One of the most urgent problems in obstetrics and neonatology is fetal hypoxia during pregnancy. According to some data, its frequency among the total number of births ranges between 4 and 6%, according to others, it reaches 10.5%.

Pathology associated with hypoxia, that is, with a lack of oxygen, is dangerous not only in the prenatal period, but also leads to serious consequences in children in the future. In 63% of the associated pathological changes in the body develop in the prenatal period, on average in 21% - in the intranatal period and in 5-6% - already in the neonatal period. How to determine fetal hypoxia and can it be avoided?

What is dangerous pathology?

This pathological condition, which often complicates pregnancy and childbirth, is the most common cause of fetal mortality and morbidity in infancy.

Oxygen deficiency in different periods of pregnancy and childbirth is characterized by the development of various pathologies and various consequences. So, for example, during the period of organ laying, it is possible to slow down the development of the embryo and form developmental anomalies, during the period of tissue differentiation of organs - to a delay in further development, to pathology of development or to damage to the central nervous system (in 60-80%), to a violation of the adaptive mechanisms of the fetus and newborns, an increase in the incidence of the latter.

Severe intrauterine fetal hypoxia can also be the cause of stillbirth or death of newborns in the early postpartum period (in 23%), disorders or delays in newborns of intellectual and/or psychomotor development. In addition, they have lesions of the heart and blood vessels (in 78%), central nervous (in 98% or more) and urinary (in 70%) systems, and severe eye diseases.

What is fetal hypoxia?

The term "fetal hypoxia" is used to refer to a complex of changes in its body resulting from insufficient oxygen supply to its organs and tissues or inadequate absorption (utilization) of oxygen by them.

This is not an independent disease or a primary nosological form, but a condition that is the result of pathological processes of a different nature in the “mother-placenta-fetus” system and complicating the intrauterine development of the latter.

Even in the case of an uncomplicated, physiological pregnancy, the supply of oxygen to the fetus is significantly lower compared to adults. But compensatory-adaptive mechanisms (an increase in heart rate, a large minute volume of blood, a significant oxygen capacity of blood, etc.) at any stage of development ensure its resistance to this deficiency, bringing oxygen supply to full compliance with the needs for it.

The disorder of compensatory mechanisms leads to a hypoxic state, which, depending on the duration, is divided into:

1. Chronic, developing as a result of oxygen deficiency for a long time with a complicated course of pregnancy. Chronic intrauterine fetal hypoxia is associated mainly with morphological and functional changes in the placenta, which occur, as a rule, as a result of a violation of its blood supply due to inflammatory, degenerative and other types of lesions.
2. Subacute, which is characterized by a decrease in the degree of adaptive ability of the fetus and develops 1-2 days before the onset of labor.
3. Acute, occurring already during childbirth. Acute fetal hypoxia very rarely develops during pregnancy. An unfavorable factor in terms of prognosis is its often observed development against the background of already existing chronic hypoxia.

Causes and forms of hypoxia

The idea of ​​numerous causes and mechanisms of development makes it possible to understand how to avoid fetal hypoxia during pregnancy. All causative factors are conditionally combined into three groups:

• diseases and disorders in the body of a pregnant woman, leading to oxygen deficiency - pathology in the cardiovascular and pulmonary systems, compression syndrome of the inferior vena cava, poisoning or intoxication of the body, anemia, blood loss or shock of various causes, complications during pregnancy or childbirth, accompanied by excess in the body of a woman carbon dioxide or oxygen deficiency;
• disorders in the fetal-placental system that develop during post-term pregnancy, abnormal placental location or thrombosis of placental vessels, false node of the umbilical cord or thrombosis of the latter, fetal hypoxia during childbirth as a result of premature detachment of the normal located placenta, abnormalities of labor, entanglement of the umbilical cord, tension or prolapse last;
• pathology in the fetus - infection, the presence of congenital malformations, hemolytic disease, anemia, prolonged compression of the head during childbirth.

Forms of hypoxia in accordance with the mechanisms of its development

Arterial-hypoxemic

Which include:

• hypoxic, resulting from impaired oxygen supply to the uteroplacental circulation;
• transplacental - the result of circulatory disorders in the placenta or in the fetal-placental system and disorders of the gas exchange function of the placenta.

Hemic

Associated with anemia due to blood loss or hemolytic syndrome, as well as a decrease in the degree of affinity for oxygen of fetal hemoglobin.

Ischemic

Developing due to:

• low cardiac output with cardiac and vascular anomalies, insufficient contractility of the heart muscle or severe cardiac arrhythmias;
• increased resistance in the vessels (mechanical compression, thrombosis of the uterine arteries, etc.), including due to a violation of the properties of the blood.

mixed

Representing a combination of two or more mechanisms of oxygen deficiency.

In practice, arterial-hypoxemic and mixed forms are most common.

Oxygen deficiency is the main factor in the mechanism of development of metabolic disorders, the functioning of organs and, as a result, the development of a terminal state. A decrease in the degree of oxygen saturation of the blood leads to a violation of its respiratory function and the development of an acidic environment. Changed conditions are the cause of the violation of many parameters of constancy and self-regulation of the internal environment of the body.

Initially, the universal compensatory reaction is aimed at protecting vital systems and organs and preserving their function. This happens by stimulating the hormonal function of the adrenal glands and increasing the release of catecholamines by them, as a result of which the fetal heart rate during hypoxia initially quickens. In addition, the centralization of blood circulation (redistribution of blood) develops due to vasospasm in certain organs that are not vital (lungs, intestines, spleen, kidneys, skin).

All this helps to improve blood circulation in vital organs (heart, brain, adrenal glands, placenta) and, accordingly, to increase oxygen delivery to them by reducing its delivery to “less important” organs and tissues, which leads to the development of metabolic acidosis (acid environment) in the latter.

Significant and prolonged hypoxia causes depletion of compensatory mechanisms, inhibition of the function of the adrenal cortex, a decrease in the content of catecholamines and cortisol in the blood. This causes a deterioration in endocrine regulation by the function of vital centers, a decrease in the frequency of heart contractions and a decrease in blood pressure, a slowdown in blood flow, stagnation of blood in the veins and its accumulation in the portal vein system.

Such disorders are accompanied by a change in blood viscosity and its flowing properties, microcirculation disorders, gas exchange disorders in them, a decrease in pH, an increase in the permeability of the walls of small vessels, swelling of tissues, etc.

Pronounced changes in macrodynamics and microdynamics, accompanied by metabolic disorders, cause tissue ischemia and even necrosis, primarily in the brain, as well as small, sometimes massive hemorrhages in it and in other organs, dysfunction of the respiratory and cardiovascular centers of the brain and etc.

Consequences of hypoxia in a child after birth

The severity and duration of these effects depend on the degree and duration of hypoxia. Depending on its intensity, there are:

• mild degree, or functional hypoxia - there are only hemodynamic disorders;
• deep, which is accompanied by a reversible violation of all types of metabolism;
• severe, or destructive, in which irreversible damage develops at the cellular level.

Clinical picture and diagnosis

Clinical signs and subjective symptoms of fetal hypoxia during pregnancy are very poor and difficult to recognize. This requires listening to the heartbeats by a gynecologist using a stethoscope.

As a result of auscultation of heartbeats, the assumption of the presence of a pathological condition may arise when there is a deviation from the norm (increase or, conversely, decrease) in the number of heartbeats. In these cases, it is necessary to conduct additional (instrumental-diagnostic) studies.

Is it possible to determine fetal hypoxia for a pregnant woman on her own?

A general idea of ​​the mechanisms of this condition helps a woman to understand that the lack of oxygen intake or utilization by the fetus necessarily leads to a change in the nature of its motor activity. You can recognize this with a correct assessment of your sensations during fetal movements.

How does the fetus behave during hypoxia?

At the initial stages of the pathological condition, a pregnant woman notes an increase in the frequency and intensity of movements. In the case of a long-term lack of oxygen or its progression, the degree of motor activity decreases up to the complete cessation of movement.

A decrease in the number of movements to 3 or less within one hour is a clear sign of hypoxic suffering and is a direct indication for the immediate conduct of additional studies to decide on the choice of further tactics for managing pregnancy.

Instrumental and diagnostic signs of fetal hypoxia in the later stages, sometimes even earlier, are detected through such indirect methods as echography, cardiotocography, blood flow in the vessels of the uterine-placental-fetal system, determination of the fetal biophysical profile, oxygen and carbon dioxide pressure, acid-base state and lactic acid content in the woman's blood, biochemical examination of amniotic fluid, the level of certain hormones, etc.

The most accurate and informative methods in late pregnancy (in the third trimester) are cardiotocography, ultrasound scanning and dopplerometry.

The initial signs of oxygen "starvation" during cardiotocography are:

• an increase in heart rate to 170 beats per minute or a decrease to 100 beats;
• a decrease in the degree of heart rate variability (rhythm variability), which is normally 5-25 beats per minute (indicates the normal regulation of heart function by the sympathetic and parasympathetic systems);
• short-term monotonous nature of the heart rate, constituting no more than 50% of the record;
• reduced response to functional tests;
• a cardiotocogram score of 5 to 7 points.

With a pronounced oxygen deficiency, the following are observed:

• significant (more than 170 beats per minute) tachycardia or bradycardia, less than 100 beats per minute;
• pronounced decrease in rhythm variability;
• the monotony of the heart rate, which is more than 50% of the record;
• a paradoxical response to functional tests and a late (after 10-30 seconds) reaction in the form of a decrease in the fetal heart rate in response to its movement (during a non-stress test);
• the cardiotocogram score is 4 points or less.

In the diagnosis of great importance is the Doppler study of blood circulation in the vessels of the brain and the fetal aorta. This technique at an earlier date, compared with cardiotocography, reveals intrauterine hypoxia in pregnant women and allows them to recommend constant careful monitoring and treatment.

Hypoxia during childbirth is also manifested by disorders of the heart. The most accessible diagnostic methods during this period are auscultation and cardiotocography.

Diagnostic symptoms in the first stage of labor include:

1. The initial signs (regardless of presentation) are bradycardia, which is about 100 beats per minute, an intermittent monotonous heart rhythm, a response to contractions, which is expressed in a late decrease in heart rate to 70 beats.
2. Pronounced signs are bradycardia, reaching 80 beats per minute with cephalic presentation or tachycardia (up to 200 beats) with breech presentation, persistent arrhythmia and monotony of the heart rhythm independent of presentation. In addition, responses to contractions, expressed in long-term late decreases in the frequency of the rhythm in the form of W-shaped complexes in the case of head presentation and a combination of its increase with a decrease (up to 80 beats per minute) - in breech presentation.

In the second stage of labor:

1. Initial signs - bradycardia up to 90 beats or an increase in the frequency of contractions (tachycardia) up to 200 beats per minute, intermittent monotonous heart rate, after attempts - a late decrease in heart rate to 60 beats per minute.
2. Pronounced signs are bradycardia up to 80 or tachycardia over 190 beats per minute, persistent monotonous rhythm, rhythm disturbance, late and prolonged slowing of the rhythm (up to 50 beats) with cephalic or pelvic presentation, with W-shaped complexes.

In addition, the presence of meconium in the amniotic fluid also speaks in favor of a threatening situation (but only with head presentation). It may be in the form of separate suspended fragments (with initial signs) or a dirty emulsion (in severe cases). However, its presence can be the result not only of acute hypoxia, but also of long-term or short-term oxygen deficiency that occurred before the onset of labor. Birth is possible without asphyxia if hypoxic episodes are not repeated.

An unfavorable sign during the first and second stages of labor, in contrast to the prenatal period, is the occurrence of a pronounced regular motor and/or respiratory activity of the fetus, which leads to severe aspiration syndrome.

Treatment and prevention of fetal hypoxia

The treatment program consists of correcting the therapy of concomitant pathology (if any), normalizing blood circulation in the placenta, improving the delivery of oxygen and energy components to the fetus, measures that increase its adaptive capabilities and the course of metabolic processes, as well as increase resistance to oxygen deficiency.

Direct treatment of fetal hypoxia is carried out using methods and drugs that contribute to:

1. Relaxation of the myometrium.
2. Expansion of the uteroplacental vessels.
3. Improving the rheological characteristics of blood.
4. Stimulation of metabolism in the myometrium and placenta.

For these purposes, bed rest is prescribed, a woman's breathing with a mixture of oxygen and air for 1 hour up to two times a day, taking a protein-oxygen cocktail, hyperbaric oxygenation - if the pregnant woman has cardiovascular insufficiency.

Of the drugs used are Sigetin, Efillin, Curantil, Trental, anticoagulants (Heparin), Methionine, folic acid, high doses of vitamin "B 12", Cocarboxylase, Lipostabil, Haloscorbin, antioxidants (vitamins "E" and "C", glutamic acid) .

In acute hypoxia, chronic hypoxia at a period of 28-32 weeks in the absence of the necessary result from the treatment, deterioration of the biophysical profile and cardiotocogram, the presence of oligohydramnios, the appearance of meconium in the amniotic fluid, emergency delivery is indicated regardless of the gestational age.

During the labor period, as a preparation for surgical () or obstetric (perineo- or episiotomy, the imposition of obstetric forceps, vacuum extraction, extraction by the pelvic end) the resolution of childbirth is used breathing with humidified oxygen, intravenous administration of glucose, Eufillin, Cocarboxylase and ascorbic acid, Sigetin.

Prevention consists in early prenatal diagnosis, treatment of concomitant diseases (cardiovascular and pulmonary pathology, diabetes mellitus, etc.), identification, thorough examination, as well as timely hospitalization and treatment of women at risk.

Oxygen starvation, or hypoxia, is a pathological process associated with insufficient oxygen supply to cells due to its lack in the surrounding atmosphere, disorders of the blood or the cells themselves. Hypoxia can manifest itself in both acute and chronic forms, but always requires immediate recognition and therapy due to possible irreversible consequences for the body.

Hypoxia is not a separate disease or syndrome. This is a general pathological process that underlies a variety of diseases and is caused by an extraordinary variety of reasons, ranging from the composition of the surrounding air to the pathology of certain types of cells in the human body.

Although oxygen starvation has certain symptoms, it is a non-specific process that can play a key role in the pathogenesis of many diseases. Hypoxia occurs in adults, newborn babies, fetuses growing in utero and has rather stereotypical structural manifestations that differ only in severity.

In the initial phase of oxygen deficiency, compensatory-adaptive mechanisms are activated, implemented mainly by the cardiovascular system, respiratory organs, and intracellular biochemical reactions. As long as these mechanisms work, the body does not feel a lack of oxygenation. As they are depleted, a decompensation phase begins with a developed picture of tissue hypoxia and its complications.

Clinically compensated acute oxygen starvation is achieved by an increase in heart rate and respiration, an increase in pressure and cardiac output, the release of reserve erythrocytes from depot organs, if necessary, the body "centralizes" blood circulation, directing blood to the most vulnerable and hypoxia-sensitive tissues - the brain and myocardium. The remaining organs for some time are able to tolerate the lack of oxygen relatively painlessly.

If the gas balance of the blood is restored before the defense mechanisms are exhausted, the victim of hypoxia can count on a full recovery. Otherwise, irreversible intracellular structural changes will begin, and the consequences will most likely not be avoided.

At chronic oxygen deficiency the defense mechanism is somewhat different: the number of constantly circulating red blood cells increases, the proportion of hemoglobin and enzymes in them increases, the alveolar and vascular networks of the lungs expand, breathing becomes deeper, the myocardium thickens, maintaining sufficient cardiac output. Tissues "acquire" a more extensive microcirculatory network, and cells - additional mitochondria. With the decompensation of these mechanisms, active production of collagen by connective tissue cells begins, culminating in diffuse sclerosis and dystrophy of the organ cells.

In prognostic terms, acute hypoxia seems to be more dangerous. due to the fact that the reserves of compensation are temporary, and the body does not have time to adjust to a new breathing regime, so untimely treatment threatens with serious consequences and even death. Chronic oxygen starvation, on the contrary, causes persistent adaptive reactions, so this condition can last for years, the organs will perform their function even with moderate sclerosis and dystrophy.

Varieties of oxygen starvation

The classification of hypoxic conditions has been revised many times, but its general principle has been preserved. It is based on identifying the cause of the pathology and determining the level of damage to the respiratory chain. Depending on the etiopathogenetic mechanism, there are:

• Exogenous oxygen starvation - associated with external conditions;
• Endogenous form - in diseases of internal organs, endocrine system, blood, etc.

Endogenous hypoxia happens:

• Respiratory;
• Circulatory - with damage to the myocardium and blood vessels, dehydration, blood loss, thrombosis and thrombophlebitis;
• Hemic - due to the pathology of erythrocytes, hemoglobin, enzyme systems of red blood cells, with erythropenia, lack of hemoglobin (anemic), poisoning with poisons that block hemoglobin, the use of certain drugs (aspirin, citramon, novocaine, vikasol, etc.);
• Tissue - due to the inability of cells to absorb blood oxygen due to disorders in various parts of the respiratory chain under conditions of normal oxygenation;
• Substrate - occurs due to a lack of substances that serve as a substrate for oxidation during tissue respiration (hunger, diabetes);
• Overload - a variant of physiological oxygen starvation due to excessive physical activity, when oxygen reserves and the capabilities of the respiratory system become insufficient;
• Mixed.

According to the rate of development of pathology, a fulminant form (up to 3 minutes), acute (up to 2 hours), subacute (up to 5 hours) and chronic, which can last for years, are distinguished. In addition, hypoxia can be general and local.

Why is oxygen becoming scarce?

The development of oxygen starvation is based on exogenous and endogenous causes. External ones are caused by a lack of oxygen in the air, which can be clean, but mountainous, urban, but dirty.

Exogenous hypoxia appears when:

1. Low oxygen content in the inhaled air - mountainous terrain, frequent flights (for pilots);
2. Being in a confined space with a large number of people, in a mine, wells, on a submarine, etc., when there is no communication with open air;
3. Inadequate room ventilation;
4. Work under water, in a gas mask;
5. Dirty atmosphere, gas pollution in large industrial cities;
6. Breakage of equipment for anesthesia and artificial pulmonary ventilation.

Endogenous hypoxia associated with internal adverse conditions that predispose to a lack of oxygen in the blood:

As you can see, the causes of endogenous oxygen starvation are extremely diverse. It is difficult to name an organ, the defeat of which in one way or another would not affect the respiration of cells. Especially severe changes occur in the pathology of erythrocytes and hemoglobin, blood loss, lesions of the respiratory center, acute occlusion of the arteries of the lungs.

In addition to hypoxia in adults, it is also possible lack of oxygen in the fetus during fetal development or a newborn baby. The reasons for it are:

• Diseases of the kidneys, heart, liver, respiratory organs in the expectant mother;
• Severe anemia in pregnancy;
• Late with pathology of hemocoagulation and microcirculation;
• Alcoholism, drug addiction of the expectant mother;
• Intrauterine infection;
• Anomalies of the placenta and umbilical vessels;
• congenital deformities;
• Anomalies of labor activity, trauma in childbirth, placental abruption, entanglement of the umbilical cord.

Structural changes and symptoms with lack of oxygen

With a lack of oxygen in the tissues, characteristic ischemic-hypoxic changes develop. Brain damage is caused by disorders with erythrocyte aggregation, impregnation of blood vessel walls with plasma and their necrotic changes. As a result, vascular permeability increases, the liquid part of the blood enters the perivascular space, giving rise to edema.

A severe lack of oxygen in the blood contributes to irreversible changes in neurons, their vacuolization, chromosome breakdown and necrosis. The more severe hypoxia, the more pronounced dystrophy and necrosis, moreover, cell pathology can increase even after the cause of oxygen deficiency has been eliminated.

So, in severe hypoxia, several days after the restoration of oxygenation in neurons that did not have structural changes before, irreversible degenerative processes begin. Then these cells are absorbed by phagocytes, and softening areas appear in the parenchyma of the organ - voids in place of destroyed cells. In the future, this threatens chronic and.

Chronic hypoxia is accompanied by a lower intensity of necrotic reactions, but it provokes the multiplication of glial elements that play a supporting and trophic role. Such gliosis underlies.

brain changes in chronic dyscirculatory encephalopathy

Depending on the depth of oxygen deficiency in tissues, it is customary to isolate several degrees of severity of pathology:

1. Light - signs of hypoxia become noticeable only during physical exertion;
2. Moderate - symptoms occur even at rest;
3. Severe - severe hypoxia with dysfunction of internal organs, cerebral symptoms; precedes coma;
4. Critical - coma, shock, agony and death of the victim.

The lack of oxygen in the body is manifested mainly by neurological disorders, the severity of which depends on the depth of hypoxia. As metabolic disorders worsen, the kidneys, liver, and myocardium are involved in the pathogenetic chain, the parenchyma of which is also extremely sensitive to a lack of oxygenation. In the terminal phase of hypoxia, multiple organ failure occurs, severe hemostasis disorders with bleeding, necrotic changes in the internal organs.

Clinical signs of oxygen starvation are characteristic of all types of pathology, while lightning-fast hypoxia may not have time to manifest itself with any symptoms due to the sudden (in a matter of minutes) death of the victim.

Acute oxygen starvation develops over 2-3 hours, during which the organs have time to feel the lack of oxygen. First, the body will try to correct it by accelerating the pulse, increasing pressure, however, compensatory mechanisms are quickly depleted due to the severe general condition and the nature of the underlying disease, hence the symptoms of acute hypoxia:

• bradycardia;
• Decreased blood pressure;
• Irregular, shallow, rare breathing or its pathological types.

If oxygen deficiency is not eliminated at this moment, then irreversible ischemic-dystrophic changes in vital organs will develop, the victim will plunge into a coma, agony and death will occur from multiple organ failure, cardiac arrest.

Subacute and chronic varieties lack of oxygen in the body in an adult or a child is manifested by hypoxic syndrome, which, of course, affects the most vulnerable organ to lack of oxygen - the brain. Against the background of oxygen deficiency in the nervous tissue, ischemia and death of neurons begin, circulatory disorders occur with microthrombosis and hemorrhage, and edema progresses.

Symptoms of oxygen starvation of the brain are:

1. Euphoria, agitation, unmotivated anxiety, restlessness;
2. Motor excitation;
3. Reduced criticism of one's condition, inadequate assessment of what is happening;
4. Signs of oppression of cortical structures - cranialgia, noises in the ears or head, dizziness, lethargy;
5. Violations of consciousness up to coma;
6. Spontaneous urination and defecation;
7. Nausea, vomiting;
8. Loss of coordination, inability to walk and make purposeful movements;
9. Convulsive muscle contractions with irritation from outside - begin with the facial muscles, then the muscles of the limbs and abdomen are involved; the most severe form is opisthotonus, when all the muscles of the body contract, including the diaphragm (as in tetanus).

As hypoxic-ischemic disorders deepen in the tissues, cardialgia joins neurological symptoms, the pulse becomes more frequent over 70 heart beats per minute, hypotension increases, breathing becomes irregular, shortness of breath increases, body temperature decreases.

Against the background of metabolic disorders and disorders of peripheral blood flow (cyanosis) of the skin develops, however, in case of intoxication with cyanides, carbon monoxide, nitro compounds, the skin of the victim may, on the contrary, turn pink.

Chronic oxygen starvation with constant cerebral hypoxia is accompanied by mental disorders in the form of hallucinations, delirious state, agitation, disorientation, memory loss and dementia. In severe hypotension, perfusion of already suffering tissues decreases, coma develops with inhibition of vital nerve centers and death.

A milder course of chronic hypoxia observed in residents of megacities, office workers and other closed poorly ventilated premises is accompanied by drowsiness, weakness, fatigue, headaches, mood swings, a tendency to depressive disorders, a decrease in the ability to concentrate at work, dizziness. Such hypoxia brings rather subjective discomfort, makes it difficult to perform professional duties, but does not threaten life. Nevertheless, it is necessary to deal with it in order to maintain an active life and adequate working capacity.

Oxygen starvation in the fetus and newborn

Oxygen starvation has a very unfavorable effect on the fetus developing during pregnancy, whose cells constantly multiply, forming tissues, and therefore are very sensitive to hypoxia. Today, pathology is diagnosed in every tenth newborn baby.

Fetal hypoxia can occur in both acute and chronic forms. In the early stages of gestation, chronic oxygen starvation provokes a slowdown in the formation of the embryo, congenital malformations, and in the later stages - disorders of the central nervous system, growth retardation, and a decrease in adaptive reserves.

Acute oxygen starvation during childbirth is usually associated with complications of childbirth itself - rapid or too prolonged labor, clamping of the umbilical cord, weakness of labor forces, placental abruption, etc. In this case, dysfunction of the internal organs of the fetus is pronounced, tachycardia of up to 160 or more strokes is observed heart rate per minute or bradycardia less than 120 beats. Heart sounds are muffled, movements are weak. The most severe variant of intrauterine hypoxia is asphyxia.

Chronic hypoxia develops slowly, with a moderately pronounced lack of oxygen, while malnutrition is diagnosed - a slowdown in weight gain by the fetus, more rare movements, bradycardia.

A developing baby can subsequently lead to a convulsive syndrome or cerebral palsy. Perhaps the formation of congenital anomalies of the heart, pneumopathy due to impaired maturation of the lung tissue.

Asphyxia during childbirth is extremely dangerous due to the death of a newborn, severe brain damage with necrosis and hemorrhage, respiratory disorders, and multiple organ failure. This condition requires resuscitation.

Oxygen starvation of the fetus is manifested:

• Tachycardia at the beginning of hypoxia and slowing of the pulse with its aggravation;
• Deafness of heart sounds;
• An increase in motor activity at the beginning of the development of pathology and in mild degrees, and a decrease with a deep lack of oxygen;
• The appearance of meconium in the amniotic fluid;
• An increase in hypoxia with periods of tachycardia and hypertension, followed by bradycardia and hypotension;
• The appearance of edema in the tissues;
• Hemorrhages due to a violation of blood viscosity, a tendency to intravascular aggregation of red blood cells;
• Disorders of electrolyte metabolism, acidosis.

serious consequences oxygen starvation during pregnancy can be birth trauma to the fetus, intrauterine death, severe asphyxia in the womb or during childbirth. Children born or born under conditions of oxygen starvation are hypotrophic, poorly adapted to life outside the fruiting place, suffer from neurological and mental disorders in the form of delayed speech and mental development, convulsive syndrome, and cerebral palsy.

In a newborn child with hypoxia, a sharp bradycardia, the absence of crying and the first breath, a sharp cyanosis of the skin, the absence of spontaneous respiration and a sharp metabolic imbalance are possible, requiring emergency care.

Treatment of oxygen starvation

Treatment of oxygen starvation should be comprehensive and timely, aimed at eliminating the cause of hypoxia and restoring adequate perfusion and tissue oxygenation. In acute forms and asphyxia, emergency therapy and resuscitation are necessary.

Regardless of the type of oxygen starvation, hyperbaric oxygenation is used as one of the main methods of pathogenetic therapy, in which oxygen is supplied to the lungs under high pressure. Due to the high pressure, oxygen can immediately dissolve in the blood, bypassing the connection with the erythrocyte, so its delivery to the tissues will be fast and not dependent on the morphological and functional features of red blood cells.

Hyperbaric oxygenation allows you to saturate the cells with oxygen, promotes the expansion of the arteries of the brain and heart, the work of which is enhanced and improved. In addition to oxygenation, cardiotonic agents, drugs to eliminate hypotension are prescribed. If necessary, transfusion of blood components is performed.

Hemic hypoxia is treated:

1. Hyperbaric oxygen therapy;
2. Hemotransfusions (blood transfusion);
3. The introduction of drugs-carriers of active oxygen - perftoran, for example;
4. Methods of extracorporeal detoxification - hemosorption, plasmapheresis to remove toxins from the blood;
5. The use of drugs that normalize the respiratory chain - ascorbic acid, methylene blue;
6. The introduction of glucose to meet the energy needs of cells;
7. Glucocorticosteroids.

Oxygen starvation during pregnancy requires hospitalization in the clinic and correction of both obstetric and extragenital pathology of the woman with the restoration of adequate blood circulation in the placenta. Rest and bed rest, oxygen therapy are prescribed, antispasmodics are introduced to reduce uterine tone (papaverine, eufillin, magnesia), drugs that improve blood rheology (chimes, pentoxifylline).

In chronic fetal hypoxia, vitamins E, C, group B, administration of glucose, antihypoxic agents, antioxidants and neuroprotectors are indicated. As the condition improves, the pregnant woman masters breathing exercises, water aerobics, undergoes physiotherapy (ultraviolet irradiation).

If severe fetal hypoxia cannot be eliminated, then in the period from the 29th week of gestation, it is necessary to urgently deliver the woman by caesarean section. Natural childbirth in chronic oxygen deficiency is carried out with monitoring of fetal cardiac activity. If a child is born in conditions of acute hypoxia or asphyxia, he is given resuscitation assistance.

In the future, babies who have undergone hypoxia are observed by a neurologist, the participation of a psychologist and a speech therapist may be required. With severe consequences of hypoxic brain damage, children need long-term drug therapy.

Dangerous complications of oxygen starvation are:

• Persistent neurological deficit;
• parkinsonism;
• dementia;
• Coma development.

Often, after hypoxia, not cured in a timely manner, psychological problems and fatigue remain.

Prevention oxygen starvation is to prevent conditions accompanied by a lack of oxygen: an active lifestyle, walking in the fresh air, physical activity, good nutrition and timely treatment of somatic pathology. "Office" work requires ventilation of the premises, and the types of professions that are more dangerous in terms of hypoxia (miners, divers, etc.) require strict observance of precautionary measures.

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hypoxia is a pathological condition characterized by oxygen deficiency in the body, which occurs due to its insufficient intake from the outside or against the background of a violation of the utilization process at the cellular level.

The term "hypoxia" comes from the addition of two Greek words - hypo (little) and oxygenium (oxygen). That is, the literal translation of hypoxia is a lack of oxygen. In common parlance, the term hypoxia is usually deciphered as oxygen starvation, which is quite fair and correct, since, ultimately, during hypoxia, all cells of various organs and tissues suffer from a lack of oxygen.

General characteristics of hypoxia

Definition

Hypoxia refers to typical pathological processes that can occur in the body in various diseases and conditions. This means that hypoxia is not specific, that is, it can be caused by various factors, and accompany a wide variety of diseases, and be a key link in the development of pathological changes in various ailments. That is why hypoxia refers to typical general pathological processes, such as inflammation or dystrophy, and, accordingly, is neither a diagnosis nor even a syndrome.

It is the essence of hypoxia as a typical pathological process that makes it difficult to understand it at the everyday level, at which a person is accustomed to dealing with specific diseases that manifest clear signs and main symptoms. In the case of hypoxia, a person, as a rule, also considers the pathological process to be a disease and begins to look for its main manifestation and symptoms. But such a search for the main manifestation of hypoxia as a disease interferes with understanding the essence of this pathological process. Consider the difference between a general pathological process and a disease with examples.

Each person faced with some kind of diagnosis tries to find out what it means, that is, what exactly is wrong in the body. For example, hypertension is high blood pressure, atherosclerosis is the deposition of fatty plaques on the walls of blood vessels, narrowing their lumen and impairing blood flow, etc. In other words, each disease is a certain set of symptoms that come from the defeat of a particular organ or tissue. But the totality of symptoms characteristic of each disease does not appear just like that, but is always due to the development of some general pathological process in a particular organ. Depending on what kind of general pathological process takes place and which organ is affected, one or another disease develops. For example, at the beginning of a general pathological inflammatory process in the lungs, a person can develop a wide variety of diseases caused specifically by inflammation of the lung tissue, such as, for example, pneumonia, bronchopneumonia, tuberculosis, etc. With a dystrophic general pathological process in the lungs, a person may develop pneumosclerosis, emphysema, etc.

In other words, the general pathological process determines the type of disturbances occurring in an organ or tissue. And the emerging disorders, in turn, cause characteristic clinical symptoms from the affected organ. That is, the same general pathological process can affect different organs and is the main mechanism for the development of various diseases. That is why the concepts of "symptoms" are not used to characterize general pathological processes, they are described from the standpoint of disorders arising at the cell level.

And hypoxia is just such a general pathological process, and not a symptom, not a syndrome, and not a disease, as a result of which the essence of disorders arising at the cellular level, and not symptoms, is given to describe it. Changes at the cellular level that occur during hypoxia can be divided into two groups - these are adaptive reactions and decompensation. And first, the body in response to hypoxia activates adaptive reactions that can for some time maintain a relatively normal functioning of organs and tissues under conditions of oxygen starvation. But if hypoxia continues for too long, then the body's resources are depleted, adaptive reactions are no longer supported, and decompensation occurs. The stage of decompensation is characterized by the appearance of irreversible changes in organs and tissues, which in any case are manifested by negative consequences, the severity of which varies from organ failure to death.

Development of hypoxia

Compensatory reactions during hypoxia are due to oxygen deficiency at the cell level, and therefore their effects are aimed at improving the supply of oxygen to tissues. In the cascade of compensatory reactions, to reduce hypoxia, mainly the organs of the cardiovascular and respiratory systems are involved, and there is also a change in biochemical processes in the cells of tissues and organ structures, which are most affected by a lack of oxygen. Until the potential of compensatory reactions is completely wasted, organs and tissues will not suffer from oxygen deficiency. But if, by the time the compensatory mechanisms are depleted, an adequate supply of oxygen is not restored, then a slow decompensation will begin in the tissues with cell damage and disruption of the functioning of the entire organ.

In acute and chronic hypoxia, the nature of compensatory reactions is different. So, in acute hypoxia, compensatory reactions consist in increased respiration and blood circulation, that is, blood pressure rises, tachycardia occurs (heart rate is more than 70 beats per minute), breathing becomes deep and frequent, the heart pumps more blood per minute than normal . In addition, in response to acute hypoxia from the bone marrow and spleen, all the "reserves" of erythrocytes that are necessary to carry oxygen to the cells enter the systemic circulation. All these reactions are aimed at normalizing the amount of oxygen delivered to the cells by increasing the volume of blood passing through the vessels per unit of time. In very severe acute hypoxia, in addition to the development of these reactions, centralization of blood circulation also occurs, which consists in redirecting all available blood to vital organs (heart and brain) and a sharp decrease in blood supply to the muscles and organs of the abdominal cavity. The body directs all oxygen to the brain and heart - organs that are critical for survival, and, as it were, “deprives” those structures that are currently not needed for survival (liver, stomach, muscles, etc.).

If acute hypoxia is eliminated within a period of time during which compensatory reactions do not deplete the body's reserves, then the person will survive, and after a while all his organs and systems will work perfectly normally, that is, oxygen starvation will not leave serious disorders. If hypoxia continues longer than the period of effectiveness of compensatory reactions, then by the time it is eliminated, irreversible changes will occur in organs and tissues, as a result of which, after recovery, the person will have various disruptions in the work of the most affected organ systems.

Compensatory reactions in chronic hypoxia develop against the background of severe long-term diseases or conditions, therefore, they also have the character of constant changes and deviations from the norm. First of all, to compensate for the lack of oxygen in the blood, the number of red blood cells increases, which makes it possible to increase the amount of oxygen carried by the same volume of blood per unit time. In addition, the activity of an enzyme increases in erythrocytes, which facilitates the transfer of oxygen from hemoglobin directly to the cells of organs and tissues. New alveoli form in the lungs, breathing deepens, the volume of the chest increases, additional vessels form in the lung tissue, which improves the flow of oxygen into the blood from the surrounding atmosphere. The heart, which has to pump more blood per minute, hypertrophies and increases in size. In tissues suffering from oxygen starvation, changes also occur that are aimed at more efficient use of a small amount of oxygen. Thus, the number of mitochondria (organelles that use oxygen to ensure cellular respiration) increases in cells, and many new small vessels are formed in tissues, which ensure the expansion of the microvasculature. It is precisely because of the activation of microcirculation and a large number of capillaries during hypoxia that a person develops a pinkish skin color, which is mistaken for a "healthy" blush.

Adaptive reactions in acute hypoxia are exclusively reflex, and therefore, when oxygen starvation is eliminated, they stop their action, and the organs completely return to the mode of functioning in which they existed before the development of an episode of hypoxia. In chronic hypoxia, however, adaptive reactions are not reflex, they develop due to the restructuring of the functioning of organs and systems, and therefore their action cannot be quickly stopped after the elimination of oxygen starvation.

This means that during chronic hypoxia the body can change its mode of functioning in such a way that it will fully adapt to conditions of oxygen deficiency and will not suffer from it at all. In acute hypoxia, complete adaptation to oxygen deficiency cannot occur, since the body simply does not have time to restructure the modes of functioning, and all its compensatory reactions are designed only to temporarily maintain the functioning of organs until adequate oxygen supply is restored. That is why the state of chronic hypoxia can be present in a person for many years, without interfering with his normal life and work, and acute hypoxia in a short period of time can lead to death or irreversible damage to the brain or heart.

Compensatory reactions during hypoxia always lead to a change in the mode of functioning of the most important organs and systems, which causes a wide range of clinical manifestations. These manifestations of compensatory reactions can be conditionally considered symptoms of hypoxia.

Types of hypoxia

The classification of hypoxia was made repeatedly. However, practically all classifications do not fundamentally differ from each other, since once identified on the basis of the causative factor and the level of damage to the oxygen transport system, the varieties of hypoxia are justified. Therefore, we will give a relatively old classification of hypoxia into types, which, nevertheless, is accepted in the modern scientific community as the most complete, informative and justified.

So, at present, according to the most complete and reasonable classification, hypoxia, depending on the mechanism of development, is divided into the following types:

1. Exogenous hypoxia (hypoxic hypoxia) - due to environmental factors.

2. Endogenous hypoxia - due to various diseases or disorders that a person has:

• Respiratory (respiratory, pulmonary) hypoxia.
• Circulatory (cardiovascular) hypoxia:
  • Ischemic;
  • congestive.
• Hemic (blood) hypoxia:
  • anemic;
  • Caused by inactivation of hemoglobin.
• Tissue (histotoxic) hypoxia.
• substrate hypoxia.
• overload hypoxia.
• Mixed hypoxia.

Depending on the rate of development and course, hypoxia is divided into the following types:

• Lightning (instantaneous) - develops within a few seconds (no longer than 2 - 3 minutes);
• Acute - develops within a few tens of minutes or hours (no longer than 2 hours);
• Subacute - develops within a few hours (no longer than 3 - 5 hours);
• Chronic - develops and lasts for weeks, months or years.

Depending on the prevalence of oxygen starvation, hypoxia is divided into general and local.

Consider the various types of hypoxia in detail.

Exogenous hypoxia

Exogenous hypoxia, also called hypoxic, is caused by a decrease in the amount of oxygen in the inhaled air. That is, due to the lack of oxygen in the air, with each breath less oxygen enters the lungs than normal. Accordingly, blood comes out of the lungs that is not sufficiently oxygenated, as a result of which a small amount of gas is brought to the cells of various organs and tissues, and they experience hypoxia. Depending on atmospheric pressure, exogenous hypoxia is divided into hypobaric and normobaric.

Hypobaric hypoxia due to low oxygen content in rarefied air with low atmospheric pressure. Such hypoxia develops when climbing to great heights (mountains), as well as when rising into the air on open aircraft without oxygen masks.

Normobaric hypoxia develops at a low oxygen content in air with normal atmospheric pressure. Normobaric exogenous hypoxia can develop when you are in mines, wells, on submarines, in diving suits, in cramped rooms with a large crowding of people, with general air pollution or smog in cities, as well as during surgery with a malfunction of anesthesia and respiratory equipment.

Exogenous hypoxia is manifested by cyanosis (cyanosis of the skin and mucous membranes), dizziness and fainting.

Respiratory (respiratory, pulmonary) hypoxia

Respiratory (respiratory, pulmonary) hypoxia develops in diseases of the respiratory system (for example, bronchitis, pulmonary hypertension, any pathology of the lungs, etc.), when the penetration of oxygen from the air into the blood is difficult. That is, at the level of the pulmonary alveoli, there is a difficulty for the rapid and effective binding of hemoglobin to oxygen that has entered the lungs with a portion of inhaled air. Against the background of respiratory hypoxia, complications can develop, such as respiratory failure, cerebral edema and gaseous acidosis.

Circulatory (cardiovascular) hypoxia

Circulatory (cardiovascular) hypoxia develops against the background of various circulatory disorders (for example, a decrease in vascular tone, a decrease in total blood volume after blood loss or dehydration, an increase in blood viscosity, increased clotting, centralization of blood circulation, venous stasis, etc.). If the circulatory disorder affects the entire network of blood vessels, then hypoxia is systemic. If blood circulation is disturbed only in the area of ​​​​an organ or tissue, then hypoxia is local.

With circulatory hypoxia, a normal amount of oxygen enters the blood through the lungs, but due to circulatory disorders, it is delivered to organs and tissues with a delay, as a result of which oxygen starvation occurs in the latter.

According to the mechanism of development, circulatory hypoxia can be ischemic and congestive. Ischemic form hypoxia develops with a decrease in the volume of blood passing through organs or tissues per unit time. This form of hypoxia can occur with left ventricular heart failure, myocardial infarction, cardiosclerosis, shock, collapse, vasoconstriction of some organs, and other situations when blood sufficiently saturated with oxygen is for some reason passed through the vascular bed in a small volume.

stagnant form hypoxia develops with a decrease in the speed of blood movement through the veins. In turn, the speed of blood movement through the veins decreases with thrombophlebitis of the legs, right ventricular heart failure, increased intrathoracic pressure and other situations when blood stagnation occurs in the venous bed. With a congestive form of hypoxia, venous, rich in carbon dioxide, blood does not return to the lungs in time to remove carbon dioxide and saturate with oxygen. As a result, there is a delay in the delivery of the next portion of oxygen to organs and tissues.

Hemic (blood) hypoxia

Hemic (blood) hypoxia develops in violation of the qualitative characteristics or a decrease in the amount of hemoglobin in the blood. Hemic hypoxia is divided into two forms - anemic And caused by changes in the quality of hemoglobin. Anemic hemic hypoxia is caused by a decrease in the amount of hemoglobin in the blood, that is, anemia of any origin or hydremia (blood dilution due to fluid retention in the body). And hypoxia, due to a change in the quality of hemoglobin, is associated with poisoning by various toxic substances that lead to the formation of forms of hemoglobin that are not able to carry oxygen (methemoglobin or carboxyhemoglobin).

With anemic hypoxia oxygen normally binds and is carried by the blood to organs and tissues. But due to the fact that there is too little hemoglobin, an insufficient amount of oxygen is brought to the tissues and hypoxia occurs in them.

When the quality of hemoglobin changes its amount remains normal, but it loses its ability to carry oxygen. As a result, when passing through the lungs, hemoglobin is not saturated with oxygen and, accordingly, the blood flow does not deliver it to the cells of all organs and tissues. A change in the quality of hemoglobin occurs when a number of chemicals are poisoned, such as carbon monoxide (carbon monoxide), sulfur, nitrites, nitrates, etc. When these toxic substances enter the body, they bind to hemoglobin, as a result of which it ceases to carry oxygen to the tissues, who are experiencing hypoxia.

Acute hypoxia

Acute hypoxia develops quickly, within a few tens of minutes, and persists for a limited period of time, ending either in the elimination of oxygen starvation or irreversible changes in the organs, which will eventually lead to serious illness or even death. Acute hypoxia usually accompanies conditions in which blood flow, the quantity and quality of hemoglobin change dramatically, such as, for example, blood loss, cyanide poisoning, heart attack, etc. In other words, acute hypoxia occurs in acute conditions.

Any variant of acute hypoxia must be eliminated as soon as possible, since the body will be able to maintain the normal functioning of organs and tissues for a limited period of time until compensatory-adaptive reactions are exhausted. And when the compensatory-adaptive reactions are completely exhausted, under the influence of hypoxia, the most important organs and tissues (primarily the brain and heart) will begin to die, which will ultimately lead to death. If it is possible to eliminate hypoxia, when tissue death has already begun, then a person can survive, but at the same time he will have irreversible dysfunctions in the functioning of the organs most affected by oxygen starvation.

In principle, acute hypoxia is more dangerous than chronic, since it can lead to disability, organ failure or death in a short time. And chronic hypoxia can exist for years, giving the body the opportunity to adapt and live and function quite normally.

Chronic hypoxia

Chronic hypoxia develops over several days, weeks, months or even years, and occurs against the background of long-term diseases, when changes in the body occur slowly and gradually. The body "gets used" to chronic hypoxia by changing the structure of cells under existing conditions, which allows the organs to function quite normally, and the person to live. In principle, chronic hypoxia is more favorable than acute, since it develops slowly, and the body is able to adapt to new conditions with the help of compensation mechanisms.

Fetal hypoxia

Fetal hypoxia is a state of oxygen starvation of a child during pregnancy, which occurs when there is a lack of oxygen supplied to it through the placenta from the mother's blood. During pregnancy, the fetus receives oxygen from the mother's blood. And if a woman's body for some reason cannot deliver the required amount of oxygen to the fetus, then it begins to suffer from hypoxia. As a rule, the cause of fetal hypoxia during pregnancy is anemia, diseases of the liver, kidneys, heart, blood vessels and respiratory organs in the expectant mother.

A mild degree of hypoxia does not adversely affect the fetus, and moderate and severe can have a very negative effect on the growth and development of the baby. So, against the background of hypoxia, necrosis (dead tissue areas) can form in various organs and tissues, which will lead to congenital malformations, premature birth, or even intrauterine death.

Fetal hypoxia can develop at any gestational age. Moreover, if the fetus suffered from hypoxia in the first trimester of pregnancy, then there is a high probability of the appearance of developmental anomalies incompatible with life, as a result of which his death and miscarriage occur. If hypoxia affected the fetus during the 2nd - 3rd trimesters of pregnancy, then the central nervous system may be affected, as a result of which the born child will suffer from developmental delay and low adaptive abilities.

Fetal hypoxia is not a separate independent disease, but only reflects the presence of any serious disturbances in the work of the placenta, or in the mother's body, as well as in the development of the child. Therefore, when signs of fetal hypoxia appear, doctors begin to search for the cause of this condition, that is, they find out which disease led to oxygen starvation of the child. Further, the treatment of fetal hypoxia is carried out in a complex manner, simultaneously using drugs that eliminate the underlying disease that caused oxygen starvation, and drugs that improve oxygen delivery to the child.

Like any other, fetal hypoxia can be acute and chronic. Acute hypoxia occurs when there is a sharp disruption of the mother's body or the placenta and, as a rule, needs urgent treatment, because otherwise it quickly leads to the death of the fetus. Chronic hypoxia can exist throughout pregnancy, negatively affecting the fetus and leading to the fact that the child is born weak, retarded, possibly with defects in various organs.

The main signs of fetal hypoxia are a decrease in its activity (the number of shocks is less than 10 per day) and bradycardia below 70 beats per minute according to the results of CTG. It is by these signs that pregnant women can judge the presence or absence of fetal hypoxia.

For an accurate diagnosis of fetal hypoxia, a Doppler study of the vessels of the placenta, CTG (cardiotocography) of the fetus, ultrasound (ultrasound examination) of the fetus, a non-stress test are performed and the child's heartbeat is heard with a phonendoscope.

Hypoxia in newborns

Hypoxia in newborns is a consequence of oxygen starvation of the baby in childbirth or during pregnancy. In principle, this term is used exclusively at the household level and it means the condition of a child, either born in a state of hypoxia (for example, due to entanglement of the umbilical cord), or suffering from chronic hypoxia during pregnancy. In fact, there is no such condition as hypoxia of newborns in its everyday, everyday sense.

Strictly speaking, there is no such term in medical science, and the condition of a newborn child is assessed not by speculative assumptions about what happened to him, but by clear criteria that allow you to say for sure whether the baby suffers from hypoxia after birth. Thus, the assessment of the severity of hypoxia of a newborn child is carried out according to Apgar score, which includes five indicators that are recorded immediately after the birth of the child and after 5 minutes. The assessment of each indicator of the scale exposes in points from 0 to 2, which are then summed up. As a result, the newborn receives two Apgar scores - immediately after birth and after 5 minutes.

A completely healthy baby who does not suffer from postpartum hypoxia receives an Apgar score of 8-10 either immediately after delivery or 5 minutes later. A child suffering from moderate hypoxia receives an Apgar score of 4 to 7 immediately after birth. If after 5 minutes this child received an Apgar score of 8 - 10 points, then hypoxia is considered eliminated, and the baby has fully recovered. If the child in the first minute after birth receives 0-3 points on the Apgar scale, then he has severe hypoxia, for the elimination of which he must be transferred to intensive care.

Many parents are interested in how to treat hypoxia in a newborn, which is completely wrong, because if the baby received an Apgar score of 7-10 5 minutes after birth, and after discharge from the maternity hospital develops and grows normally, then nothing needs to be treated, and he successfully survived all the consequences of oxygen starvation. If, as a result of hypoxia, the child has any disorders, then they will need to be treated, and not to give the baby prophylactically various drugs to eliminate the mythical "hypoxia of the newborn."

Hypoxia in childbirth

In childbirth, the child may suffer from a lack of oxygen, which leads to negative consequences, up to the death of the fetus. Therefore, during all childbirth, doctors monitor the baby's heartbeat, since it is from it that you can quickly understand that the child began to suffer from hypoxia and an urgent delivery is needed. In case of acute fetal hypoxia in childbirth, to save him, an urgent cesarean section is performed for a woman, since if childbirth continues naturally, the baby may not live to see the birth, but die from oxygen starvation in the womb.

The following factors can be the causes of fetal hypoxia during childbirth:

• Preeclampsia and eclampsia;
• Shock or cardiac arrest in a woman in labor;
• uterine rupture;
• Severe anemia in a woman in labor;
• Bleeding with placenta previa;
• entanglement with the umbilical cord of the child;
• Prolonged childbirth;
• Thrombosis of the vessels of the umbilical cord.

In practice, fetal hypoxia during childbirth is very often provoked by intense uterine contractions caused by the administration of oxytocin.

Consequences of hypoxia

The consequences of hypoxia can be different, and depend on the period of time during which oxygen starvation was eliminated and how long it lasted. So, if hypoxia was eliminated during the period when the compensatory mechanisms were not exhausted, then there will be no negative consequences, after a while the organs and tissues will completely return to normal operation. But if hypoxia was eliminated during the period of decompensation, when compensatory mechanisms were exhausted, then the consequences depend on the duration of oxygen starvation. The longer the period of hypoxia turned out to be against the background of decompensation of adaptive mechanisms, the stronger and deeper the damage to various organs and systems. Moreover, the longer hypoxia lasts, the more organs are damaged.

During hypoxia, the brain suffers most severely, since it can withstand 3-4 minutes without oxygen, and from 5 minutes necrosis will already begin to form in the tissues. The heart muscle, kidneys and liver are able to endure a period of complete absence of oxygen for 30 to 40 minutes.

The consequences of hypoxia are always due to the fact that in cells in the absence of oxygen, the process of oxygen-free oxidation of fats and glucose begins, which leads to the formation of lactic acid and other toxic metabolic products that accumulate and eventually damage the cell membrane, leading to its death. When hypoxia lasts long enough from the poisonous products of improper metabolism, a large number of cells die in various organs, forming whole areas of dead tissues. Naturally, such areas sharply impair the functioning of the organ, which is manifested by the corresponding symptoms, and in the future, even with the restoration of oxygen flow, it will lead to a persistent deterioration in the functioning of the affected tissues.

The main consequences of hypoxia are always caused by disruption of the central nervous system, since it is the brain that suffers primarily from oxygen deficiency. Therefore, the consequences of hypoxia are often expressed in the development of a neuropsychic syndrome, which includes parkinsonism, psychosis and dementia. In 1/2 - 2/3 of cases, the neuropsychic syndrome can be cured. In addition, the consequence of hypoxia is exercise intolerance, when, with minimal exertion, a person develops palpitations, shortness of breath, weakness, headache, dizziness, and pain in the region of the heart. Also, the consequences of hypoxia can be hemorrhages in various organs and fatty degeneration of muscle cells, myocardium and liver, which will lead to disruption of their functioning with clinical symptoms of insufficiency of one or another organ, which can no longer be eliminated in the future.

Hypoxia - causes

The causes of exogenous hypoxia may be the following factors:

• Discharged atmosphere at altitude (mountain sickness, altitude sickness, illness of pilots);
• Being in tight spaces with a large crowd of people;
• Being in mines, wells or in any closed premises (for example, submarines, etc.) with no communication with the external environment;
• Poor ventilation of premises;
• Work in diving suits or breathing through a gas mask;
• Strong air pollution or smog in the city of residence;
• Malfunction of anesthesia and respiratory equipment.

The following factors can be the causes of various types of endogenous hypoxia:

• Respiratory diseases (pneumonia, pneumothorax, hydrothorax, hemothorax, destruction of alveolar surfactant, pulmonary edema, pulmonary embolism, tracheitis, bronchitis, emphysema, sarcoidosis, asbestosis, bronchospasm, etc.);
• Foreign bodies in the bronchi (for example, accidental ingestion of various objects by children, suppression, etc.);
• Asphyxia of any origin (for example, with compression of the neck, etc.);
• Congenital and acquired heart defects (non-closure of the foramen ovale or Batal duct of the heart, rheumatism, etc.);
• Damage to the respiratory center of the central nervous system during injuries, tumors and other diseases of the brain, as well as when it is inhibited by toxic substances;
• Violation of the mechanics of the act of breathing due to fractures and displacements of the bones of the chest, damage to the diaphragm or muscle spasms;
• Disorders of the heart, provoked by various diseases and pathologies of the heart (heart attack, cardiosclerosis, heart failure, electrolyte imbalance, cardiac tamponade, pericardial obliteration, blockade of electrical impulses in the heart, etc.);
• A sharp narrowing of blood vessels in various organs;
• Arteriovenous shunting (transfer of arterial blood into veins through vascular shunts before it reaches organs and tissues and gives oxygen to cells);
• Stagnation of blood in the system of the inferior or superior vena cava;
• Thrombosis;
• Poisoning by chemicals that cause the formation of inactive hemoglobin (for example, cyanides, carbon monoxide, lewisite, etc.);
• Anemia;
• Acute blood loss;
• Syndrome of disseminated intravascular coagulation (hypoxia, clinical symptoms do not have time to appear, because death occurs within a very short period of time (up to 2 minutes). acute form hypoxia lasts up to 2-3 hours, and during this period there is a failure of all organs and systems at once, primarily the central nervous system, respiration and heart (heart rate slows down, blood pressure drops, breathing becomes irregular, etc.). If hypoxia is not eliminated during this period, then organ failure turns into coma and agony, followed by death.

  Subacute and chronic forms hypoxia are manifested by the so-called hypoxic syndrome. Against the background of hypoxic syndrome, symptoms from the central nervous system first appear, since the brain is most sensitive to oxygen deficiency, as a result of which foci of necrosis (dead areas), hemorrhages and other variants of cell destruction quickly appear in its tissues. Due to necrosis, hemorrhage and death of brain cells against the background of oxygen deficiency at the initial stage of hypoxia, a person develops euphoria, he is in an excited state, he is tormented by motor anxiety. One's own state is not evaluated critically.

  In addition to the symptoms of depression of the cerebral cortex, a person also has pain in the region of the heart, irregular breathing, shortness of breath, a sharp decrease in vascular tone, tachycardia (an increase in heart rate of more than 70 beats per minute), a drop in blood pressure, cyanosis (cyanosis of the skin), decrease in body temperature. But when poisoned with substances that inactivate hemoglobin (for example, cyanides, nitrites, nitrates, carbon monoxide, etc.), human skin becomes pinkish in color.

  With prolonged hypoxia with a slow development of CNS damage, a person may experience mental disorders in the form of delirium ("delirious tremens"), Korsakov's syndrome (loss of orientation, amnesia, replacement of fictional events with real ones, etc.) and dementia.

  With further progression of hypoxia, blood pressure drops to 20-40 mm Hg. Art. and there is a coma with the extinction of brain functions. If blood pressure falls below 20 mm Hg. Art., then death occurs. In the period before death, a person may experience agonizing breathing in the form of rare convulsive attempts to inhale.

  Altitude hypoxia (mountain sickness) - causes and mechanism of development, symptoms, manifestations and consequences, opinion of the master of sports in mountaineering and physiologists - video

  Degrees of hypoxia

  Depending on the severity of the course and the severity of oxygen deficiency, the following degrees of hypoxia are distinguished:

  • Light(usually detected only during physical exertion);
  • Moderate(phenomena of hypoxic syndrome appear at rest);
  • heavy(the phenomena of the hypoxic syndrome are strongly pronounced and there is a tendency to go into a coma);
  • critical(The hypoxic syndrome has led to coma or shock, which can end in death agony).

  Treatment of oxygen starvation

  In practice, mixed forms of hypoxia usually develop., as a result of which the treatment of oxygen deficiency in all cases should be comprehensive, aimed at simultaneously eliminating the causative factor and maintaining an adequate supply of cells of various organs and tissues with oxygen.

  To maintain a normal level of oxygen supply to cells in any type of hypoxia, hyperbaric oxygenation is used. This method consists in forcing oxygen into the lungs under pressure. Due to the high pressure, oxygen dissolves directly in the blood without binding to erythrocytes, which makes it possible to deliver it to organs and tissues in the required amount, regardless of the activity and functional usefulness of hemoglobin. Thanks to hyperbaric oxygen therapy, it is possible not only to supply the organs with oxygen, but also to expand the vessels of the brain and heart, so that the latter can work at full strength.

  In addition to hyperbaric oxygen therapy, in circulatory hypoxia, cardiac drugs and drugs that increase blood pressure are used. If necessary, a blood transfusion is performed (if blood loss has occurred that is not compatible with life).

  With hemic hypoxia, in addition to hyperbaric oxygen therapy, the following therapeutic measures are carried out:

  • Transfusion of blood or red blood cells;
  • The introduction of oxygen carriers (Perftoran, etc.);
  • Hemosorption and plasmapheresis to remove toxic metabolic products from the blood;
  • The introduction of substances capable of performing the functions of respiratory chain enzymes (vitamin C, methylene blue, etc.);
  • The introduction of glucose as the main substance that gives cells energy for the implementation of vital processes;
  • The introduction of steroid hormones to eliminate the pronounced oxygen starvation of tissues.
  In principle, in addition to the above, to eliminate hypoxia, any treatment methods and drugs can be used, the action of which is aimed at restoring the normal functioning of all organs and systems, as well as maintaining the vital functions of the body.

  Prevention of hypoxia

  An effective prevention of hypoxia is to prevent conditions in which the body may experience oxygen starvation. To do this, you need to lead an active lifestyle, be outdoors every day, exercise, eat well and treat existing chronic diseases in a timely manner. When working in an office, you need to periodically ventilate the room (at least 2-3 times during the working day) in order to saturate the air with oxygen and remove carbon dioxide from it.
  

(literal translation from Greek - “little oxygen”) - a state oxygen starvation of the whole organism and individual organs and tissues, caused by various external and internal factors.

Causes of hypoxia

1. Hypoxic (exogenous)- with a decrease in the oxygen content in the inhaled air (stuffy unventilated rooms, high altitude conditions, high-altitude flight without oxygen equipment);
2. Respiratory (respiratory)- in the event of a complete or partial violation of the movement of air in the lungs (example: suffocation, drowning, swelling of the bronchial mucosa, bronchospasm, pulmonary edema, pneumonia, etc.);
3. Hemic (blood)- with a decrease in the oxygen capacity of the blood, i.e. when the blood loses its ability to attach oxygen to erythrocyte hemoglobin (the main oxygen carrier). Most often occurs with carbon monoxide poisoning, with hemolysis of red blood cells, with anemia (anemia);
4. Circulatory- with cardiovascular insufficiency, when the movement of blood enriched with oxygen to tissues and organs is difficult or impossible (example: myocardial infarction, heart defects, vasculitis, vascular damage in diabetes, etc.);
5. Histotoxic (tissue)- in violation of the absorption of oxygen by the tissues of the body (example: some poisons and salts of heavy metals can block the enzymes involved in "tissue respiration");
6. reloading- due to excessive functional load on the organ or tissue (example: excessive load on the muscles during hard work, when the need for oxygen is higher than its actual inflow into the tissue);
7. mixed- a combination of several of the above options.

Signs and symptoms of hypoxia, mechanisms of protection of the body from hypoxia

Signs of hypoxia are very diverse and almost always depend on the degree of its severity, the duration of exposure and the cause of occurrence. We will give the most basic symptoms and explain their causes of development.

Hypoxia is acute (develops after a few minutes, hours) from the onset of exposure to the causative factor or may be chronic (develops slowly, over several months or years).

Acute hypoxia has a more pronounced clinical picture and severe rapidly developing consequences for the body, which may be irreversible. Chronic hypoxia, because develops slowly, allows the patient's body to adapt to it, so patients with severe respiratory failure on the background of chronic pulmonary diseases live for a long time without dramatic symptoms. At the same time, chronic hypoxia also leads to irreversible consequences.

The main mechanisms of protection of the body from hypoxia

1) An increase in the frequency of breathing, to enhance the supply of oxygen to the lungs and its further transport by the blood. At first, breathing is frequent and deep, however, as the respiratory center is depleted, it becomes rare and superficial.

2) An increase in heart rate, an increase in blood pressure and an increase in cardiac output. Thus, an organism experiencing oxygen hunger tries to “distribute” as much and as quickly as possible oxygen into the tissues.

3) The release of deposited blood into the bloodstream and increased formation of red blood cells - to increase the number of oxygen carriers.

4) Slowing down the functioning of certain tissues, organs and systems in order to reduce oxygen consumption.

5) Transition to "alternative energy sources". Since there is not enough oxygen to fully meet the energy needs of the body, alternative energy sources are launched to ensure almost all processes occurring in the body. This defense mechanism is called anaerobic glycolysis, i.e. the breakdown of carbohydrates (the main source of energy that is released during their breakdown) without the participation of oxygen. However, the reverse side of this process is the accumulation of unwanted products such as lactic acid, as well as a shift in the acid-base balance to the acid side (acidosis). Under conditions of acidosis, the full severity of hypoxia begins to manifest itself. Microcirculation in the tissues is disturbed, breathing and blood circulation become inefficient, and eventually there is a complete depletion of reserves and cessation of breathing and blood circulation, i.e. death.

The above mechanisms in acute short-term hypoxia are quickly depleted, which leads to the death of the patient. In chronic hypoxia, they are able to function for a long time, compensating for oxygen starvation, but bring constant suffering to the patient.

First of all, the central nervous system suffers. The brain always receives 20% of all oxygen in the body, this is the so-called. The "oxygen debt" of the body, which is explained by the colossal need of the brain for oxygen. Mild disorders during brain hypoxia include: headaches, drowsiness, lethargy, fatigue, impaired concentration. Severe signs of hypoxia: disorientation in space, impaired consciousness up to coma, cerebral edema. Patients suffering from chronic hypoxia acquire severe personality disorders associated with the so-called. hypoxic encephalopathy.

Change in the shape of the nails and distal phalanges of the fingers. In chronic hypoxia, the nails thicken and acquire a rounded shape resembling "watch glasses". The distal (nail) phalanges of the fingers thicken, giving the fingers the appearance of "drumsticks".

Diagnosis of hypoxia

In addition to the characteristic symptom complex described above, laboratory and instrumental research methods are used to diagnose hypoxia.

Pulse oximetry is the easiest way to determine hypoxia. It is enough to put a pulse oximeter on your finger and in a few seconds the saturation (saturation) of the blood with oxygen will be determined. Normally, this figure is not lower than 95%.

Study of the gas composition and acid-base balance of arterial and venous blood. This type allows for a quantitative assessment of the main indicators of the body's homeostasis: partial pressure of oxygen, carbon dioxide, blood pH, the state of carbonate and bicarbonate buffer, etc.

The study of gases of exhaled air. For example, capnography, CO-metry, etc.

Therapeutic measures should be aimed at eliminating the cause of hypoxia, combating oxygen deficiency, correcting changes in the homeostasis system.

Sometimes, to combat hypoxia, simply ventilating the room or walking in the fresh air is enough. In cases of hypoxia, which was the result of diseases of the lungs, heart, blood or poisoning, more serious measures are required.

. Hypoxic (exogenous)– use of oxygen equipment (oxygen apparatus, oxygen balloons, oxygen pillows, etc.);

. Respiratory (respiratory)- the use of bronchodilators, antihypoxants, respiratory analeptics, etc., the use of oxygen concentrators or centralized oxygen supply up to mechanical ventilation. In chronic respiratory hypoxia, oxygen treatment becomes one of the main components;

. Hemic (blood)- blood transfusion, stimulation of hematopoiesis, oxygen treatment;

. Circulatory- corrective operations on the heart and (or) blood vessels, cardiac glycosides and other drugs with a cardiotropic effect. Anticoagulants, antiplatelet agents to improve microcirculation. In some cases, it is used oxygen therapy .

. Histoxic (tissue)- antidotes for poisoning, artificial ventilation of the lungs, drugs that improve the utilization of oxygen by tissues, hyperbaric oxygenation;

As can be seen from the foregoing, in almost all types of hypoxia, oxygen treatment is used: from breathing with a mixture of oxygen cartridges or oxygen concentrator before before artificial ventilation. In addition, to combat hypoxia, drugs are used to restore the acid-base balance in the blood, neuro and cardioprotectors.

Oxygen cartridges are a budgetary and convenient means of treating hypoxia. They do not require adjustment, special handling skills, maintenance, they are convenient to take with you. Below is a selection of the most popular models of oxygen cartridges:

Hypoxia is a state of oxygen starvation that can be experienced both by the body as a whole and by its individual organs or organ systems.

A variety of factors can provoke hypoxia, including:

• Reduced oxygen content in the inhaled air (for example, during a stay in high mountainous areas);
• Partial or complete violation of air exchange in the lungs due to drowning, suffocation, edema of the lungs or bronchial mucosa, bronchospasm, etc.;
• A decrease in the oxygen capacity of the blood or, in other words, a decrease in the amount of hemoglobin capable of attaching oxygen, because it is he who performs the function of its main transporter (blood hypoxia can occur against the background of carbon monoxide poisoning, anemia or erythrocytolysis);
• Pathological conditions resulting from cardiovascular insufficiency and in which the movement of oxygenated blood to various tissues and organs is difficult or completely impossible (for example, with heart defects, diabetic vascular disease, etc.);
• Disturbances in the processes of oxygen uptake by body tissues (signs of hypoxia may develop due to blocking the activity of enzymes that take part in tissue respiration, toxic substances or salts of heavy metals);
• An increase in the functional load on a tissue or organ (symptoms of hypoxia can be provoked by hard physical work or increased sports loads, when the need for oxygen exceeds its actual intake into the body).

In some cases, oxygen starvation is the result of a combination of the factors listed above.

Hypoxia can also be observed in children during their prenatal development. If such a condition is noted for a long period, it can cause serious disturbances in the metabolism of the fetus. In especially severe cases, the consequences of hypoxia can be ischemia, necrosis of the child's tissues, and even his death.

The main causes of intrauterine fetal hypoxia are:

• Diseases transferred by the mother, including diseases of the heart, blood vessels, lungs, as well as diseases accompanied by a decrease in the concentration of hemoglobin in the blood;
• Congenital malformations of the fetus;
• Violations of the function of the umbilical cord and placenta, including deterioration of placental gas exchange due to premature detachment of the placenta, and interruption of the umbilical circulation due to the formation of knots, compression or entanglement of the fetus;
• Anemia, characterized by a reduced content of hemoglobin in the blood;
• Prolonged mechanical squeezing of the fetus.

Symptoms of hypoxia

Signs of hypoxia are quite diverse and are determined by the degree of severity of the condition, the duration of exposure to the body of an unfavorable factor, as well as the reactivity of the body itself.

In addition, the symptoms of hypoxia are determined by the form in which it occurs. In general, depending on the rate of development of the pathological process, there are:

• lightning fast;
• acute;
• Subacute;
• chronic hypoxia.

Fulminant, acute and subacute forms, in contrast to chronic hypoxia, are characterized by a more pronounced clinical picture. Symptoms of oxygen starvation develop in a fairly fast time frame, not giving the body the opportunity to adapt to them. Therefore, the consequences of acute hypoxia are often more serious for a person than the consequences of chronic oxygen starvation, which is gradually accustomed to. In some cases, they are irreversible.

Chronic hypoxia develops slowly. Thus, patients who are diagnosed with severe forms of respiratory failure on the background of chronic lung diseases can live for years without any dramatic symptoms. However, it should be noted that, like the acute form of oxygen starvation, the chronic one also leads to irreversible consequences. They just develop over a longer period of time.

The most common signs of hypoxia in acute form are:

• The appearance of shortness of breath;
• Increasing the frequency of breathing and its depth;
• Dysfunction of individual organs and systems.

The chronic form is most often characterized by an increase in the activity of erythropoiesis (the process of formation of erythrocytes in the bone marrow) against the background of the development of a pathological condition in which the concentration of erythrocytes per unit volume of blood significantly exceeds those considered physiologically normal. In addition, in the body there is a violation of the function of various organs and their systems.

Treatment of hypoxia

The treatment of hypoxia involves the appointment of a set of measures aimed at eliminating its cause, combating the lack of oxygen, as well as making adjustments to the body's homeostasis system.

In some cases, to eliminate the effects of hypoxia, it is enough to ventilate the room or walk in the fresh air. If the condition is provoked by more serious causes and is associated with diseases of the blood system, lungs, cardiovascular system, or poisoning with toxic substances, the following can be recommended for the treatment of hypoxia:

• Therapy using oxygen equipment (masks, pillows, balloons, etc.);
• Appointment of antihypoxants, bronchodilators, respiratory analeptics, etc.;
• The use of oxygen concentrators;
• Artificial ventilation of the lungs;
• Blood transfusion and stimulation of hematopoiesis;
• Surgical operations correcting the function of the heart and blood vessels;
• Prescribing drugs with a cardiotropic effect;
• The use of antidotes in combination with artificial ventilation of the lungs and the appointment of drugs whose action is aimed at improving the utilization of oxygen by tissues (in case of poisoning).