PATHOPHYSIOLOGY OF EXTERNAL BREATHING
Respiratory insufficiency – the clinic-physiological concept. This such pathological state, when the tension О2 in blood arterial is reduced (arterial hypoxemia) and the tension СО2 exceeds
Many specialits consider as respiratory insufficiency also such state, when the respiratory parameters of blood are within the limits of physiological variation, but it is provided with excessive action of external breath device, which exhausts and limits reserve possibilities of an organism.
Forms of respiratory insufficiency
On clinical course is distinguished two forms of respiratory insufficiency – acute and chronic. They differ among themselves on speed of functional disturbances increase.
Acute respiratory insufficiency understand such state, when this syndrome develops fast, within minutes, of hours or day and has propersity impetuously to progress. Fast accures arterial hypoxemia, hypercapnia, develops acidosis, there are disorders of the central nervous system. All this can be completed coma and death.
Typical example of acute respiratory insufficiency is asphyxia. This state, theatening for life, when in blood don’t enter oxygen, and from blood the carbonic gas is not removed. Asphyxia occurs, as a rule, owing to sharp contraction or complete closing of respiratory ways. More often it happens for want of external compression of respiratory ways, find in them of foreign bodies, narrowing larynx (allergic edema), find in respiratory ways and alveolars of liquid (sink, aspiration of vomit mass), swelling of lung, double-side pneumothorax. Besides asphyxia can arise in case of a strong oppression of respiratory centre, disturbance of transfer of impulses ieuro-muscular synapses (on respiratory muscles), massive traumas of thorax. Duration acute asphyxia the person – 3-4 mines.
Acute respiratory insufficiency
In course of asphyxia is distinguished three periods. The first period is characterized by excitation of respiratory centre, increase of cardiac rate and increase of arterial pressure. The excitation of respiratory centre is stipulated, mainly, accumulation in an organism of carbonic gas, which acts directly and reflective. Some significance in stimulation of breath has oxygen tension in blood and irritation of aorta and sinoauriculares zones chemoreceptors. In the beginning of the first period breath has character of inspiratory dispnea when the breath prevails above an exhalation. At the end of the first period the breath is delayed, and begin to prevail powerful expiration movement (expirational dispnea). The increase of arterial pressure also is explained by delay of carbonic gas. The second period of asphyxia is characterized by predominance of the parasympathetic nervous system. The breath becomes significant less often. The cardiac rate decreases, arterial pressure is reduced. In the third period the oppression both frequencies is stoped, and depth of breath, then breath temporarity is stoped (preterminal pause), and on background of stop there are some single, more and more low respiratory movements (gasping-breath). The appearance it is explained to that after a paralysis of respiratory centre are excited of neurons caudal part of medulla oblongata. They also give some respiratory movements before the complete stop of breath.
The chronic respiratory insufficiency is characterized by slower increase of hypoxemia and hypercapnia, and they do not reach such degree, as for want of acute insufficiency due to the expense of inclusion of compensator mechanisms (erythrocytosis, increase of hemoglobin in erytrocytes).
It is known, that the external breath is provided with three processes – ventilating lung, diffusion of gases (О2 and СО2) through alveolar wall and pathogenesis of blood through capillaries lung. The disorder of any of these processes can serve as the reason of respiratory insufficiency. On pathogenesis is distinguished two forms of respiratory insufficiency – ventilation and alveolar-respiratory.
Ventilation respiratory insufficiency
The essence of ventilation insufficiency is that in a alveolars for unit time enter less air than in norm.
This state is called alveolar-hypoventilation. The reasons of alveolar hypoventilation can be or connected to the apparatus of breath, or are not connected to it (outlungs of the reason). To outlungs to the reasons the following concern.
1. Disturbance of respiratory centre function, due to by effects of medical drugs, cerebral-brain traumas with epidural or subdural hematoma malignant tumours of brain, absceses of brain, meningitis, disorder brain circulation blood.
2. Disorder of the motoneurons function of spinal cord, which innervation respiratory muscles (tumour of spinal cord, syringomyelia, poliomyelitis).
3. Disorder of the functioervous-muscular device of breath:
а) lesion of nerves – for want of avitaminosis, inflammation, trauma;
b) blockade of impulses transfer iervous – muscular synapses – myasthenia, action of myorelaxantes;
c) lesion of respiratory muscles-myositis, dystrophies, periodic paralysis, hypocaliemia, hypophosphoremia.
4. Limitation of thorax mobility, which can be caused by inherent or ecquired deformation of ribs and vertebral, ossification of costales cartilages, grown of preular parts, ascites, meteorism, obesity, pain for want of neuralgia of intercostales nerves.
5. Disorder of thorax integrity and pleural cavity (pneumothorax).
The reasons of respiratory insufficiency, which are connected to the apparatus of breath, concern disorders of air ways patency and decrease of an amount of functioning alveoles. Depending on pathogenesis is distinguished three forms of ventilation respiratory insufficiency -obstructive, restrictive and dysregulative (disorder of breath due to disorders central regulation).
Obstructive insufficiency. Obstruction of respiratory ways is narrowing their lumen and increase of resistance to movement of air. The damage can be located as in upper respiratory ways (with diameter of
Upper respiratory paths is understood cavity of mouth, nasal meatuses, pharynx, larynx, trachea, large bronchus. Obstruction it may be is caused internal and externals mechanical trauma. Internal trauma most frequently it arises as complication of trachea-intubation, less often – after operation on larynx. External mechanical trauma – fractures of lower jaw, cervical cartilages, larynx cartilages, epiglossus, trachea, damage of language basis, mouth, neck. The mechanism of obstruction is spasm, edema also paralysis of voice slot, damage or off set of larynx cartilages, hematoma, edema of mucous membrane or serrounding tissues. Variety of an internal trauma – burns and inhalating of poisoning gases. In these cases develops edema of mucous upper respiratory paths. Bleeding in respiratory ways is observed after operating interferences on head and neck, after tonsilectomy, tracheostomy. Sometimes bleeding happens spontaneous, for example from nose. The bleeding especially is dangerous when the patient is in coma or under narcosis, that is when the drainage of respiratory paths is impossible. Aspiration of foreign body is observed in children in the age from 6 months to 4 years more often. In the adult aspiration of foreign body occurs, usually, during reception of food, especially in state of alcoholic intoxication. Ather causes of ebstruction lower respiratory ways – necrotic ludvig`s angina (suprogenis necrotic flegmona of oral bottom cavity of an infectious origin), subpharynx abscess, which cause is aerobic and anaerobic microflora, аngioneurotic edema, which develops as response on allergen and is accompanied of nettle-rash, asthma, rhinitis.
To obstruction of lower respiratory ways results aspiration of the liquid environments – of vomit mass, of blood, of water, and allergy response mainly on medical preparations – antibiotics and protein substitutes. It develops immediately, during 30 mines and appears hardly expressed laryngo- and bronchospasm.
Obstructive respiratory insufficiency arises also for want of chronic unspecific diseases lung – chronic bronchitis, emphysema, bronchoectasis, bronchial astma.
Emphysema is an illness, in which rupture interalveolar septums and lungs capillaries.
Emphysema
By basis it is considered degraded collagen and elastic fibres of proteolytic enzymes, which thrown out from phagocytes under influences of the external factors – microorganisms, dust particles, tobacco smoke. In etiology of emphysema some role is allocated of hereditary predisposition, which essence consists in synthesis of defective collagen and elasthyne, insufficient synthesis of proteolytic enzymes inhibitors.
The mechanism of obstruction for want of emphysema explain so. Walls of bronchioles very thin and pliable. The lumen them is supported transpulmonaris more pressure. The more elasticity lung, the should be transpulmonaris more pressure to overcome elastic recoil. Bronchioles for want of it will be in an extended state. When the elasticity lung is reduced, it is enough for their stretch low transpulmonaris pressure. The force, which acts on walls bronchioles from within, decreases and also their lumen is narrowed. The decrease of lumen conducts to sharp increase of resistance to movement of air.
As a result of it the breath is difficulty. But even more exhalation is difficulty. For want of emphysema it becomes active. the pressure in pleurae cavity increases, and bronchioles are compressed from the outside of lungs fabric. With the cource of time bronchioles compress completely, and the exhalation becomes impossible. Air becomes isolated in alveoles, which remain is blowed up.
Emphysema
The mechanism of obstruction for want of bronchial asthma is multicomponent.
At the first place is аccumulation of viscous glasslike mucus in bronchus. It is connected with hypertrophy of mucous glands and hyperproductions by them mucus (hypercrinia). The viscous mucus is difficultly discharge and congest (mucostasis).
The important role in the mechanism of mucostasis plays hyperplasia of goblet cells, which supersede cells of ciliata epithelium. Besides, arises edema mucous, spasm of circular and longitudinal smooth bronchus muscules.
In the patients with bronchial asthma develops increased reactivity of bronchial muscles on specific and unspecific stimulus. The highest degree hyperreactivity is observed at once time or after an attack. Strong stimulus, which provokes bronchoconstriction in the patients of bronchial asthma, is the physical load.
Restrictive insufficiency. This form of respiratory insufficiency arises, when the extensibility lung is reduced, that is when they be not capable easily to be straightened. To carry out a breath, it is necessary to increase transpulmonary pressure, and it can be made at the expense of increase of respiratory muscles action. restrictive insufficiency arises in case inflammation and edema lung.
Lungs edema
Owing to arterial both venous hyperemia and swelling of interstitial tissue the alveoles is compressed from the outside and completely are not straightened. By often cause is fibrose lung, that is grow up rough fibrose connective tissue on place perished elements of parenhima, elastic fibres and capillaries.
Lungs fibrose
By fibrose are finished such illnesses, as emphysema, silicosis, anthracosis and other. To decreasing of extensibility lung may lead disturbance of surfactant system. Under surfactant is understood surface-active substances, which reduce a surface tension in an alveole. influencing on a surface tension, surfactant regulates elastic recoil of lung. as the major function it is necessary to consider prevention of alveolares collapse. It acts as the antistick factor, providing stability of alveole.
The deficiency of surfactant can arise in case of insufficient synthesis it or excessive remove from a surface of alveoles. The insufficient synthesis is characterized for illness of hyaline membranes iewborn, for want of which destroy intraalveolares septum and in alveoles is stored hyaline with epithelial cells and form elements of blood. Ecquired decrease of surfactant is observed for want of asphyxia, acidosis, pneumonia, pollution of air. The defect of surfactant predetermines high surface tension of alveoles and high resistance lung for want of expansion by their inhaled air.
Besides, by cause of restrictive insufficency may be аtelectasis ( fall of alveoles and stopping of their ventilation), рneumothorax, deformation of thorax, paralysis of respiratory muscles.
Disorder of the central regulation of breath. Under influence reflective, humoral and direct influences the respiratory centre changes the function. Those disorders of breath regulation, which limit alveolar ventilation, can serve as the reason of respiratory insufficiency. It is distinguished the following forms of breath disturbances central genesis.
Bradypnea – rare breath. It can arise reflectative in case of increase of arterial pressure (reflex from baroreceptors of aorta and carotide bodies), and also for want of hyperoxia (reflex from hemoreceptors of the same zones). The deep and rare breath arises for want of narrowing of upper respiratory ways. It is named stenotic. The reason bradypnea happens a direct lesion of neurons of respiratory centre for want of long hypoxia, under influence of narcotic substances, for want of organic changes in a brain (inflammation, insult) or functional disorders of the central nervous system (neurosis, hysteria).
Polypnea (tachypnea) – friquent surface breath. It arises reflectative for want of to fever, hysteria, pain in area of thorax, peritoneum, pleura.
Hyperpnea – deep and friquent breath. It has compensator character, however excessive stimulation of respiratory centre in pathological conditions (decrease of partial pressure О2, anemia, acidosis) provokes rather intensive breath, which can lead to washout СО2 from organism and paralysis of respiratory centre. For want of diabetic mellitus there is a so-called noisy breath (Kussmaul’s breath), due to metabolic acidosis.
Apnea – temporary stopping of breath. This manifestation of inhibition neurons of respiratory centre under influence hypoxia or intoxication, for want of organic lesion of brain. Apnea occurs affer hyperventilation, when tension of СО2 in blood is dropped lower threshold for respiratory centre of level, and also during fast rise of arterial pressure (reflex from baroreceptors of vessels).
Periodic breath. This such disorder of respiratory rhythm, when the periods of respiratory movements alternate with periods of apnea. There are two main types of periodic breath – Chein-Stoks and Bioth. In the first case the amplitude of respiratory movements cyclic is increased up to expressed hyperpnoe and decreases to apnea. For want of breath Bioth amplitude of respiratory movements is constant. The appearance of periodic breath is sign of respiratory centre hypoxia (insufficiency of heart, uremia, meningitis, encephalitis).
Dyspnea. This sensation of air shortage and simultaneously necessity to strengthen breath. The person consciously tries to be saved of unpleasant sensations. In a unconscious state dyspnea it does not happen. In conditions of pathology dyspnea can cause the following factors: а) insufficient oxygenation of blood in lung (low partial pressure of oxygen in inhaled air, difficulty of ventilation lung, disorder of lungs hemodynamics); b) disorder of gases transport by blood (insufficiency of blood flow, anemia, inactivation of hemoglobin); c) metabolic acidosis (diabetis mellitus); d) functional and organic lesion of brain (hysteria, encephalitis, insult). In creation of dyspnea the large role belongs to reflexes from respiratory ways, parenhima of lung, aorta and carotide bodies.
The breath for want of dyspnea as a rule is friquent and deep, and exhalation becomes active. Depending on with what components of breath – inhalation or the exhalation – prevails is distinguished inspiratory and expiratory dyspnea. The first type of dyspnea is observed for want of asphyxia, second – for want of bronchial asthma and emphysema.
Alveolar-respiratory insufficiency
This type of respiratory insufficiency arises in that case, when is reduced gas exchange between alveolar air and blood. Two variants of such insufficiency are possible:
1) due to inadequacy of ventilation and perfusion of lung;
2) owing to difficulty diffusion of gases through alveolar wall.
Disturbances of correlation“ventilation / perfusion”. That the gas structure of blood was supported, the important significance has not only absolute value of alveolar ventilation, but also normal ratio between alveolar ventilation and perfusion of lung. The amount of blood, which proceeds through lung for 1 mines, is equalled 4.5-
That volume of inhaled air, which is distributed in alveoles, where blood flow is absent or sharply is reduced, does not take part in gas exchange between alveolar air and blood of lung capillaries and does not support gas composition of blood.
The optimum ratio of alveolar ventilation and perfusion of lung makes 4:5. It can be changed to side of increase or to side of decrease. the increase of correlation ventilation / perfusion is characterized for effect of dead space. The predominance perfusion above ventilation is characterized for effect of vein-arterial shunt. In both cases normal gas composition of blood to supply impossible. If the ventilation prevails the tension of oxygen in blood flowing from alveoles will be sufficient, but from blood too much carbonic acid will be remove. As the consequence arises hypocapnia. If the ventilation lags from perfusion arises hypoxemia and hypercapnia.
In clinic frequently there are cases, when decreases perfusion of lung. It is being in case disturbance of the right heart contraction (infarct of myocardium, cardiosclerosis, myocarditis, exudative pericarditis), heart insufficiency and vessels (stenosis of lung artery, stenosis of right atrio-ventricular ostium, shock), thrombembolism of lung artery.
disturbances of diffusion have not the so important significance in pathogenesis of respiratory insufficiency, as disorders of ventilation and perfusion. Nevertheless sometimes diffusion the ability of alveoles becomes the defining factor. Diffusion ability of lung decreases for want of alveolar surface decrease (resection of lung, cavity, abscess, atelectasis, emphysema) or thickening of a alveolar-capillary membrane (fibrosis, sarcoidosis, pneumoconiosis, sclerodermya, pneumonia, emphysema, has swelled lung).
Disorder of gases transition through alveolar membrane name as a syndrome of alveolar-capillary blockade. The main clinical symptom it is hypoxemia.
Hypoxia
During evolutionary development the alive organisms have acquired an effective method of energy obtaining – biological oxidation. It is possible only under condition of continuous tissues maintenance by oxygen.
The main stocks in an organism are in significant – 0.025-0.030 l/kg of body weight, that is approximately 2l for the person of
Hypoxia is typical pathological process, which arises owing to insufficient oxygen supply of tissues or insufficient use it by tissues. Hypoxia underlies many diseases or accompanies with them. Four main hypoxia types are distinguished – hypoxic, hemic, circulational and histotoxic.
Characteristics of different kinds of hypoxia
|
Hypoxia |
Norm |
Hemic |
Circulatory |
Tissual
|
Hypoxic |
|
|
oxygen capacity of blood |
20 |
10 |
20 |
20 |
20 |
|
|
arterial blood |
quantity О2 |
19 |
9,5 |
19 |
19 |
14,8 |
|
saturation О2 |
95 |
95 |
95 |
95 |
74 |
|
|
pО2 mmHg |
100 |
100 |
100 |
100 |
45 |
|
|
venous blood |
quantity О2 |
14,8 |
5,3 |
10,6 |
18 |
10,6 |
|
saturation О2 |
74 |
53 |
53 |
90 |
53 |
|
|
pО2 mmHg |
41 |
28 |
28 |
80 |
21 |
|
|
arterial – venous difference of О2 |
4,2 |
4,2 |
8,4 |
1,0 |
4,2 |
|
Hypoxic hypoxia
The essence of this hypoxia kind is oxygen tension reducion in arterial blood, the hemoglobin saturation by oxygen decreases and as a result the contents of oxygen decreases. Thus hypoxemia develops.
Some reasons to cause tension reduction of oxygen in blood, which is flowing from lung are known. First of all, it is necessary to mention the partial oxygen pressure decrease in inhaled air. The person meets this factor ascent on the mountain (climbers, contributors). On a sea level the partial oxygen pressure is equalled to
As a rule, action of low partial oxygen pressure in a human organism is short-term. The chronic influence is tested by the inhabitants of mountain areas. 92 % the population of earth has put up at low districts (up to
The decrease of partial oxygen pressure in the air in low districts is possible when it is replacement by other gases. For example, the oxygen can be replaced with methan in mines, carbonic gas- in shafts, argon -on some productions.
The second hypoxical hypoxia variety is connected to respiratory insufficiency, with main processes disorder, which provide external breath, – ventilation, diffusion and perfusion. Respiratory hypoxia results the gas metabolism disorder of the lung function for normal partial oxygen pressure in atmospheric air. In practice any external breath disorders can cause a respiratory hypoxia.
On the Earth alveolar hypoventilation arises in such cases:
а) an oppression of respiratory centre – overdose of drugs, brain swelling, brain insult;
b) patency of respiratory ways disorder – dyphteria, laryngospasm, larynx swelling, getting into tracheal foreign body;
c) thorax damage;
d) respiratory muscles and intercostals of nerves disease.
Oxygen diffusion disorder through alveolar wall happens in case of respiratory lung surface decrease (athelectasis, pneumothorax, hydrothorax), thickening and change of alveolar wall histological structure (fibrosis, swelling, pneumoconiosis, pneumonia).
Some role in development of respiratory type hypoxic hypoxia belongs to lung perfusion disorders, and one more point – disorders of perfusional ventilational ratio. Hypoxia arises in case of limited lung perfusion or development so-called intralungs the shunt.
In case of perfusion decrease, pulmonic blood capillaries gets arterialised almost completely ( 95 %), but total arterial blood volume, which departs from pulmonic and gets into general blood circulation, is less of norm. Therefore general blood arterialisation is lower than 95 %.
Pulmonary shunt develops in case of indurations appearance lung tissue with partial bronchioles obturation, for example due to pneumonia will be derivated. The ventilation of these inflamations is limited, and perfusia is rather intensive due to hyperemia. Blood, which flows through capillaries at weakly ventilationed areas of the inflammatory lung sites, is not arterialised. Mixing up with oxygenated enough blood from good ventilated alveole, it reduces a general oxygenation degree of arterial blood, which flows out of lung.
Arterial and venous blood mixing takes place in fact of some defects cardio-vascular system, for example, with nonclosure Botall’s flowing. General oxygenation of arterial blood is also lower.
Hemic hypoxia
Basis of this hypoxia type is decrease of blood oxygen capacity. Two variants: anemic and toxic are possible.
In case of anemic form, the total circulating hemoglobin level – owing to blood loss, erythrocytes hemolysis in blood, channel or bone brain bloodmaking function oppression decreases.
Toxic form arises in case of hemic toxines poisoning. The general content of hemoglobin in blood remains normal, but the contents of functionally active hemoglobin decreases. The part of hemoglobin turns into such compounds, which are not capable to execute oxygen transport function.
More often hemoglobin gets linked with charcoal gas (carbon oxide, CO). This compound is named carboxihemoglobin. It’s in 300 times more stable than oxyhemoglobin, therefore hypoxia arises even with insignificant CO concentration in the air. Hemoglobin gets switched out off the transport function, oxygen capacity in blood decreases, hypoxia occurs.
Another one form toxic hemical hypoxia is known, which arises ground methhemoglobinemia origin. Methhemoglobinemia are divided in two groups origin – hereditary (primary) and acquired (secondary). Hereditary methhemoglobinemia are stipulated atypic hemoglobin synthesis, derivation of endogenic products, which turn hemoglobin to methhemoglobin; enzymes systems deficiency, which restore methemoglobin into hemoglobin. Among exogenic methemoglobin makers the majors are following: nitrogen compounds (oxides, nitrites), aminocompounds (hydroxilamine, aniline, phenylhydrasine, paraaminobensous acid), oxidizers (chlorates, permanganates, hynones, pyridin, naphtaline), oxy–restoring paint (methylene blue, kresilblau), medications (novocaine, pylocarpine, phenacetine, barbyturates, aspirin, resorcin and others).
Iormally the contents of methhemoglobin in blood makes 0,3-3 g/l. Hemoglobin oxydisers can lift it’s level to extremely high digits. If methhemoglobin concentration reaches up to 75 %, the death occurs.
Methhemoglobinemia is the purest form of hemic hypoxia. It’s mechanism is incorporated in erythrocyte itself in heme. It is known, that hemoglobin connects oxygen in labile way not changing the valency of iron atom, which is in two-valent peroxyde form. In action of just mentioned oxidizers there is an orbital electron offset, and the heme iron gets transformed from two-valent into three-valent. Hemoglobin, turning into methhemoglobin (ferrohemoglobin), loses it’s active centre, and oxygen transport function at the same time. Oxygen capacity of blood decreases.
Iatural conditions in the person has got a methhemoglobin continuous derivation. This physiological methhemoglobinemia is stipulated by effect of molecular oxygen upon hemoglobin. In a parallel to methhemoglobin derivation there is a constant demethhemoglobinisation, that is opposite methhemoglobin transformation into hemoglobin. This process is carried out by erythrocytes reductase system and unoxydated products – lactate, pyruvate and others. Thus the dynamic equilibrium between the both hemoglobin and methhemoglobin contents, is supported, to hypoxia does not arise.
In conditions of intoxication methhemoglobinmakers can oxidized hemoglobin directly or undirectly. The second mechanism is reduced to enzymes systems damage, which catalyses restoring of methhemoglobin back into hemoglobin.
Showing of methhemoglobinemia depends on individual resistance of an organism – on general metabolism intensity on antioxydase and reductase systems activity erythrocytes age and hemoglobin type. The oxidation speed, for example, Нb F is higher than Нb А.
Circulatory hypoxia
This is such hypoxia kind, which is stipulated by of circulation blood speed decrease, that is oxygen delivery to tissues slowing down. It arises owing to general blood flow slowing down in case of cardio-vascular insufficiency, or owing to local blood supply disorders. Pure circulatory hypoxia does not happen really exist. It is observed only as a local phenomenon in fact of separate organs ischemia. If blood circulation disorders seize the large or small circle, other circulatory hypoxia forms are connected for sure.
In case of pure circulational hypoxia the main respiratory parameters in blood are not changed. Oxygen capacity in blood is normal the tension of oxygen in arterial blood is normal, hemoglobin oxygenation is normal too. Hypoxia arises because of volume decreases of oxygen, which is transported to tissues per one a time unit. In case of blood slow passing through tissues the last utilise more oxygen thaormally, therefore most indicative change on the part of respiratory blood parameters is arterial-venous difference increase by oxygen. This parameter testifies the blood flow speed decrease and reflects the essence of mentioner hypoxia type.
Not only absolute but relative blood circulation insufficiency can also cause circulational hypoxia. Relative insufficiency is such a state, when the oxygen consumption exceeds it’s greatest possible delivery to tissues. As an example one can give an myocardium. In sympathetic hyperactivity, conditions adrenaline stimulates myocardium operation adrenoreceptors cardiomyocytic and increases it’s oxygen consumption. At the same time adrenaline dilatates the coronary vessels acting β-adrenoreceptors. Although, even the maximal most possible coronary blood flow increase, is still lag behind the increased necessity in oxygen. Hypoxia arises, which is also circulatory.
Histotoxic hypoxia
In this hypoxia kind basis is the tissues inability of oxygen utilisating, therefore it’s main parameter is the low arterioal-venous difference. Neither, the contents of oxygen in blood, nor it’s delivery to tissues are not broken, but tissue use it less for one time unit, than it is necessary for maintenance their energy needs. The reason of this phenomenon is the decrease of respiratory enzymes activity.
Three enzymes systems participate in electron transport from substrat to molecular oxygen – pyridindependent dehydrogenases, flavindependent dehydrogenases, cytochromes. Any of these systems blockade will result in disorder of electron transport throughout on a respiratory chain and will cause histotoxic hypoxia. Respiratory chain enzymes are oppressed with cyanides, monoiodacetatis, drugs, spirit, formaldehyde, aceton, ethylurethane, sulfurhydrogen, cocain, carbon oxyde and other substances. Typical example of hystotoxical hypoxia – cyanic poisoning, which oppresses cytochromoxydase. The cytochromes oxidazing – restoring processes get blocked with local anestetics (novocaine). Flavine enzymes lose their activity in case of riboflavine (vit. B2) deficiency. Pyridine enzymes activity is slowing down with nicotine acid deficiency.
These four hypoxia kinds can be isolated seldom. The combination of two or more hypoxia kinds is more often observed in practice. Such combinations are mixed hypoxias.
Metabolism in state of hypoxia
In a basis of hypoxia damaging effect upon the organism stays the АТP decrease in cells lays. The contents other macroergic compound – creatinephosphate decreases in a brain and heart very fast. The АТP stocks in cells are practically absent. The АТP synthesis in biological oxidation process during hypoxia lays behind АТP disintegration by the time of a cell live. The decrease of macroergic compounds in cells results in disorder of all metabolism forms, ultra structural and functional cell damage. Major changes of carbohydrate metabolism are the following: anaerobic glycolysis increase, glycogen stocks exhausting, accumulation of pyruvic and lactic acids, metabolic acidosis.
The protein metabolism disorders manifest in such changes: the synthesis oppression and simultaneously acceleration of fibers disintegration, increase of residual blood nitrogen contents, ammonia accumulation.
The fatty metabolism in case of hypoxia is characterized by such features: intensive fat disintegration in depot, accumulation of fatty acids in tissues, ketoacids accumulation in blood.
Cerebral and heart activity disorder in state of hypoxia
Nervous system is the most sensitive to oxygen starvation. Such digits testify to it. The average intensity of oxygen consumption by an organism at all makes 0,38 ml/mines per
Brain cortex neurons can work perfectly in conditions of complete blood flow termination only for 5-6 minutes. Oblongatal braieurons maintain the complete blood supply termination for 20-30 minutes, spinal cord neurons – up to 60 minutes. Heavy and long hypoxia causes a defect of blood supply and breath centres, reflex activity disorder. Cramps, the unconsciousness appears. The speed of oxygen consumption by a brain begins to decelerate, while the oxygen partial pressure in air falls below
The myocard is very sensitive to oxygen starvation.It takes on the second place after the nervous system. Increasing heavy hypoxia oppresses contract and rhythmic heart activity. In a basis of these disorders the suppression of biological oxidation and energy deficiency lays.
Compensatory responses in state of hypoxia
The compensatory responses of an organism, which are directed to hypoxia removal are divided into four groups – respiratory, hemodynamic, bloodly and tissuel.
The respiratory responses appear as dyspnea, with acceleration and deepening of breathing. It is named altitude, or hypoxic, or compensatory. Dispnea arises in reply to an hemoreceptors aortae arc and sinocarotide zones irritation with hypoxic blood. Due to dyspnea pulmonary ventilation is increased. The compensatory significance of lung hyperventilation is not absolute, because after excessive and long hyperventilation occurs hypocapnia. It has aegatively effect upon breath regulation, as carbonic acid intensively washout from blood physiological irritation of respiratory centre. Sudden unconsciousness during the height rise can be explained just by respiratory centre paralysis.
The hemodynamic compensator responses include:
а) tachycardia – result of sympathetic tonus increase;
b) stock blood volume increase at the expense of adrenaline action upon myocardium adrenoreceptors;
c) cardiac output increase as a result of tachycardia and stock volume increase;
d) the blood flow acceleration – it is connected in main to cardiac output increase;
e) blood circulation centralization that is peripheral vessels narrowing and vessels of the vital organy extension owing to there is redistribution of blood to brain, heart, lung in fact of simultaneous blood supply limitation of skin, muscles, intestines, spleen.
The group of bloodly compensatory responses includes such a responses as:
а) erythrocytosis – first of all in responce of an blood output from depot, and later by blood form stimulation;
b) the increase of hemoglobin charge in erythrocytes;
c) hemoglobin to oxygen similarity increase in lung (shift of oxyhemoglobin dissociation curve to the left) and decrease it this similarity in tissues (shift of oxyhemoglobin dissociation curve to the right).
Tissuel compensatory responses are the decrease of metabolism, activation of glycolysis, activation of respiratory chain enzymes.
Adaptation to hypoxia
Hypoxia – is not only a damaging, but is also a training factor. During hypoxia training period emergency adaptation is formed first. In case of long hypoxia perfomanse a certain mode the emergency adaptation turns into long-term adaptation. Adapted organisms have got energetic and plastic resources are spent very economically.
In case of the hypoxia training termination the state of desadaptation occurs. The positive properties, of adapted organism bought during trainings, are getting gradually lost.It is important not to infringe a mode of trainings at all stages of adaptive process. The mode disorder is dangerous. Dangerous life disorders arise in such cases, which increase sensitivity to hypoxia. Adaptation, desadaptation, failure adaptation problem is very important. It has practical significance in people selection and preparation for certain professional mastering by the (divers, spaceman) and for examination the territories with extremal life conditions (space, ocean, mountain).
