrothorax;

4. pneumothorax;

5. extensive inflammation of the alveoli;

6. large tumors of the lung parenchyma;

7. surgical removal of part of the lung.

Clinical and functional signs of obstruction:

1. An early complaint of shortness of breath at a previously allowable load or during a “cold”.

2. Cough, more often with scanty sputum, causing for some time a feeling of heavy breathing (instead of relieving breathing after a regular cough with sputum separation).

3. The percussion sound is not changed or at first acquires a tympanic hue above the posterolateral sections of the lungs (increased airiness of the lungs).

4. Auscultation: dry wheezing. The latter, according to B.E. Votchal, should be actively detected during forced expiration. Auscultation of wheezing during forced expiration is valuable in terms of judging the spread of bronchial obstruction in the pulmonary fields. Respiratory noises change in the following half-breath: vesicular breathing - hard vesicular - hard indefinite (drowns out wheezing) - weakened hard breathing.

5. More late signs lengthening of the expiratory phase, participation in the breathing of the auxiliary muscles; retraction of intercostal spaces, lowering of the lower border of the lungs, limitation of the mobility of the lower edge of the lungs, the appearance of box percussion sound and the expansion of its distribution zone.

6. Decrease in forced pulmonary samples (Tiffno index and maximum ventilation).

In the treatment of obstructive insufficiency, the leading place is occupied by preparations of the bronchodilating series.

Clinical and functional signs of restriction.

1. Dyspnea during exercise.

2. Rapid shallow breathing (short - quick inhalation and quick exhalation, called the phenomenon of a “slamming door”).

3. Excursion of the chest is limited.

4. Percussion sound shortened with a tympanic hue.

5. The lower border of the lungs is above normal.

6. The mobility of the lower edge of the lungs is limited.

7. Weakened vesicular breathing, rales or popping rales.

8. Decrease in vital lung capacity (VC), total lung capacity (OEL), decrease in tidal volume (DO) and effective alveolar ventilation.

9. Often there are violations of the uniform distribution of ventilation-perfusion ratios in the lungs and diffuse disorders.

Separate spirography Separate spirography or bronchospirography allows you to determine the function of each lung, and therefore the reserve and compensatory capabilities of each of them.

Using a double-lumen tube inserted into the trachea and bronchi and equipped with inflatable cuffs for obstructing the lumen between the tube and bronchial mucosa, it is possible to get air from each lung and record the respiration curves of the right and left lungs separately using a spirograph.

Separate spirography is indicated to determine functional parameters in patients undergoing lung surgery.

There is no doubt that a clearer idea of \u200b\u200bthe violation of bronchial patency gives a record of the curves of the air flow velocity during forced expiration (peak fluorimetry).

Pneumotachometry - is a method for determining the speed and power of an air stream during forced inspiration and expiration using a pneumotachometer. After resting, the test subject exhales as quickly as possible into the tube (the nose is disconnected using the nose clip). This method is mainly used to select and evaluate the effectiveness of bronchodilators.

The average values \u200b\u200bfor men - 4.0-7.0 l / l for women - 3.0-5.0 l / s. With samples with the introduction of bronchospasmolytic drugs, bronchospasm can be differentiated from organic lesions of the bronchi. Exhalation power decreases not only with bronchospasm, but also, although to a lesser extent, in patients with weak respiratory muscles and with sharp stiff chest.

General plethysmography (OCG) is a method of direct measurement of the value of bronchial resistance R with calm breathing. The method is based on the synchronous measurement of air flow velocity (pneumotachograms) and pressure fluctuations in a sealed cabin where the patient is placed. The pressure in the cabin changes synchronously with fluctuations in alveolar pressure, which is judged by the proportionality coefficient between the volume of the cabin and the volume of gas in the lungs. Plethysmographically, small degrees of narrowing of the bronchial tree are better detected.

Hydroxymetry - This is a thorough determination of the degree of oxygen saturation of arterial blood. These readings of the oximeter can be recorded on moving paper in the form of a curve - an oximeter. The principle of the photometric determination of the spectral features of hemoglobin is the basis of the action of an oximeter. Most oxyhemometers and oxyhemographs do not determine the absolute value of oxygen saturation of arterial blood, but make it possible to only monitor changes in blood oxygen saturation. For practical purposes, oximetry is used for functional diagnostics and evaluation of treatment effectiveness. For diagnostic purposes, oxigemometry is used to assess the state of the function of external respiration and blood circulation. So, the degree of hypoxemia is determined using various functional tests. These include switching the patient’s breathing from air to breathing with pure oxygen and, conversely, a test with a breath hold on inhalation and exhalation, a test with a physical dosed load, etc.



/ 13
The worst Best

The state of the body in which the external respiration system does not provide the normal gas composition of arterial blood or its maintenance at a normal level is achieved due to excessive functional tension of this system. Thus, in the concept of "respiratory failure" respiration is considered only as external respiration, that is, as a gas exchange process between the atmosphere and blood of the pulmonary capillaries, as a result of which arterialization of mixed venous blood occurs. At the same time, arterial blood normal in gas composition does not yet indicate the absence of respiratory failure, since due to the tension of the compensatory mechanisms of the respiratory system, krbvi gases remain within normal limits for a long time and decompensation occurs only with II-III degree of respiratory failure. The term "pulmonary insufficiency" is sometimes used as a synonym for "respiratory failure", but the lung as an organ does not exhaust all the processes that ensure external respiration, and in this sense, the use of the concept of "respiratory failure", or "insufficiency of external respiration", is more correct, so as it covers some extrapulmonary mechanisms of insufficiency, for example, associated with damage to the respiratory muscles. Respiratory failure is often combined with heart failure. This combination is reflected in the terms “pulmonary-cardiac” and “cardiopulmonary insufficiency”. Sometimes there are "restrictive" and "obstructive" forms of respiratory failure. It should be borne in mind that restriction and obstruction are types of impaired ventilation ability of the lungs and characterize only the state of the ventilation apparatus. Therefore, it is more correct when analyzing the causes of chronic respiratory failure to distinguish (according to N, N. Kanaev) 5 groups of factors leading to impaired external respiration:

1 Damage to the bronchi and respiratory structures of the lungs:

a) damage to the bronchial tree: increased tone of the smooth muscles of the bronchi (bronchospasm), edematous-inflammatory changes in the bronchial tree, violation of the supporting structures of the small bronchi, decreased tone of the large bronchi (hypotonic dyskinesia);

b) damage to the respiratory structures (lung tissue infiltration, lung tissue destruction, lung tissue dystrophy, pneumosclerosis);

c) a decrease in the functioning pulmonary parenchyma (underdevelopment of the lung, compression and atelectasis of the lung, absence of part of the lung tissue after surgery).

2. Damage to the musculoskeletal framework of the chest and pleura (limiting the mobility of the ribs, limiting the mobility of the diaphragm, pleural adhesions).

3. Damage to the respiratory muscles (central and peripheral paralysis of the respiratory muscles, degenerative changes in the respiratory muscles).

4. Circulatory disturbance in the small circle (reduction of the vascular bed of the lungs, pulmonary arterioles spasm, stagnation of blood in the small circle).

5. Violation of the regulation of respiration (oppression of the respiratory center, respiratory neurosis, violation of local regulatory relations).

The main clinical criterion for respiratory failure is shortness of breath. Depending on its severity with different physical stress, it is customary to distinguish 3 degrees of respiratory failure. At grade I, shortness of breath occurs during physical exertion that exceeds daily, cyanosis is usually not detected, fatigue occurs quickly, but auxiliary respiratory muscles are not involved in breathing. With II degree, dyspnea occurs when most of the usual daily activities are performed, cyanosis is mild, fatigue is pronounced, and the auxiliary muscles of breathing are activated during exercise. At the III degree, shortness of breath is already noted at rest, cyanosis and fatigue are pronounced, the auxiliary muscles are constantly involved in breathing.

Functional diagnostic research, even if it includes only general spirography and a study of blood gases, can provide the clinician with significant help in determining the degree of respiratory failure. In the absence of violations of the ventilation ability of the lungs, the presence of a patient with respiratory failure is unlikely. Moderate (and sometimes significant) obstructive disorders are most often associated with respiratory failure of the first degree. Significant obstruction suggests I or II degree, and severe obstruction - II or III degree of respiratory failure. Restrictive disorders have a relatively small effect on the gas transport function of the external respiration system. Significant and even sharp restriction is most often accompanied only by respiratory failure of the II degree. Hypoxemia at rest most often indicates respiratory failure or blood circulation. Moderate hypoxemia may indicate I degree of respiratory failure, severe hypoxemia is evidence of its more severe degrees. Persistent hypercapnia almost always accompanies II-III degree of respiratory failure.

Acute respiratory failure (ARF) is characterized by the rapid development of a condition in which pulmonary gas exchange becomes insufficient to provide the body with the necessary amount of oxygen. The most common causes of ARF are: obstruction of the airways by a foreign body, aspiration of vomit, blood or other fluids; broncho - or laryngospasm; swelling, atelectasis, or collapse of the lung; thromboembolism in the pulmonary artery system; dysfunction of the respiratory muscles (poliomyelitis, tetanus, spinal cord injuries, the effects of exposure to organophosphorus substances or muscle relaxants); oppression of the respiratory center in case of poisoning with drugs, sleeping pills or with traumatic brain injury; massive acute inflammatory processes in the pulmonary parenchyma; shock lung syndrome; a sharp pain syndrome that impedes the normal implementation of respiratory excursions.

In assessing the severity of ARF associated with impaired ventilation, the study of the partial pressure of CO 2 and O 2 in arterial blood is important.

ODN therapy requires intensive resuscitation measures aimed at eliminating the causes of hypoventilation, stimulating active spontaneous breathing, anesthesia in cases of severe traumatic injuries, mechanical ventilation (including auxiliary), oxygen therapy and correction of CBS.

Respiratory failure

Respiratory failure (NAM) - the inability of the respiratory system to maintain normal blood gas composition at rest or under load. DN is characterized by a decrease in oxygen stress of less than 80 mm Hg. and increasing the voltage of carbon dioxide more than 45 mm Hg DN is manifested by respiratory hypoxia, as well as respiratory acidosis. The DN complex is distinguished, in which a change in the gas composition of the blood occurs only with tension and decompensation, when a change in the gas composition is observed at rest, it happens: acute and chronic.

According to pathogenesis, they are divided into:

Alveolar ventilation impairment

Impaired diffusion of gases in the lungs

Violation of blood perfusion in the vessels of the lungs

Violation of perfusion-ventilation ratios

1. Violation of alveolar ventilation

Violation of nervous regulation.

Arise:

In case of damage or inhibition of the respiratory center due to trauma, hemorrhage, tumor, abscesses, under the influence of biodepressants.

In violation of the function of spinal motor neurons due to injuries of the spinal cord, tumor, polio.

In case of damage to the intercostal and phrenic nerves due to injuries of neuritis, vitamin deficiency, etc.

In violation of neuromuscular transmission, with botulism, myasthenia gravis, and the action of muscle relaxants.

In case of damage to the respiratory muscles - intercostal muscles and diaphragm.

With this form of respiratory failure, the work of the respiratory muscles is disrupted, due to which the MOD, BS decrease, hypoxia quickly develops and compensation is impossible, therefore this form of DN leads to the development of asphyxiation.

Obstructive disorders

With obstruction of the respiratory tract. May occur at the level of the main respiratory tract and at the level of the small bronchi.

Obstruction of the main respiratory tract occurs with: laryngospasm, laryngeal edema, foreign bodiesah larynx, trachea and bronchi.

Obstruction of the small bronchi occurs with bronchospasm, with edema, with hypersecretion of mucus.

With obstruction, the exhalation phase is more difficult. This leads to the development of expiratory dyspnea. In this case, the depth of breathing increases, and the frequency decreases. With severe obstruction in the lungs, the residual volume increases, which can lead to the development of acute emphysema.

Compensation of obstructive disorders is carried out by enhancing the work of the respiratory muscles. However, the disadvantage of this compensation is that the intensively working respiratory muscles consume a large amount of oxygen, which exacerbates hypoxia.

Restorative Disorders

Restriction is a violation of lung expansion during the inspiration phase. Restrictive disorders can occur as a result of intrapulmonary and extrapulmonary causes. The first include:

Pulmonary fibrosis (develops as a result of tuberculosis, sarcoidosis, chronic pneumonia, autoimmune diseases).

Distress syndrome of newborns (occurs due to a violation of the synthesis of surfactant - most often observed in premature infants) and adults (develops when the surfactant is destroyed, which can happen with shock, inhalation of toxic substances, and inflammatory processes in the lungs).

Extrapulmonary causes: pneumothorax or accumulation of air in the chest and pleural cavity - with injuries, hydrothorax - accumulation of fluid in the pleural cavity - in the form of exudate with exudative pleurisy.

With restrictive disorders, the inspiratory phase suffers, inspiratory dyspnea develops, decreases until the respiratory rate increases, breathing becomes frequent, but shallow. Increased respiration is a compensatory mechanism for maintaining respiratory volume. The disadvantage of this compensation is that little air enters the alveoli, and most of it ventilates the anatomically dead airspace.

2. Disturbance of gas diffusion in the lungs

M= Ks/ LΔP

M - diffusion, K - gas diffusion coefficient (depends on the permeability of the alveolar-capillary membrane), S - total area of \u200b\u200bthe diffusion surface, L - the length of the diffusion path, Δ P - the gradient of the concentration of oxygen and carbon dioxide between the alveolar air and blood.

Thus, the causes of diffusion disturbance are an increase in the diffusion path of the gas, a decrease in the total area of \u200b\u200bthe diffusion surface, and a decrease in the permeability of the alveolar-capillary membrane.

The diffusion pathway consists of the wall of the alveoli, capillary and interstitial space between them. An increase in the diffusion pathway occurs with pulmonary fibrosis (tuberculosis, sarcoidosis), as well as with fluid accumulation in the interstitial space, which is observed with pulmonary edema. The same reasons affect the decrease in permeability of the alveolar-capillary membrane and the decrease in the total area of \u200b\u200bthe diffuse surface of the lungs. They occur with all types of restrictive disorders.

3. Violation of blood perfusion in the vessels of the lungs

It occurs with circulatory disorders in a small circle. The reasons:

Inadequate blood flow to the pulmonary circulation due to valve stenosis or the mouth of the pulmonary trunk (due to thromboembolism pulmonary arteries)

An increase in pressure in the pulmonary circulation, due to which pulmonary hypertension develops and pulmonary vessels are sclerotic. This occurs when the ductus arteriosus is open (Batalov duct), with defects in the atrial and interventricular septa

With stagnation of blood in the pulmonary circulation, which occurs with left ventricular heart failure and leads to pulmonary edema.

4. Violation of perfusion-ventilation ratios

It develops with an increase in functionally dead space in the lungs (a set of alveoli that are well perfused but poorly ventilated). This occurs with diffuse lesions of the lung tissue and multiple atelectasis. At the same time, the number of perfused alveoli increases (with chronic emphysema, obstructive and restrictive diseases).

Dyspnea

These are subjective sensations of lack of air, accompanied by an objective violation of the frequency and depth of breathing.

1. Respiratory dyspnea. It is manifested by difficulty in the phase of inspiration. It is observed with restrictive disorders of alveolar ventilation.

2. Expiratory dyspnea. It manifests itself as a difficulty in the exhalation phase. It is observed with obstructive violations of the ventilation phase.

3. Mixed dyspnea. The phases of inspiration and expiration are disturbed.

The main role in the formation of shortness of breath is played by the proprioreceptors of the respiratory muscles, the irritation of which occurs when the work of the respiratory muscles is enhanced. In this case, the signal enters the respiratory center, the stress reaction is also activated, and the information enters the limbic system, where the feeling of lack of air or the inability to fully breathe is formed. In addition, other receptors play a role in the formation of dyspnea: chemoreceptors of the sinocarotid zone and aortic arch, which respond to hypoxia and hypocapnia; bronchial stretch receptors and alveolar decline receptors respond to obstructive and restrictive disorders; as well as interstitial J-receptors, which are activated by increasing pressure in the interstitial space, which happens with edema.

Pathological types of breathing

Hyperpnea - deep breathing, which develops with obstruction, with an increase in the tone of the sipmatic system, with acidosis. A type of hyperpnea is Kussmaul's large acidotic respiration, which is observed in diabetic ketoacidosis.

Tachypnea - This is an increase in respiratory rate. It occurs with restrictive disorders in violation of the tone of the sympathetic system.

Bradypnea - rare breathing. It occurs with obstruction, with depression of the respiratory center, with an increase in systemic blood pressurewith alkalosis.

Apnea - lack of breathing. It may be short-term with periodic forms of breathing; there may be a complete respiratory arrest.

Apneystic breath - characterized by a long convulsive breath, interrupted by a short exhalation, occurs when the inspiratory section of the respiratory center is irritated due to hemorrhage.

Agonal breath - single breaths, alternating with periods of apnea of \u200b\u200bdifferent durations, occur when the afferent impulses are disturbed in the respiratory center and are characterized by the residually fading activity of the respiratory center itself.

Chain stokes breathing. It is characterized by increasing in strength respiratory movements, which alternate with periods of apnea. It occurs with hypercapnia or with a violation of the sensitivity of the respiratory center to carbon dioxide.

Biot's Breath - characterized by periods of apnea, after which respiratory movements of the same amplitude follow, observed with various lesions of the central nervous system.

Asphyxia - choking, a form of respiratory failure, occurs with total obstruction of the airways, or with severe violation of the nervous regulation and - respiratory muscles.

During asphyxiation, two stages are distinguished:

Compensation (there is a pronounced sympatho-adrenal system, which is accompanied by excitement, panic and fear, attempts to clear the airways and make breathing movements). Characteristic: centralization of blood circulation, tachycardia and increased blood pressure.

Decompensation (due to a decrease in the partial pressure of oxygen in the blood, central nervous system depression occurs, which leads to loss of consciousness, cramps, respiratory arrest, a drop in systolic blood pressure, and bradycardia, which leads to death).

Restrictive type (from lat. restrictio - restriction) hypoventilation is observed with limited expansion of the lungs. The causal mechanisms of such limitations can lie inside or outside the lungs.

Intrapulmonary forms are due to increased elastic resistance of the lungs. This occurs with extensive pneumonia, pneumofibrosis, atelectasis and other pathological conditions. Of great importance for the development of a restrictive type of restriction of lung expansion is surfactant deficiency. Many factors lead to this, ranging from impaired pulmonary hemodynamics, influenza virus to the damaging effects of tobacco smoke, increased oxygen concentration, inhalation of various gases.

Restrictive respiratory disorders of extrapulmonary origin occur when limiting chest excursion. This may be due to pulmonary pathology (pleurisy) or chest (rib fractures, excessive ossification of the costal cartilage, neuritis, chest compression). The defeat of the musculoskeletal framework of the chest and pleura prevents the expansion of the lungs and reduces their airflow. At the same time, the number of alveoli remains the same as normal.

On the one hand, an increase in tensile strength during inspiration requires more work of the respiratory muscles. On the other hand, in order to maintain the proper volume of MOD while reducing the amount of inspiration, it is necessary to increase the frequency of respiratory movements, which occurs due to shortening of the expiration, that is, breathing becomes more frequent and superficial. Various reflexes also take part in the development of shallow breathing. So, with irritation of irritant and juxtamedullary receptors, it can be tachypical, but already due to shortening of the breath. The same effect can be with irritation of the pleura.

Hyperventilation

Hypoventilation type respiratory disorders were considered above. They most often lead only to a decrease in the supply of oxygen to the blood. Much less often, in this case, insufficient removal of carbon dioxide occurs. This is due to the fact that CO 2 more than twenty times easier passes through the airborne barrier.

Hyperventilation is another matter. At the beginning of it, there is only a slight increase in the oxygen capacity of the blood due to a slight increase in the partial pressure of oxygen in the alveoli. But then the removal of carbon dioxide increases and may develop respiratory alkalosis. To compensate, the electrolyte composition of the blood may change with a decrease in the level of calcium, sodium and potassium in the blood.

Hypocapnia can lead to a decrease in oxygen utilization, since in this case the oxyhemoglobin dissociation curve shifts to the left. This will primarily affect the functions of those organs that take a greater amount of oxygen from the flowing blood: on the heart and brain. In addition, one should not forget that hyperventilation is carried out due to the intensification of the work of the respiratory muscles, which, with its sharp increase, can consume up to 35% and most oxygen.

Hyperventilation hypocapnia may result in increased excitability of the cerebral cortex. In conditions of prolonged hyperventilation, emotional and behavioral disorders, and with significant hypocapnia, loss of consciousness may occur. One of the characteristic signs of severe hypocapnia, with a decrease in PaCO 2 to 20-25 mm Hg, is the appearance of convulsions and spasm of skeletal muscle. This is largely due to a violation of the exchange of calcium and magnesium between the blood and skeletal muscles.

Obstructive bronchitis. In the genesis of bronchial obstruction, the leading role belongs to swelling of the mucosa as a result of inflammation and excessive secretion of mucus. With bronchitis, an isolated violation of the airway occurs. The heterogeneity of the mechanical properties of the lungs acts as one of the most characteristic manifestations of obstructive pathology. Zones with different bronchial resistance and extensibility have different temporal characteristics, therefore, at the same pleural pressure, the process of emptying and filling with air occurs at different speeds. As a result, the distribution of gases and the nature of ventilation in various parts of the lungs are inevitably violated.

Ventilation of areas with low temporal characteristics with increased breathing is significantly impaired and the ventilated volume decreases. This is manifested by a decrease in lung distensibility. The efforts exerted by patients, accelerating and teaching breathing, lead to an even greater increase in the ventilation of well-ventilated areas and to a further deterioration in the ventilation of poorly ventilated parts of the lungs. There is a kind of vicious circle.

When breathing, non-ventilated areas undergo compression and decompression, which consumes a significant proportion of the energy of the respiratory muscles. The so-called ineffective work of breathing increases. Compression on exhalation and stretching on inspiration of the "air bubble" lead to a change in the volume of the chest, which does not provide a reciprocating movement of air into and out of the lungs. Constant chronic overload of the respiratory muscles leads to a decrease in their contractility and disruption of the normal functioning mode. The weakening of the respiratory muscles in such patients is also evidenced by a decrease in the ability to develop large respiratory efforts.

Due to the simultaneous contraction of blood vessels, the total blood flow through the collapsed part of the lung decreases. The compensatory reaction of this is the direction of blood to the ventilated sections of the lungs, where there is good oxygen saturation of the blood. Often up to 5/6 of all blood passes through such sections of the lungs. As a result, the total coefficient of the ventilation-perfusion ratio drops very moderately, and even with complete loss of ventilation of the whole lung in the aortic blood, only a slight decrease in oxygen saturation is observed.

Obstructive bronchitis, manifesting itself as a narrowing of the bronchi (and this leads to an increase in bronchial resistance), causes a decrease in the volume of expiratory flow in 1 second. In this case, the leading value in the pathological difficulty in breathing belongs to obstruction of small bronchioles. These parts of the bronchi easily close with: a) a contraction of smooth muscles in their wall, b) the accumulation of water in the wall, c) the appearance of mucus in the lumen. There is an opinion that the chronic form of obstructive bronchitis is formed only when persistent obstruction occurs, lasting at least 1 year and not being eliminated under the influence of bronchodilators .

Neuro-reflex and humoral mechanisms of regulation of the muscles of the bronchi.In connection with the relatively weak innervation of the bronchioles from the sympathetic nervous system their reflex effect (when performing muscular work, under stress) is not great. To a greater extent, the influence of the parasympathetic department (n. Vagus) can be manifested. Their mediator acetylcholine leads to some (relatively moderate) spasm of bronchioles. Sometimes parasympathetic effect it is realized with irritation of some receptors of the lungs themselves (see below), with occlusion of small pulmonary arteries with microemboli. But the parasympathetic effect can be more pronounced when bronchospasm occurs in some pathological processes, for example, with bronchial asthma.

If the effect of the mediator of the sympathetic nerves of NA is not so significant, then the hormonal pathway, due to exposure through the blood of A and HA of the adrenal glands, through β-adrenergic receptors causes the expansion of the bronchial tree. Biologically active compounds that form in the lungs themselves, such as histamine, a slow-acting anaphylactic substance released from mast cells during allergic reactions, are powerful factors leading to bronchospasm.

Bronchial asthma. In bronchial asthma, the leading role in bronchial obstruction is active constriction due to spasm of smooth muscle. Since smooth muscle tissue is represented mainly in large bronchi, bronchospasm is expressed mainly by their narrowing. However, this is not the only mechanism of bronchial obstruction. Of great importance allergic edema bronchial mucosa, which is accompanied by a violation of patency of the bronchi of a smaller caliber. Often there is an accumulation in the bronchi of a viscous, difficult to detach vitreous secretion (dyskrinia), while the obstruction can become purely obstructive. In addition, the inflammatory infiltration of the mucous membrane with a thickening of the basement membrane of the epithelium is often joined.

Bronchial resistance increases both when inhaling and when exhaling. With the development of an asthmatic attack, respiratory disorders can increase with menacing swiftness.

In patients with bronchial asthma more often than with other lung pathologies, it is observed alveolar hyperventilation as a manifestation of violations of the central regulation of respiration. It takes place, both in the phase of remission, and in the presence of even severe bronchial obstruction. During an asthma attack, there is often a phase of hyperventilation, which, with an increase in the asthmatic state, is replaced by a phase of hypoventilation.

Catching this transition is extremely important because respiratory acidosis is one of the most important criteria for the severity of the patient's condition, which determines medical tactics. With an increase in PaCO 2 above 50-60 mm Hg there is a need for emergency intensive care.

Arterial hypoxemia in bronchial asthma, as a rule, does not reach a severe degree. In the phase of remission and with a mild course, moderate arterial hypoxemia may occur. Only during an attack of RaO 2 can be reduced to 60 mm Hg. and lower, which also turns out to be an important criterion in assessing the patient's condition. The main mechanism for the development of hypoxemia is a violation of ventilation-perfusion relations in the lungs. Therefore, arterial hypoxemia can be observed in the absence of hypoventilation.

Weak movements of the diaphragm, overstretching of the lungs and large fluctuations in intrapleural pressure lead to the fact that during the attack, blood circulation also suffers. In addition to tachycardia and severe cyanosis on inspiration, systolic pressure can sharply decrease.

As mentioned earlier in asthma, the diameter of the bronchioles during exhalation becomes smaller than during inhalation, which occurs from the fall of the bronchioles due to increased exhalation, additionally compressing the bronchioles from the outside. Therefore, the patient can inhale without difficulty, and exhale with great difficulty. Clinical examination can be detected along with a decrease in expiratory volume and a decrease in the maximum expiratory flow rate.

Chronic non-specific lung diseases (COPD). The main feature of COPD is mainly the bronchogenic genesis of their development. This is precisely what determines the fact that, with all forms of this pathology, the leading syndrome is bronchial obstruction. Obstructive pulmonary disease affects 11-13% of people. In the so-called developed countries, mortality from this type of pathology doubles for every 5 years. The main reason for this situation is smoking and environmental pollution (see section "Ecology").

The nature of COPD, their severity, as well as other mechanisms of external respiration disorders, have their own characteristics.

If the ratio of alveolar ventilation to the minute volume of breathing is normal is 0.6-0.7, then with severe chronic bronchitis it can decrease to 0.3. Therefore, to maintain the proper volume of alveolar ventilation, a significant increase in the minute volume of breathing is necessary. In addition, the presence of arterial hypoxemia and the resulting metabolic acidosis require a compensatory increase in lung ventilation.

The increase in lung distensibility explains the relatively rare and deep breathing, the tendency to hyperventilation in patients with emphysema type chronic bronchitis. On the contrary, with the bronchitis type, a decrease in lung distensibility causes less deep and more frequent breathing, which, given the increase in the dead airspace, creates the prerequisites for the development of hypoventilation syndrome. It is no coincidence that, of all the indicators of respiration mechanics, the closest correlation of PaCO 2 was established precisely with the extensibility of the lungs, while with bronchial resistance such a connection is practically absent. In the pathogenesis of hypercapnia, a significant place, along with violations of the mechanics of respiration, belongs to a decrease in the sensitivity of the respiratory center.

Peculiar differences are also noted from the side of blood circulation in a small circle. The bronchitis type is characterized by the early development of pulmonary hypertension and "pulmonary heart". Despite this, the minute volume of blood circulation, both at rest and under load, is significantly greater than with the emphysematous type. This is due to the fact that with the emphysematous type, due to the low volumetric blood flow velocity, even with a lesser degree of arterial hypoxemia, tissue respiration suffers more than bronchitis, in which, even with arterial hypoxemia, but sufficient volumetric blood flow, tissue supply is much better organism O 2. Hence, the emphysematous type can be defined as hypoxic, and bronchitis as hypoxemic.

In the presence of bronchial obstruction, an increase in OOL and its relationship to VC is naturally noted. The VC most often remains within the normal range, although its deviations can be noted, both in the direction of decrease and increase. As a rule, the unevenness of ventilation increases. Diffusion disorders are usually observed in about half the cases. In some cases, the role of reducing the diffusion capacity of the lungs in the pathogenesis of arterial hypoxemia in this disease is undoubted, however, the leading importance in its development belongs to the violation of ventilation-perfusion relations in the lungs and the anatomical bypass of venous blood into the arterial bed, bypassing the pulmonary capillaries.

In the early stages of the disease, the severity of arterial hypoxemia is small. The most characteristic shift in the acid-base state of the blood is metabolic acidosis, caused primarily by intoxication of the body. Hypoventilation, respiratory disorders of the acid-base state of the blood, and severe arterial hypoxemia are characteristic of a far-reaching stage of the pathological process, in the clinical picture of which is no longer bronchiectasis, but severe bronchitis.

Chronical bronchitis. The most common form of bronchopulmonary pathology among COPD is chronic bronchitis. This is a periodically exacerbating chronic inflammatory process that proceeds with a predominant lesion of the respiratory tract of a diffuse nature. One of the common manifestations of this disease is generalized bronchial obstruction.

An in-depth functional study allows patients with non-obstructive bronchitis to identify initial respiratory disorders. The methods used for these purposes can be divided into 2 groups. Some make it possible to evaluate indicators of mechanical inhomogeneity of the lungs: a decrease in volumetric air flow velocities during forced expiration of the second half of the VC, a decrease in lung distensibility as breathing becomes more frequent, a change in the uniformity of ventilation, and others. Another group allows one to evaluate pulmonary gas exchange disorders: a decrease in PaO 2, an increase in alveolar arterial gradient of PO 2, capnographic violations of ventilation-perfusion relationships, etc. This is what is found in patients with moderate lung pathology (non-obstructive bronchitis, smoker's bronchitis) and are combined with an increase in pulmonary arterial pressure and expiratory airway closure capacity.

Atelectasis. The main reasons for their appearance are two: bronchial obstruction and violation synthesis of surfactants. With obstruction of the bronchi in non-aerated alveoli, their collapse develops in connection with the entry of gases into the bloodstream. Pressure reduction promotes fluid flow into the alveoli. The result of such changes is a mechanical compression of the blood vessels and a decrease in blood flow through these sections of the lungs. In addition, hypoxia developing here, for its part, leads to the development of vasoconstriction. The result of the redistribution of blood between the intact lung and the affected atelectatic processes will be an improvement in the gas transport function of the blood.

Atelectasis is also enhanced due to a decrease in the formation of surfactants, which normally interfere with the action of surface tension of the lungs.

The purpose of the surfactant covering - the inner surface of the alveoli and reduces the surface tension by 2-10 times, ensures that the alveoli are preserved from collapse. However, in some pathological conditions (not to mention newborn premature babies), the amount of surfactant decreases so much that the surface tension of the alveolar fluid is several times higher than normal, which leads to the disappearance of the alveoli - and especially the smallest. This happens not only with the so-called hyaline cartilage diseases, but also with the long stay of workers in a dusty atmosphere. The latter leads to the appearance of lung atelectasis.

4.1.16. Respiratory problems with pulmonary tuberculosis.

This pathology most often develops in the upper lobes of the lungs, where aeration and blood circulation are usually reduced. Respiratory disorders are detected in most patients with active pulmonary tuberculosis, in a significant number of patients in the inactive phase, and in many people cured of it.

The direct causes of the development of respiratory disorders in patients with active pulmonary tuberculosis are specific and nonspecific changes in the lung tissue, bronchi and pleura, as well as tuberculous intoxication. In inactive forms of tuberculosis and in cured persons, specific and mainly nonspecific changes in the lung tissue, bronchi and pleura act as the cause of respiratory disorders. Adverse effects on breathing can be exerted by hemodynamic disturbances in the small and large circles of blood circulation, as well as regulatory disorders of toxic and reflex origin.

Among the manifestations of respiratory disorders in patients, a decrease in the ventilation capacity of the lungs is most often noted, the frequency and severity of which increase as the prevalence of the tuberculous process and the degree of intoxication increase. 3 types of ventilation disorders are found to approximately the same degree: restrictive, obstructive, and mixed.

Restrictive disorders are based on a decrease in the extensibility of lung tissue due to fibrotic changes in the lungs and a decrease in the surface-active properties of pulmonary surfactants. Of great importance are also the changes in the pulmonary pleura that are characteristic of the tuberculous process.

The obstructive ventilation disorders are based on the anatomical changes in the bronchi and peribronchial lung tissue, as well as the functional component of bronchial obstruction - bronchospasm. An increase in bronchial resistance occurs in the first months of tuberculosis and progresses with increasing duration. The highest bronchial resistance is determined in patients with fibro-cavernous tuberculosis and in patients with extensive infiltrates and dissemination in the lungs.

Bronchospasm is detected in about half of patients with active pulmonary tuberculosis. The frequency of its detection and severity increase with the progression of the tuberculous process, an increase in the duration of the disease and the age of the patients. The least severity of bronchospasm is observed in patients with fresh limited pulmonary tuberculosis without decay. Greater severity is characteristic of patients with fresh destructive processes, and the most severe violations of bronchial obstruction occur with fibro-cavernous pulmonary tuberculosis.

In general, with pulmonary tuberculosis, restrictive ventilation disorders are more important than with non-specific diseases. The frequency and severity of obstructive disorders, in contrast, are slightly less. However, the dominant is a violation of bronchial obstruction. They are caused mainly by metatuberculous nonspecific changes in the bronchi, which naturally occur during a long-existing specific process. In addition, in a number of patients, pulmonary tuberculosis develops against the background of a long-term nonspecific inflammatory process, most often, chronic bronchitis, which determines the nature and severity of existing respiratory disorders.

The increase in elastic and inelastic (mainly bronchial) breathing resistance leads to an increase in the energy cost of ventilation. An increase in respiratory work was not observed only in patients with focal pulmonary tuberculosis. With an infiltrative and limited disseminated process, the work of breathing, as a rule, is increased, and with common disseminated and fibro-cavernous processes, it increases even more.

Another manifestation of tuberculosis-related lesions of the pulmonary parenchyma, bronchi and pleura is uneven ventilation. It is found in patients, both in the active and inactive phase of the disease. Uneven ventilation contributes to the mismatch between ventilation and blood flow in the lungs. Excessive ventilation of the alveoli relative to blood flow leads to an increase in the functional dead airspace, a decrease in the proportion of alveolar ventilation in the total volume of ventilation, an increase in the alveolar-arterial gradient of PO 2, which is observed in patients with limited and widespread pulmonary tuberculosis. Zones with a low ventilation / blood flow ratio are responsible for the development of arterial hypoxemia, which is the leading mechanism for reducing PaO 2 in patients.

In the predominant number of patients with hematogenously disseminated and fibro-cavernous pulmonary tuberculosis, a decrease in the diffusion capacity of the lungs is detected. Its decrease progresses with an increase in the prevalence of radiologically detected changes in the lungs and the severity of ventilation disorders in a restrictive manner. A decrease in the diffusion capacity of the lungs occurs due to a decrease in the volume of functioning lung tissue, a corresponding decrease in the gas exchange surface, and a violation of the permeability of the airborne gas barrier.

Arterial hypoxemia in such patients is detected mainly during physical exertion and much less often - at rest. Its severity varies widely; in patients with fibro-cavernous pulmonary tuberculosis, the saturation of arterial blood O 2 can decrease to 70% or less. The most pronounced hypoxemia is observed in chronic processes of a long duration, combined with obstructive bronchitis and emphysema, with the development of pronounced and progressive ventilation disorders.

Among the causes of arterial hypoxemia, ventilation-perfusion disorders play a leading role. Another reason for the possible development of hypoxemia is a violation of the diffusion conditions of O 2 in the lungs. As the third possible mechanism of arterial hypoxemia, there may be intrapulmonary artery bypass grafting of the small and large circles of blood circulation.

In order for the human lungs to function normally, several important conditions must be observed. Firstly, the possibility of free passage of air through the bronchi to the smallest alveoli. Secondly, a sufficient number of alveoli that can support gas exchange and thirdly, the possibility of increasing the volume of the alveoli during the act of breathing.

According to the classification, it is customary to distinguish several types of lung ventilation disorders:

• Restrictive
• Obstructive
• Mixed

The restrictive type is associated with a decrease in the volume of lung tissue, which happens with the following diseases: pleurisy, pneumofibrosis, atelectasis and others. Extrapulmonary causes of impaired ventilation are also possible.

The obstructive type is associated with a violation of air conduction along the bronchi, which can happen with bronchospasm or with another structural lesion of the bronchus.

The mixed type is distinguished by a combination of violations of the two above types.

Methods for diagnosing lung ventilation disorders

To diagnose a violation of lung ventilation for one type or another, a number of studies are carried out to assess the indicators (volume and capacity) that characterize lung ventilation. Before dwelling on some studies in more detail, we consider these basic parameters.

• Tidal volume (DO) - the amount of air that enters the lungs in 1 breath with calm breathing.
• The reserve volume of inspiration (Rovd) is the amount of air that can be inhaled as much as possible after a calm inspiration.
• Exhaled reserve volume (RO) - the amount of air that can be exhaled additionally after a quiet exhalation.
• Inspiratory capacity - determines the ability of the lung tissue to stretch (the sum of DO and RVD)
• Vital lung capacity (VC) - the amount of air that can be inhaled as much as possible after deep exhalation (the sum of DO, Rovd \u200b\u200band Rovyd).

As well as a number of other indicators, volumes and capacities, on the basis of which the doctor can conclude that there is a violation of lung ventilation.

Spirometry

Spirometry is a type of study that is based on a series of respiratory tests with the participation of the patient in order to assess the degree of various pulmonary disorders.

Goals and objectives of spirometry:

• severity assessment and diagnosis of lung tissue pathology
• assessment of the dynamics of the disease
• assessment of the effectiveness of the used therapy of the disease

Procedure

During the study, the patient in a sitting position inhales and exhales air with maximum force into a special apparatus, in addition, indices of inspiration and expiration with calm breathing are recorded.

All these parameters are recorded using computer devices on a special spirogram, which the doctor decrypts.

Based on the spirogram parameters, it is possible to determine by what type - obstructive or restrictive, there was a violation of lung ventilation.

Pneumotachography

Pneumotachography is a research method in which the speed of movement and volume of air is recorded on inhalation and exhalation.

Recording and interpretation of these parameters allows you to identify diseases that are accompanied by impaired patency of the bronchi in the early stages, for example, bronchial asthma, bronchiectatic disease and others.

Procedure

The patient sits in front of a special device, to which it is connected using a mouthpiece, as with spirometry. Then the patient takes several consecutive deep breaths and exhalations several times. Sensors record these parameters and build a special curve, on the basis of which the patient reveals a violation of conduction along the bronchi. Modern pneumotachographs, in addition, are equipped with various devices with which you can register additional indicators of respiratory function.

Peak flowmetry

Peak flowmetry is a method by which it is determined at what speed a patient can exhale. This method is used to evaluate how narrow the airways are.

Procedure

The patient in a sitting position performs a quiet breath and exhale, then deeply inhales and exhales the maximum air into the mouthpiece of the peak flow meter. After a few minutes, he repeats this procedure. Then the maximum of two values \u200b\u200bis recorded.

CT of the lungs and mediastinum

Computed tomography of the lungs is a method of X-ray examination, which allows you to obtain layered sections-pictures and based on them to create a three-dimensional image of the organ.

Using this technique, you can diagnose pathological conditions such as:

• chronic pulmonary embolism
• occupational lung diseases associated with inhalation of particles of coal, silicon, asbestos and other
• identify tumor lesions of the lungs, condition lymph nodes and the presence of metastases
• identify inflammatory lung diseases (pneumonia)
• and many other pathological conditions

Bronchophonography

Bronchophonography is a method that is based on the analysis of respiratory sounds recorded during a respiratory act.

When the lumen of the bronchi or the elasticity of their walls changes, then bronchial conduction is disrupted and turbulent air movement is created. As a result of this, various noises are generated, which can be registered using special equipment. This method is often used in children's practice.

In addition to all of the above methods, to diagnose lung ventilation disorders and the causes that caused these disorders, bronchodilation and bronchoconstriction tests with various drugs, a study of blood gas composition, fibronchoscopy, lung scintigraphy and other studies are also used.

Treatment

The treatment of such pathological conditions solves several basic problems:

• Restoring and supporting vital ventilation and blood oxygenation
• Treatment of the disease that caused the development of ventilation disorders (pneumonia, a foreign body, bronchial asthma and others)

If the cause was a foreign body or a blockage of the bronchus with mucus, then these pathological conditions can simply be eliminated using fibrobronchoscopy.

However, more frequent causes of this pathology are chronic diseases of the lung tissue, for example, chronic obstructive pulmonary disease, bronchial asthma and others.

Such diseases are treated for a long time with the use of complex drug therapy.

With pronounced signs of oxygen starvation, oxygen inhalations are performed. If the patient breathes independently, then using a mask or nasal catheter. During a coma, intubation and mechanical ventilation are performed.

In addition, various activities to improve drainage function bronchi, for example antibiotic therapy, massage, physiotherapy, physiotherapy exercises in the absence of contraindications.

A terrible complication of many disorders is the development of respiratory failure of varying severity, which can lead to death.

In order to prevent the development of respiratory failure with impaired ventilation, it is necessary to try to diagnose and eliminate possible risk factors during the course of time, as well as to control the manifestations of already existing chronic lung pathology. Only timely consultation of a specialist and well-chosen treatment will help to avoid negative consequences in the future.

In contact with

The role of the upper respiratory tract and nasal breathing in the life of the body

Dissociated breathing

Terminal respiration

Periodic breathing

Dyspnea

Violations of the respiratory function, accompanied by various types of respiratory disorders.

Mechanisms of impaired external respiration (respiratory failure)

TOPIC 9 Pathophysiology of external respiration

Breath- this is a set of processes that result in oxygen consumption by body cells and their release of carbon dioxide . That is, the respiratory system ultimately performs the function of maintaining the gas exchange of cells. The respiratory system consists of the following links:

I external respiration, including:

ü ventilation of the alveoli with external air;

ü gas exchange between the alveolar air and the blood of the capillaries of the alveoli;

ü transport of gases by blood;

II. Cell respiration including:

ü exchange (by diffusion) of gases between cells and tissue capillaries;

ü oxygen consumption by cells and their emission of carbon dioxide.

The voltage of oxygen and carbon dioxide in the blood depends on the state of the function of external respiration,

The main manifestation of impaired respiratory function is the so-called respiratory failure. At the XV All-Union Congress of Therapists (1962), this state of the body was defined as such in which the normal intensity of external respiration is insufficient to ensure normal partial tension of oxygen and carbon dioxide in the blood.

Therefore, in case of respiratory failure, arterial hypoxemia and hypercapnia occur, or the gas composition of the blood is maintained due to overstrain of the external respiration apparatus.

Distinguish three types of mechanisms of disturbance of external respiration:

1. violation of ventilation of the alveoli:

2. violation of the ventilation of the alveoli and their blood supply (perfusion);

3. violation of the diffusion of gases through the alveolar-capillary membrane

Consider the listed mechanisms of disturbance of external respiration in detail.

1. Violation of alveolar ventilation may manifest itself in the form of:

Ø hypoventilationwhich may be due alveolar obstruction (obstructive type of hypoventilation) and violation of the elasticity of the lungs and musculoskeletal frame of the chest (restrictive type of alveolar hypoventilation) or (fig. 1).

ü obstructive hypoventilation type: characterized reduced airway patency. This type of pathology is based on an increase in the so-called resistive, or non-elastic, resistance to air flow, which leads to a lag in the value of alveolar ventilation from the needs of the body. Obstructive disorders have their own characteristics, depending on in which section of the respiratory tract (upper or lower) they are mainly localized.

Patency Disorders upper respiratory tract arise with their partial or complete obstruction (blockage), for example, when foreign bodies or vomit get into the trachea, retraction of the tongue, swelling of the larynx, compression by the tumor, spasm of the muscles of the larynx. In these cases, the so-called stenotic respiration ( inspiratory dyspnea), characterized by a slowdown in the inspiratory phase.

The main mechanisms of impaired patency lower respiratory tract are bronchiolo- and bronchospasm, the decline of bronchioles with the loss of elastic properties by the lungs, inflammatory edema of the wall of small bronchi, accumulation of blood in them, exudate, compression of small bronchi under the influence of increased transmural pressure (for example, during coughing). When obstructing the lower respiratory tract to exhale, additional respiratory muscles are included. As a result, the pressure in the pleural cavity becomes positive, which leads to an increase in intrapulmonary pressure and expiratory closure of the airways at the level of small bronchi, bronchioles and alveolar passages. Ultimately, there is an overflow of lungs with air. Such a pathogenetic mechanism is activated in case of bronchitis, broncho-asthmatic condition.

Obstructive type of alveolar hypoventilation may also occur with loss of light elastic properties, since the width of the lumen of small airways depends on the elasticity of the lung tissue, stretching the bronchioles. Such violations are characteristic of bronchial asthma and emphysema. In violation of patency of the lower respiratory tract observed expiratory dyspneacharacterized by rare deep breathing with lengthening of the expiratory phase;

ü restrictive type of hypoventilation: external respiration is a type of alveolar hypoventilation resulting from restrictions on lung expansion. Such violations are usually found with extensive pneumonia, pneumofibrosis, atelectasis, tumors and lung cysts. Diffuse interalveolar and peribronchial connective tissue proliferation , and decreased synthesis of surfactant accompanying these pathologies cause decreased lung capacity to stretch during inspiration . As a result, the depth of inspiration decreases, and the frequency of respiration increases due to shortening of the exhalation (the so-called short or shallow breathing);

ü dysregulation : alveolar ventilation is also reduced in violation of the nervous regulation of the respiratory muscles.

Violations of the regulation of respiration leading to alveolar hypoventilation are determined mainly respiratory disorders . These pathological abnormalities of the respiratory center may be associated with the following mechanisms:

· excitatory afferentation deficiency, which deprives the respiratory center of a certain amount of stimulating effects necessary for respiratory rhythmogenesis. A similar mechanism underlies the syndrome of neonatal asphyxia and Pickwick syndrome (pathological drowsiness, regardless of the time of day, accompanied by the development of hypoventilation;

· excess excitatory afferentationleading to frequent and shallow breathing. In this case, the alveoli are poorly ventilated by increasing the functional dead space. This occurs with thermal and pain effects (burn and pain shock), peritoneal irritation;

· excess inhibitory afferentationdepressing respiratory center. This mechanism is activated by irritation of the mucous membrane of the upper respiratory tract and leads to a reflex (trigemino-vagal reflex) respiratory arrest;

· the occurrence of chaotic afferentationleading to the disintegration of automatic and voluntary regulation of respiration. The reasons for the development of such a violation can be playing the wind instruments, singing, as well as the occurrence of powerful flows of afferent impulses of a different nature during shock, an acute period of myocardial infarction, and visceral injuries.

The rhythm and depth of breathing are affected, in particular, with disorders of the brain stem functions (centers in the medulla oblongata and the pons of Varolia), as well as limbic and other structures of the cerebral hemispheres. This happens, for example, with encephalitis, tumors, brain injuries.

The innervation of the respiratory muscles is also violated during injuries of the spinal cord or polio, tetanus, diphtheria, dystrophic damage to the nervous system (syringomyelia), as well as due to damage to the peripheral nerve trunks innervating the diaphragm and intercostal muscles.

They affect myoneural synapses, disrupt the nervous regulation of the respiratory muscles, and therefore weaken (or stop) breathing poisons such as botulinum toxin, curare, and other muscle relaxants.