Hypoxemia why when breathing pure oxygen. Pulse oximetry: the essence of the method, indications and application, norm and deviations

Hypoxemia is a pathology that can occur at any age. It can affect both adults and unborn children. Lack of oxygen cannot be called a disease, but it is quite possible to define a pathological condition. Typically, hypoxemia occurs due to diseases associated with the cardiovascular and respiratory systems. At first glance, a harmless condition is fraught with a threat to the patient’s life, so doctors approach this problem responsibly.

Hypoxemia and its causes

What is hypoxemia? Hypoxemia has a second name - oxygen deficiency. This diagnosis is made if the patient has insufficient oxygen in the blood. But this component is so important for every organ. With its deficiency, all normal processes are disrupted, and the redox balance is gradually disrupted.

It is important to know that excess oxygen is also dangerous, so you need to find that “golden mean” to avoid any deviations. In the absence of health problems, the volume of oxygen in the blood should not exceed 65%. This figure is calculated based on total body weight. If we take a standard person, the weight of oxygen in the blood should be about 40 kg.

The causes of hypoxemia include:

• Excess carbon dioxide in the environment. When this component predominates in the air, oxygen is not able to reach the tissues of the human body. The one and only source of oxygen for the blood is air. It is on its qualitative composition that the entry of O2 into the blood depends.

• Diseases associated with the lungs. When any pathology occurs in the lung tissue, they are unable to cope with the incoming oxygen. Their work is significantly slowed down, because of this gas is consumed more than it is supplied.
• Heart defects of various origins, and the circulation of blood discharge is impaired from right to left. If there are disturbances in the septum of the ventricles of the heart, then a mixing of arterial and venous blood occurs, as a result of which the tissues begin to starve. In this case, hypoxemia or hypoxia develops.
• Oxygen metabolism disorders. In this case, a small percentage of O 2 is delivered from the patient’s blood to the tissues. This condition can occur even in a completely healthy person. For example, if he overloads his body with physical exercise. Blood circulation accelerates, and oxygen, in turn, does not have time to be properly absorbed into the tissues.
• Anemia. In this disease, the occurrence of hypoxemia is very common. This happens because only hemoglobin is involved in the process of transporting O2 in the body. A decrease in this indicator leads to oxygen starvation of tissues.

Experts do not consider hypoxemia as a separate disease. They believe that this condition is caused by some kind of disorder in the human body. To get rid of hypoxemia, it is necessary to find the cause that influenced this condition.

Symptoms of hypoxemia

Symptoms of hypoxemia are usually divided into early and late.

The early ones include:

• quickening breathing;
• dilation of blood vessels;

• increased heart rate;
• pressure drop;
• rapid fatigue;
• indifference to everything around;
• frequent headaches that turn into dizziness;
• very pale skin.

Late symptoms include:

• blue tint of the skin;
• asthma;
• tachycardia;
• swelling noticeable on the legs;
• restless sleep;
• memory losses;
• loss of consciousness;
• sense of anxiety;
• trembling hands and feet.

Symptoms may vary. It all depends on the mechanism of hypoxemia. For example, frequent coughing, fever, and intoxication of the body appear with lung pathologies. They are the ones who cause oxygen starvation.

If the cause of hypoxemia is anemia, then several more symptoms are added:

1. Aversion to food.
2. Dry skin.
3. Deterioration of hair and nails.

If arterial hypoxemia manifests itself in children, then symptoms develop much faster than in adults. This is due to the fact that the child consumes almost twice as much O2. Since babies’ bodies are growing and all systems are still developing, suspicion of hypoxemia should be carefully checked.

If the diagnosis is confirmed, then specialists will quickly determine the cause of this condition and begin active treatment. In the absence of the necessary therapy, a small organism will not be able to cope with such a disease on its own. Unpleasant consequences include disturbances in brain function, respiratory failure and coma.

During the period of bearing a baby, every expectant mother should be aware of the dangers of hypoxemia. Throughout pregnancy, the fetus is supplied with oxygen through the placenta. If there is not enough oxygen in the blood of a pregnant woman, then after some time hypoxemia will develop not only in her, but also in the child.

The causes of hypoxemia in women during pregnancy include:

• neglect of daily walks;
• constant stressful situations;
• anemia;
• pathologies of the heart and blood vessels;
• kidney diseases;
• diabetes;

• incorrect location of the umbilical cord or placental abruption;
• lung pathologies;
• labor activity that began earlier or later than the due date.

The consequences of intrauterine hypoxemia for a child include:

1. Slow heart rate and breathing.
2. No crying after birth.
3. Blue skin tone.
4. Partial absence of reflexes.
5. Decreased muscle activity.

On the part of the patient, only one thing is required - timely visit to the clinic. Further all actions are carried out by specialists. The more accurately the problem is diagnosed, the more successful the treatment will be.

Diagnosis of hypoxemia

Methods for diagnosing hypoxemia for newborns, as well as for adult patients, include:

• hemoximetry, which shows the amount of O 2 in arterial blood. The normal rate ranges from 95 to 98%. If they are lowered, then the patient is prescribed the necessary treatment;

• a complete blood test, which determines the number of red blood cells and also establishes the level of hemoglobin;
• X-ray of the lungs, with which a specialist can determine the presence of problems with the respiratory system;
• An electrocardiogram and echocardiogram are done to confirm or rule out heart defects.

Methods for determining fetal oxygen deficiency include:

• Observing the movements of the unborn baby. A woman must keep track of her movements herself. When the number of movements is less than 10 times per hour, you should pay attention to this and see a doctor.
• A highly invasive procedure called a non-stress test. This study shows the pulse response to fetal movements. In the absence of acceleration, hypoxemia can be judged.
• Ultrasound examination of the unborn baby, which is carried out several times throughout the pregnancy. It determines all parameters, including the presence of oxygen deficiency.
• Doppler ultrasound is used to determine blood flow pathologies.
• Study of amniotic fluid. This test determines the transparency of amniotic fluid. When their color differs from normal, the doctor can diagnose intrauterine hypoxia.

After identifying a problem with the flow of oxygen into the blood, specialists look for the cause that caused this condition. Treatment must begin immediately, otherwise life-threatening consequences will occur.

Treatment of hypoxemia

If a very low oxygen content in the blood is determined, the patient is sent to hospital treatment. This problem cannot be dealt with at home. The patient must comply with bed rest and sleep patterns. If complications or respiratory arrest occur, the patient is prescribed artificial ventilation.

If immediately after birth the baby does not show signs of life, a special electric suction is used, then the following actions are necessary:

1. The baby is placed in an incubator, in which a humid environment is constantly maintained and oxygen is supplied.
2. Monitoring of all blood components, which is carried out by biochemical analysis.
3. Particular attention is paid to breathing, as well as the heart and blood vessels.

There are cases when acute arterial hypoxemia develops. These include bronchial asthma, pulmonary edema, accumulation of oxygen in the pleural cavity or when a foreign object enters the respiratory tract. In this situation, the patient needs urgent help.

Everyone should know what it is:

• First, it is necessary to rid the upper respiratory tract of all unnecessary things.
• Secondly, perform artificial respiration and wait for an ambulance.

In the hospital, the patient is connected to a ventilator.

The prescription of medications also depends on the cause that caused oxygen starvation.

The most popular drugs include:

• sodium oxybate;
• Actovegin;
• trimethylhydrazinium propionate;
• warfarin;
• drotaverine;
• papaverine;
• vitamins C and B.

The list of medications is far from complete. Each of them performs its own action, some complement each other. It is not surprising that in this case you cannot do without vitamins. Everyone knows their positive effect on the immune system.

For patients with hypoxemia, oxygen therapy is performed, during which the blood is saturated with O2. This gas is passed through a special tube that is attached to a mask or nasal catheter. The percentage of blood oxygen saturation after this procedure should not exceed 80%. At the same time, antihypoxic drugs are prescribed.

As for alternative medicine, in this case one should be careful about such therapy. “Grandma’s recipes” are not able to cure the problem. These remedies will help temporarily get rid of symptoms, but not from hypoxemia. It is good to combine drug treatment with folk remedies.

Many herbal teas can dilate blood vessels, thin the blood and slow down oxidative processes. Plants are also known that have the necessary components for a patient with hypoxemia.

The list of such herbs includes:

• mountain sheep;
• hawthorn berries;
• calendula;
• black currant;
• pusher;
• chokeberry.

1. Hawthorn infusion helps to actively reduce blood pressure. To prepare this remedy you will need about 30 g of hawthorn berries and 1 liter of boiled water. The fruits must be steamed in boiling water for at least 8 hours. The prepared infusion is drunk up to four times a day, 100 ml.
2. Nettle tea. You will need a teaspoon of this plant, which must be poured with boiling water. Keep the decoction in this state for an hour, then drink it instead of regular tea. This drink should not be taken by patients who suffer from kidney disease.
3. Freshly squeezed black rowan juice has a beneficial effect on blood vessels. It should be consumed no more than three times a day, one tablespoon at a time.

If the patient decides to try one of the traditional medicines, he should definitely consult with his doctor. He will evaluate the benefit or uselessness of this therapy. Independent decisions made regarding treatment are categorically excluded, since even greater harm can be caused to health.

Treatment outcome and complications

What the prognosis will be depends on the type and course of the disease. Arterial hypoxemia in its acute form is very rarely completely cured. With fulminant hypoxemia, the patient's body is in a state of shock, and in such cases the mortality rate is high. Time passes not even for minutes, but for seconds. The faster you provide qualified assistance, the more likely recovery is.

Complications of this disease include:

• disruptions in the functioning of the nervous system - the occurrence of seizures, organic brain damage, suppression of breathing, as well as the functioning of the heart and blood vessels;
• a sharp drop in blood pressure, irregular pulse;
• pulmonary edema.

Complex arterial hypoxemia in a child in the womb can also cause death. Death can occur both during pregnancy and during childbirth. In practice, there are few cases when little patients were saved, whose mothers neglected scheduled appointments and did not follow all the recommendations of the pregnancy doctor.

There is no point in postponing a visit to the doctor, especially if we are talking not only about your own health, but also about the well-being of future children. The sooner you notice the problem and start treating it, the more favorable the outcome will be.

Prevention of hypoxemia

Preventive measures include the following:

• Every day you need to spend at least half an hour in the fresh air. Especially expectant mothers should not neglect this point. In this case, walks are important not only for them, but also for the fetus.
• Every person should remember about scheduled appointments. It is on them that the onset of the disease can be detected. The sooner treatment begins, the less likely there will be any complications. Hypoxemia is not something to joke about.
• Gymnastic exercises that promote the development of the respiratory system. Many experts recommend sticking to the diaphragmatic breathing technique. This exercise involves vigorous exhalation and inactive inhalation.
• Physical activity should be approached with caution. The heart should not be overloaded. Useful activities include swimming in the pool, yoga, and running.
• Nutrition must be approached with great responsibility. The diet must contain many vitamins to replenish the body with the necessary energy. Healthy foods include fresh fruits and vegetables.

Hypoxemia can be prevented if noticed early. This condition can really be avoided if you follow the rules prescribed by doctors.

If you neglect prevention, as well as attending scheduled appointments with specialists, the consequences can be the most unpleasant. Irreversible processes will begin in all systems of the body. In this case, dealing with the problem will become much more difficult.

Normal functioning of the body is possible only with proper blood circulation, sufficiently saturated with oxygen. With oxygen deficiency, hypoxemia begins to develop, which is a consequence of both a serious illness and a malfunction of the body.

Timely treatment measures will help prevent multiple complications, and prevention will prevent the manifestation of pathology.

Description of the disease

Hypoxemia is a condition that is manifested by insufficient oxygen in a person’s blood. As a result of a decrease in this indicator, all metabolic processes slow down both in cells and tissues.

The oxygen level is indicated by two values:

• saturation;
• tension.

A decrease in the second indicator is facilitated by the uneven functioning of different parts of the lungs, which can be observed with age. As a result, oxygen begins to flow poorly to the cells, which leads to the development of health problems.

A process such as a decrease in tension and oxygen saturation leads to the development of arterial hypoxemia.

Types, classification and characteristic symptoms

All symptoms of hypoxemia are divided into early and late.

The first group includes:

• rapid breathing;
• vasodilation;
• general weakness;
• low blood pressure;
• pale skin;
• dizziness;
• cardiopalmus.

The second group of signs of pathology is characterized by:

• symptoms of cardiac and respiratory failure, such as swelling of the legs, tachycardia;
• disorders in brain function, such as fainting, insomnia, memory impairment, anxiety and others.

There may be chronic or acute hypoxemia.

It should also be noted that the symptoms of the disease will largely depend on the mechanism of its development. Pathology resulting from lung disease may be accompanied by cough, fever, and intoxication. If oxygen deficiency manifests itself against the background of anemia, then lack of appetite, dry skin, and others are observed.

Main reasons

In medical practice, there are five main reasons that can provoke this disease. They can influence both individually and in combination with each other:

1. Atypical blood shunting. With congenital or acquired heart defects, venous blood enters the aorta. Because of this, hemoglobin becomes unable to accept oxygen, resulting in a decrease in the level of the latter.
2. Hypoventilation of lung tissue. With pathologies of this organ, the frequency of exhalation and inhalation slows down. This reduces the amount of oxygen supplied relative to that consumed.
3. Anemia. As a result of a decrease in hemoglobin, the oxygen level index, which spreads through the tissues, also decreases.
4. Reduced oxygen concentration in the air.
5. Diffuse disorders. Increased physical activity helps blood circulate faster. As a result, the time required for hemoglobin to contact oxygen is significantly reduced.

In addition, there are several other factors that can cause hypoxemia:

• excessive smoking;
• heart disease;
• pathologies of the bronchi and lungs;
• changes in atmospheric pressure;
• overweight leading to obesity;
• anesthesia

Hypoxemia can often occur in newborns. This occurs as a result of a lack of oxygen in the mother's body during gestation.

How is the treatment carried out?

Therapeutic therapy is primarily aimed at eliminating the root cause that provoked this condition.

If moderate or severe pathology occurs, treatment is carried out inpatiently. Bed rest and quality sleep are required.

Medicines are also prescribed depending on the factors that contributed to the development of the pathology. Drug therapy may include the following medications and methods:

• Anticoagulants - Heparin, Warfarin. Prescribed to prevent the formation of thromboembolism in the arteries of the lungs.
• Antihypoxants - Actovegin, Cytochrome C. Their action is aimed at restoring oxidative processes. Drugs in this group are prescribed for any form of hypoxemia.
• Papaverine and No-Shpa help reduce blood pressure and prevent pulmonary edema.
• The vitamin complex is used as a strengthening agent that combats oxygen starvation.
• Fluid therapy improves blood flow and prevents shock.

Oxygen therapy is used to increase oxygen levels in the blood. This method is recommended to be combined with taking antihypoxic drugs.

What could be the consequences?

Pathologies of mild and moderate severity are quite easy to treat. If treatment is not started in a timely manner, the development of complications such as:

• encephalopathy;
• hypotension;
• stroke;
• pulmonary edema;
• arrhythmia;
• convulsions.

If hypoxemia is observed in the fetus, then the following are possible:

• intrauterine growth retardation;
• death of the baby in the womb, during labor or immediately after he is born;
• onset of labor prematurely or with severe complications;
• lag in mental and physical development in the future.

Acute, fulminant hypoxemia can provoke the most unfavorable complications, since it contributes to hypoxemic coma of the body.

Preventive measures

In order to prevent the development of a pathology such as hypoxemia, it is necessary to follow simple recommendations, which are as follows:

• daily walks in the fresh air;
• moderate physical activity;
• performing breathing exercises;
• taking a vitamin-mineral complex, especially in autumn and winter;
• consumption of vegetables and fruits;
• timely diagnosis of pathologies of the cardiovascular and respiratory systems.

Hypoxia can be prevented. The main thing is to adhere to the rules for preventing oxygen deficiency, and if signs of illness are detected, immediately seek medical help. If you do not start treating the pathology in time, then it is possible that irreversible consequences may develop in the lungs, brain and the body as a whole.

Causes of arterial hypoxemia

Arterial hypoxemia is a consequence and a sign of impaired ability of the respiratory system to oxygenate venous blood flowing to the lungs.

The only exceptions are dyshemoglobinemia, in which, by the way, pulse oximetric monitoring of Sp02 is ineffective due to gross artifacts.

The value of pulse oximetry is not limited to recognizing arterial hypoxemia and monitoring its dynamics. Sometimes it is possible to determine the cause of impaired blood oxygenation in the lungs and, therefore, choose the optimal method of correction.

It should be noted that the capabilities of pulse oximetry in the differential diagnosis of hypoxemia are more modest than those of laboratory or monitor gas analysis, because the existing system for describing gas exchange disorders is traditionally focused on parameters such as tension, concentration and partial pressure of respiratory gases. The insufficient accuracy of SpO2 measurement and the always present probability of a shift in the oxyhemoglobin dissociation curve do not allow the use of this parameter to calculate PaO2. But still, pulse oximetry, in comparison with gas analysis, has an undeniable advantage: at present, it is the only widely available way to provide indefinitely long-term continuous monitoring of the degree of arterial blood oxygen saturation.

Continuous monitoring of arterial hemoglobin saturation, combined with an understanding of the typical mechanisms of pulmonary gas exchange disorders, allows a number of valuable conclusions to be drawn.

There are several techniques that can be used to clarify the cause of hypoxemia detected by a pulse oximeter.

1. It is necessary to take into account the clinical situation in which arterial hypoxemia occurs and compare SpO2 with the data of laboratory and instrumental studies. For example, if hypoxemia is diagnosed in a patient with fresh unrecovered blood loss, then the most likely reason for the decrease in SpO2 is a violation of regional ventilation-perfusion relationships in the lungs. Such hypoxemia is easily corrected by simple oxygen inhalation and infusion.

2. The amplitude of the photoplethysmogram in some cases allows us to confirm assumptions based on observations of SpO2. In the example above (a patient with unreplaced blood loss), the pulse oximeter display shows a decrease in PPG peaks, as well as “respiratory waves” - fluctuations in the curve synchronous with breathing - which are characteristic of hypovolemia.

3. The reaction of SpO2 to various therapeutic effects (oxygen therapy, infusion, PEEP mode, change in body position, etc.) is highly informative. Thus, persistently reduced saturation even against the background of the use of oxygen in high concentrations is characteristic of massive shunting of blood in the lungs.

4. Studying the dynamics of saturation, which is best judged by the SpO2 trend, also allows us to draw certain conclusions. An unexpected sharp decrease in SpO2 is characteristic of sudden events, such as displacement of the endotracheal tube into the bronchus or the development of tension pneumothorax. A gradual decrease in saturation, which cannot be normalized by oxygen therapy and selection of a mechanical ventilation regimen, is typical for complex gas exchange disorders that occur, for example, with RDS or total pneumonia. Labile hypoxemia is observed when sputum accumulates in the bronchi, periodically disrupting the ventilation of some regions of the lungs.

5. It is advisable to combine pulse oximetry with other methods of respiratory monitoring (capnography, oximetry, spirometry). Data from different monitors complement each other and even in complex cases help to restore the picture of pulmonary gas exchange disorders.

Causes of arterial hypoxemia. There are five of them (they can occur separately, but often they are combined):

Hypoventilation;

Decreased oxygen content in the inhaled gas;

Shunting blood in the lungs;

Hypoventilation of individual pulmonary zones;

Impaired diffusion of oxygen from the alveoli into the blood of the pulmonary capillaries.

In each of the above cases, hypoxemia deepens as the body's need for oxygen increases.

Pulse oximetry for hypoventilation and apnea. A decrease in the minute volume of pulmonary ventilation leads to a decrease in oxygen delivery to the alveoli and impaired evacuation of carbon dioxide from the alveolar space. At the same time, the delivery of carbon dioxide from the periphery to the alveoli and the extraction of oxygen from them by blood flowing through the lungs do not stop. As a result, the oxygen content in the alveolar gas decreases and the CU2 concentration increases. The gas composition of the blood flowing from the lungs changes accordingly.

With hypoventilation, arterial hypoxemia develops, detected by a pulse oximeter by a decrease in SpO2, and hypercapnia, accompanied by dilation of arterioles, an increase in PPG amplitude and tachycardia (Fig. 1.11).

The degree of hypo- or hyperventilation is traditionally assessed by CO tension in arterial blood, because the value of this indicator depends only on the correspondence of the minute volume of alveolar ventilation to the rate of carbon dioxide production. Intrapulmonary oxygen exchange obeys much more complex laws. Therefore, a decrease in Sp02 can definitely be associated with hypoventilation only when there are real clinical prerequisites for this and there is no reason to suspect the involvement of other mechanisms causing hypoxemia.

Diagnosis of hypoventilation by a decrease in SpO2 in each case requires a mandatory correlation of the value of this indicator with a specific clinical situation.

The undoubted advantage of pulse oximetry in case of hypoventilation is the timely recognition of this disorder by the most dangerous consequence - hypoxemia, which can quickly lead to serious complications.

A pulse oximeter responds to a sudden decrease in ventilation volume much earlier than a capnograph.

How quickly does arterial hypoxemia develop during respiratory arrest? For an anesthesiologist and intensivist, the answer to this question is of exceptional practical importance. After all, we are talking about the time that a specialist has to manage to intubate a patient after administering a muscle relaxant, or about the permissible duration of sputum aspiration in a patient undergoing mechanical ventilation, or about any other situation when apnea occurs or is artificially induced.

In general, the rate of occurrence and development of hypoxemia after stopping ventilation is determined by two factors: (1) the body's need for oxygen and (2) the body's oxygen reserves available for use in the physiological PaO2 range.

The oxygen requirement of an adult at rest is on average 250 ml/min. With adequate anesthesia, it decreases to 200 ml/min, and with insufficient anesthesia it can increase. An increased need for oxygen is observed during hypermetabolic conditions, such as stress.

Rice. 1.11. Apnea episodes on SpO2 trend during air breathing

The conventions of the values ​​given here are obvious. Minute oxygen consumption depends on body weight and metabolic state, which in turn is determined by many factors: muscle tremors, hyperthermia or septic shock. The leader among hypermetabolic conditions is malignant hyperthermia syndrome - a rare complication of general anesthesia, in which the need for oxygen increases tenfold.

Oxygen reserves in the body are small and in an adult breathing air they average 1.5 liters, and when breathing pure oxygen they increase to 4-4.5 liters. Therefore, preliminary ventilation of the patient with oxygen (preoxygenation) significantly increases the permissible duration of subsequent apnea. This can be verified by viewing SpO2 trends recorded, for example, during intubations during induction of anesthesia*.

The volume of oxygen in the lungs when breathing atmospheric air is about 450 ml, and when breathing pure oxygen it increases to 3 liters (the size of the functional residual capacity, FRC - the volume of gas contained in the lungs at the end of a quiet exhalation).

Any pathology that leads to a decrease in FRC or impairs the use of this oxygen reserve shortens the period between the moment of respiratory arrest and the onset of arterial hypoxemia.

Listed below are the main reasons for the decrease in FRC, knowledge of which allows us to identify from the general mass of patients a group of special risk in relation to the accelerated development of hypoxemia during apnea:

Obesity;

High intra-abdominal pressure (intestinal paresis, ascites, pregnancy, etc.), especially in the supine position or in the Trendelenburg position;

Relaxation of the diaphragm;

Reducing the amount of working lung tissue (extensive lung resections, pneumonia, atelectasis, RDS, sputum plugs, pneumo- or hemothorax, etc.);

General anesthesia;

Newborn period.

A number of problems associated with preoxygenation are discussed in more detail in Chap. "Oximetry".

The main causes of violation of intrapulmonary gas utilization:

Alveolar dead space (thrombosis and embolism of pulmonary vessels) - oxygen in such areas is not available for use;

The presence in the lungs of large areas with a pronounced predominance of ventilation over blood flow (low pressure in the pulmonary artery, for example, with hypovolemia).

Human blood contains about 850 ml of oxygen, mainly bound to hemoglobin. When breathing pure oxygen, its supply increases to approximately 950 ml. With apnea or hypoventilation, this reserve begins to be used up from the moment the oxygen level in the alveolar gas drops below normal. The rate of deepening of hypoxemia largely depends on the amount of gas contained in the blood.

With unreplenished blood loss or anemia, the safe duration of apnea is shortened.

In children, especially newborns, hypoxemia due to apnea develops much faster than in adults.

How soon does a pulse oximeter detect hypoventilation or apnea?

When breathing atmospheric air, there is practically no excess oxygen in the lungs, which could maintain normal PaO2 levels for some time under apnea conditions. Therefore, any delay in the delivery of new portions of oxygen to the alveoli quickly leads to a decrease in the partial pressure of this gas in the lungs and the occurrence of arterial hypoxemia. A noticeable decrease in saturation occurs within 30 s after a sudden reduction in the volume of ventilation, but a portion of arterial blood carrying this information requires 5-10, and in case of circulatory disorders - up to 40 s or more, to reach the pulse oximetry sensor. Add 2 to 15 seconds to this time to update the numbers on the display monitor. Thus, a pulse oximeter requires an average of 40 to 60 s (and up to 2 min in case of low minute volume) to detect hypoventilation or apnea caused by a sudden event, such as tongue retraction, kinking of the endotracheal tube, recurarization or depressurization of the respirator circuit .

In terms of the speed of reaction to sudden hypoventilation, a pulse oximeter is second only to a high-speed oximeter - a monitor designed to measure the concentration of oxygen in exhaled gas, and in case of apnea - also to a capnograph, which in this case records the cessation of fluctuations in the concentration of carbon dioxide.

Before the introduction of pulse oximetry, doctors treating such patients were forced to be guided only by the above factors and act in accordance with the expected scenario for the development of events. Pulse oximetry made it possible to measure what previously had to be judged by a very unreliable external sign - the rate of appearance and increase in cyanosis. As a result, the permissible period of tracheal intubation in an obese patient or the effectiveness of preoxygenation before sputum aspiration in a patient with RDS ceased to be convincing physiological abstractions, but turned into specific digital indicators that are easy to monitor in any patient.

Thus, thanks to the daily practice of working under monitor control, it was possible to reconsider the clinical significance of diffusion hypoxia that occurs during recovery from anesthesia with nitrous oxide, determine the preoxygenation regime before tracheal intubation, and understand some other assumptions, recommendations and rituals.

The most important role of monitoring is to provide an opportunity for an understanding specialist to see and evaluate the operation of the pathophysiological mechanisms in the patient. This is why in anesthesiology and intensive care, monitoring serves as a bridge between physiological concepts and the reality of clinical practice. The habit of analyzing monitoring data and “fitting” them into a specific clinical situation is very useful, since this is how the ability to understand the essence of what is happening is formed and meaningful clinical experience is accumulated. In the end, the monitor is a kind of additional sense organ for the doctor, and it is a shame to use its capabilities at the level of the simplest conditioned reflexes.

In those cases. When hypoventilation develops gradually, over several hours or days (as, for example, with polyradiculoneuritis or myasthenic crisis), the capnograph and pulse oximeter react to it synchronously. In such situation

The undoubted advantage of pulse oximetry is the possibility of performing long-term monitoring in a non-intubated patient. The dynamics of the increase in breathing disorders can be monitored by the SpO2 trend (Fig. 1.12).

Unfortunately, the possibilities of pulse oximetry described above are applicable only when the patient is breathing atmospheric air. With an increase in the oxygen concentration in the inhaled or inhaled gas, even a small tidal volume is enough to ensure that the required amount of oxygen enters the alveoli.

During oxygen therapy, even deep hypoventilation may not be accompanied by a decrease in SpO2 and, accordingly, may not be detected by a pulse oximeter.

Hypoxemia caused by hypoventilation is quickly and completely eliminated in two ways (they can be combined):

increasing the volume of ventilation and increasing the oxygen concentration in the respiratory mixture. Oxygen therapy allows you to overcome the most dangerous manifestation of hypoventilation in the shortest possible time (without eliminating the hypoventilation itself), and pulse oximetry allows you to monitor the result; Very often this is enough to buy time to take more radical measures.

What should be the concentration of oxygen in the respiratory mixture to eliminate hypoxemia caused by hypoventilation? It is known that this indicator depends on the degree of decrease in minute volume of ventilation and on the body’s need for oxygen. However, in practical work this knowledge is useless, because no one ever calculates FiQ2

Rice. 1.12. SpO2 trend with gradually progressive hypoventilation

in advance. The parameter is always chosen intuitively and often turns out to be higher or lower than necessary. In many cases, changes in the patient's condition subsequently require a corresponding change in the oxygen concentration in the inhaled gas.

Pulse oximetry allows you to correctly select the oxygen concentration both during hypoventilation and other disorders of blood oxygenation in the lungs, and to continuously monitor the adequacy of oxygen therapy. (This topic is discussed in more detail below.)

It must be remembered that it is impossible to get rid of carbon dioxide retention in the body in this way. Therefore, the capnograph provides information about hypoventilation even when it is masked by oxygen therapy and is not recognized by a pulse oximeter.

Reduced oxygen content in the inhaled gas. As the oxygen content in the inspired gas decreases, the partial pressure of oxygen in the alveoli decreases. As a result, oxygen tension and, accordingly, hemoglobin saturation in the blood flowing from the lungs drop and after some time are established at a new, lower level. In this case, the pulse oximeter detects arterial hypoxemia, the severity of which depends on the degree of decrease in Fi02.

Excessive concentration of other components of the gas mixture (usually nitrous oxide);

A significant drop in atmospheric pressure (breathing rarefied air at high altitudes or transporting a patient in an airplane with an unpressurized cabin).

The oxygen content in the gas mixture is measured by an oximeter - a monitor specifically designed for this purpose. However, oximeters are still not available in all anesthesia and intensive care departments, and the method itself, to which a separate chapter is devoted in this book, is used much less frequently than pulse oximetry. Therefore, most likely the signal about trouble will come from the pulse oximeter, and the cause of hypoxemia will have to be determined depending on the situation.

For any desaturation that occurs during anesthesia using nitrous oxide, it is necessary first to check the correct dosage of oxygen and anesthetic.

Shunt-induced hypoxemia. Pulmonary shunting is one of the most common causes of arterial hypoxemia in patients in the intensive care unit and operating room.

A shunt is a portion of the pulmonary blood flow that passes through unventilated areas of the lungs. Venous blood flowing to the lungs and entering the shunts does not change its composition and, at the exit from the lungs, it meets blood flowing from normally functioning alveoli. As a result of mixing these two flows, arterial blood is formed, the oxygen tension in which is reduced due to the admixture of venous blood (Fig. 1.13). Therefore, blood shunting is classified as a group of pulmonary gas exchange disorders, united under the name “venous admixture”.

Rice. 1.13. Shunting blood in the lungs

A variety of reasons contribute to the cessation of ventilation of individual blood supply areas of the lungs:

* complete obstruction of part of the respiratory tract with plugs of viscous sputum, aspirated vomit, blood clots, tumor, etc.; with sealed endobronchial intubation, an entire lung can instantly turn into a shunt;

Pneumonia - in pneumonic foci, the alveoli are airless, as they are filled with exudate, and the blood flow is increased due to inflammatory hyperemia;

Micro- and macroatelectasis are perhaps a particularly common cause of bypass surgery;

With alveolar pulmonary edema, areas filled with transudate turn into a shunt;

Massive shunting of blood occurs in respiratory distress syndrome (RDS) through areas of interstitial edema and consolidation of alveolar tissue, multiple microatelectasis and areas of local bronchial obstruction.

Another probable mechanism of shunting is the opening of arteriovenous anastomoses that exist in the lungs, but do not function under normal conditions. The existence of such anastomoses has been proven experimentally, but in general the problem has not been sufficiently studied. It is assumed that these anastomoses are designed to discharge part of the venous blood during a sharp increase in pressure in the pulmonary artery.

Shunting can be reduced or eliminated only by eliminating its cause. An increase in SpO2 after removing sputum, “coughing” the patient, using the PEEP (PEEP) or NPD (CPAP) modes, increasing the average pressure in the airways during mechanical ventilation, or pulling up an endotracheal tube inserted too deeply indicates that the cause arterial hypoxemia was shunted.

The degree of arterial hypoxemia directly depends on the volume of shunting. However, with the same volume of shunting, SpO2 is lower in patients with anemia, reduced cardiac output, or increased oxygen demand. In such patients, tissues intensively extract oxygen from arterial blood. As a result, venous blood flows away from the organs with a sharply reduced oxygen content. Shunting venous blood into the lungs with an abnormally low oxygen content further reduces Sp02. Therefore, correction of hypoxemia caused by shunting also includes measures to normalize systemic

hemodynamics and elimination of anemia. Pulse oximetry allows you to monitor the effectiveness of these measures”;

Unfortunately, in many cases one cannot count on quick removal of the shunt; on the contrary, the progression of pneumonia, RDS or aspiration pneumonitis is accompanied by the involvement of more and more areas of lung tissue in the pathological process, an increase in the shunt and a deepening of hypoxemia.

To gain the time needed to treat critical pulmonary pathology, oxygen therapy is used, which reduces hypoxemia during working shunts.

The mechanism of action of oxygen therapy for hypoxemia caused by a shunt is quite simple. When breathing air, blood flows away from the normally functioning pulmonary zones, the hemoglobin of which is 94-98% saturated with oxygen. In patients with thickened alveolocapillary membranes, this figure may be lower due to diffusion disorders. The use of a gas mixture with an increased concentration of oxygen makes it possible to saturate the remaining 2-6% of hemoglobin in the blood flowing through the functioning alveoli, and also to increase, albeit slightly, the amount of oxygen dissolved in the plasma. With a small volume of shunting, this additional amount of oxygen entering the blood flowing from healthy pulmonary areas is enough to raise the saturation of the blood coming from the shunts to normal levels. It is clear that with massive shunting this mechanism is ineffective and hypoxemia remains resistant to oxygen therapy.

It is believed that in cases where up to 10% of the minute volume of blood circulation is shunted in the lungs, hypoxemia can be completely eliminated by inhalation of 30% oxygen. With a 30% shunt, SpO2 can be normalized only by using pure oxygen. When the shunt volume exceeds 50% of the total blood flow, hypoxemia is resistant to oxygen therapy, and even with 100% oxygen it is possible to increase SpO2 by only a few percent. Knowing the mechanism of action of oxygen therapy during bypass surgery, it is not difficult to understand why this is so. Of course, the figures given here are indicative in nature, but are very typical for the vast majority of cases. The reaction of SpO2 to an increase in the concentration of oxygen in the inhaled gas is an important criterion in the diagnosis of blood shunting in the lungs.

Hypoxemia with regional hypoventilation. Shunting of blood in the lungs occurs when ventilation of the blood supply to the lung area is completely stopped. However, ventilation of individual pulmonary zones is often maintained, but becomes insufficient to ensure normal gas exchange in them. Regional hypoventilation occurs.

Ideally, the volume of ventilation of the lungs in general and each pulmonary region in particular; must correspond to the volume of general and regional blood flow. But even in a healthy person, in the lungs, along with such “ideal” regions, there are areas where ventilation is excessive in relation to blood flow (zones with high ventilation-perfusion ratios). The hemoglobin saturation of the blood flowing from these zones is several percent higher than in ideal regions.

There are also regions whose ventilation is insufficient to fully process the flow of venous blood (areas with low ventilation-perfusion ratios). From such areas, blood arrives with reduced saturation. Normally, excess blood saturation in some regions effectively compensates for the lack of saturation in others. In this way, a normal gas composition of arterial blood is formed (Fig. 1.14).

Rice. 1.14. The influence of differences in regional ventilation-perfusion ratios on SpO2 when breathing atmospheric air

The capabilities of this natural compensatory mechanism are limited by the oxygen capacity of the main oxygen carrier - hemoglobin and are sufficient only for normally functioning lungs.

Under pathological conditions, the volume of regions with low ventilation-perfusion ratios sometimes increases so much that full compensation becomes impossible. When the flow of underoxygenated blood from hypoventilated regions increases sharply, the few additional percent saturation gained by the small flow of blood in hyperventilated areas is unable to correct the situation. Arterial hypoxemia occurs, which a pulse oximeter helps to detect.

The development of hypoxemia according to the mechanism described above occurs only when the patient breathes air.

Increasing the oxygen concentration in the inhaled or inhaled gas (FiO2) to 25-50% can significantly increase, and in many cases completely normalize SpO2.

Hyperventilation (spontaneous or instrumental) with ventilation-perfusion imbalance also contributes to an increase in Sp02, but its effectiveness is less than that of oxygen therapy.

The appearance of areas in the lungs with low ventilation-perfusion ratios is due to two reasons: (1) a local decrease in ventilation or (2) a local increase in blood flow.

Ventilation of the region may decrease due to narrowing of the bronchus, decreased extensibility of individual sections of the lung tissue, paresis or painful limitation of the mobility of one of the domes of the diaphragm, unilateral pneumo-, hemo- or hydrothorax. The main specific causes of impaired ventilation of individual pulmonary regions:

Reduction of bronchial lumen due to accumulation of sputum;

Regional bronchiolospasm;

Swelling of the mucous membrane of the bronchioles, predominant in the lower parts of the lungs;

Compression of small bronchi by infiltrates during RDS or focal pneumonia;

Partial closure of large bronchi with a deeply inserted endotracheal tube;

Tumor, presence of a foreign body in the bronchi;

Increased stiffness of certain areas of the lung tissue, for example with interstitial edema, predominant in the lower zones;

Newly expanded atelectasis;

Expiratory closure of the airways.

A local increase in pulmonary blood flow occurs as a result of its pathological redistribution. When the pressure in the pulmonary artery decreases and becomes insufficient to lift blood into the upper zones of the lungs, blood flow is carried out mainly through the underlying sections, the ventilation of which no longer corresponds to the increased blood flow. A similar picture is observed with an increase in intrapulmonary pressure (for example, during mechanical ventilation), which compresses the alveolar capillaries in the upper zones of the lungs and thereby directs blood flow to the lower regions, where the capillary pressure is higher. A particularly pronounced decrease in Sp02 is observed when these two factors are combined, for example, during mechanical ventilation against the background of hypovolemia.

Reasons for redistribution of pulmonary blood flow, which can cause arterial hypoxemia:

Decrease in pulmonary artery pressure:

Hypovolemia, including hidden; "

General anesthesia;

The use of certain vasodilators acting on the arterioles of the small circle;

Decreased minute volume of blood circulation;

High intrapulmonary pressure:

PEEP.NPD;

Auto-PEEP.

Even a cursory acquaintance with this short list allows us to conclude that the redistribution of blood flow in the lungs is influenced by reasons of a functional nature: disorders, blood circulation, the effects of medications, ventilation modes. In these

In cases of hypoxemia, it occurs not due to damage to the bronchopulmonary apparatus, but as a result of a violation of its operating conditions. Timely correction of functional disorders leads to rapid normalization of Sp02.

So, arterial hypoxemia, caused by a decrease in regional ventilation-perfusion ratios, is generated by a wide variety of reasons (a combination of them is possible). A pulse oximeter can detect a decrease in Sp02 in a patient with bleeding, high spinal or epidural block, sputum retention, pneumothorax, or a “hard” mode of mechanical ventilation; and in all these cases, the same mechanism for the development of hypoxemia works - insufficient ventilation of individual pulmonary regions in relation to blood flow. This circumstance explains the phenomenon common to all of these situations: the rapid and complete elimination of arterial hypoxemia by inhalation of oxygen in a relatively low concentration. That is why hypoxemia caused by regional hypoventilation is more often observed in patients breathing atmospheric air. Oxygen therapy in many cases; is able to mask this type of pulmonary gas exchange disorders. The mechanism of action of oxygen therapy on gas exchange in hypoventilated regions is similar to that on the lungs as a whole during general hypoventilation: it is enough to increase the oxygen concentration in hypoventilated alveoli to normalize the saturation of the blood flowing through them.

Hypoxemia in diffusion disorders. The theoretical aspects of impaired diffusion of Oxygen through the barrier separating erythrocyte hemoglobin from alveolar gas have been developed in sufficient detail. This, unfortunately, cannot be said about the clinical assessment of diffusion disorders during anesthesia and intensive care. Despite clear ideas about the mechanisms of impaired oxygen diffusion in the lungs, practical critical care medicine currently does not have publicly available methods for identifying (not to mention accurately quantifying) diffusion disorders in a particular patient.

A decrease in the diffusion capacity of the lungs primarily affects the transfer of oxygen from the alveoli to the blood. The intrapulmonary exchange of carbon dioxide does not suffer even with severe diffusion disorders, since CO2, due to its high solubility in aqueous media, has a very high penetrating ability.

The causes of impaired diffusion of oxygen from the alveoli into the blood of the pulmonary capillaries are quite diverse:

Reduction in the total area of ​​functioning alveoli (reduction in effective respiratory surface):

Extensive resection of lung tissue, pneumonectomy;

Multiple atelectasis, lung collapse;

Extensive pneumonia;

Massive thromboembolism of the pulmonary vessels;

Thickening of the alveolocapillary membrane due to its edema or fibrosis;

In both cases, hypoxemia increases with an increase in the linear speed of blood movement through the pulmonary vessels, when the time the erythrocyte remains in the capillary is not enough to complete hemoglobin saturation:

Hyperdynamic circulatory conditions (sepsis, infusion of adrenomimetics, physical activity, etc.):

Reducing the number of functioning pulmonary vessels: pulmonary resections, thrombosis and embolism in the pulmonary system.

The three factors listed above, which limit diffusion and cause arterial hypoxemia, occur in various pathologies.

Hypoxemia caused by diffusion disorders is usually easily eliminated by oxygen inhalation.

With an increase in oxygen concentration in the alveoli, the driving force of diffusion increases - the difference in gas voltage on both sides of the alveolo-capillary membrane. As a result, hypoxemia decreases or disappears, although the reason for which it arose remains. Only in cases of extremely severe diffusion disorders can the effect of oxygen therapy be incomplete.

In clinical practice, hypoxemia developing as a result of diffusion disorders is observed very often, but, unfortunately, in each case we can only assume the presence of disorders, relying on common sense and knowledge of applied physiology.

Hypoxemia of mixed origin

Often, arterial hypoxemia is generated by several mechanisms acting simultaneously. Let's look at two examples of how to use pulse oximetry data in such patients to diagnose these mechanisms and determine pathogenetically based measures for correcting hypoxemia.

Situation: a patient, a few minutes after the injection of a local anesthetic solution into the epidural catheter, developed a clinical picture of a total spinal block with a sharp decrease in SpO2. The pulse oximeter display shows the appearance of respiratory waves.

Causes of hypoxemia: (1) general hypoventilation caused by relaxation of the intercostal muscles and diaphragm, and (2) regional hypoventilation due to redistribution of pulmonary blood flow caused by relative hypovolemia.

Problems: Mechanical ventilation, which may be required to solve the first problem, leads to a critical decrease in venous return and increases the uneven distribution of pulmonary blood flow.

Correction of hypoxemia: (1) inhalation of 100% oxygen through a mask or endotracheal tube, (2) in case of severe hypoventilation - auxiliary ventilation, preferably in high-frequency mode with minimal positive pressure, and in case of apnea - mechanical ventilation (better - HF ventilation or ventilation with active exhalation ), (3) forced infusion therapy, use of ephedrine or other vasopressors.

Hypoventilation

Comatose state

Cerebral edema

Any doubt about the adequacy of spontaneous breathing

PO2=80 mmHg.рСО2=36 mmHg.

The pathophysiological basis for the use of corticosteroids in traumatic brain injury is:

Sodium retention

Increased blood sugar levels

Anti-inflammatory effect and immunosuppression

Reduced cell membrane permeability

In severe diabetic acidosis, there is

Normal Anion Gap

Whole body hyperhydration

Hypoventilation

Plasma hyperosmolarity

Increased intracellular potassium concentration

Characteristic signs of hypoglycemic coma are

Dehydration

Convulsions

Decreased tendon reflexes

Hyperventilation

Polyuria

It is not typical for thyrotoxic crisis:

Feeling of heat in the body

Bronchospasm

Abdominal pain

Hormones of the adrenal cortex that influence carbohydrate, fat and protein metabolism include

Deoxycorticosterone acetate (DOXA)

Cortisone

Estradiol

All listed hormones

The pituitary gland influences secretion

Hypothalamus and adrenal cortex

Adrenal medulla

Pancreas

All listed glands

Changes in electrolyte balance with long-term use of ACTH or cortisone

Lead to metabolic acidosis

Lead to metabolic alkalosis

Doesn't make any major changes

Lead to a decrease in sodium in the body

Lead to a decrease in interstitial space

The optimal option for anesthesia for Caesarean section in a pregnant woman with diabetes mellitus is

Epidural anesthesia

Endotracheal anesthesia

Mask anesthesia

Combination of epidural anesthesia and endotracheal anesthesia

The optimal method of anesthesia for pain relief during normal labor and operative delivery is

Local anesthesia

Epidural anesthesia

Mask anesthesia

Endotracheal anesthesia

The dose of ketamine used for intramuscular injection for labor analgesia is

12-16 mg/kg

17-20 mg/kg

When general anesthesia is indicated, the optimal anesthetics for induction of anesthesia for Caesarean section are:

Hexenal or ketamine

Nitrous oxide

Clinical manifestations of Mendelssohn syndrome are all of the following, except:

Rapidly onset bronchiolospasm

Cyanosis, swelling of the jugular veins

Hypertension followed by collapse

Decreased central venous pressure

Pulmonary edema

Drugs for induction of anesthesia during cesarean section in pregnant women with eclampsia or preeclampsia include

Barbiturates

Sombrevin

It is not typical for the state of acute hypoxemia

Increased pulmonary artery pressure

Increased cardiac output

Regional pulmonary vasoconstriction

Decreased cerebral blood flow

Decreased myocardial blood flow

With fat embolism it is typical

Detection of fat globules in urine and retinal vessels

Mental confusion

Petechiae and increased levels of fibrinogen degradation products

All listed symptoms

Pulmonary embolism can be accurately diagnosed

By scanning or angiography of the lungs

X-ray examination of the chest

Blood lactate dehydrogenase level

All answers are correct

Patients with acute seizure disorders can be treated with

Barbiturates and benzodiazepines

Ketamine

Droperidol

All listed drugs

Ringer's lactate (Hartmann's solution)

Generates bicarbonate

Has a lactate concentration of 40 mmol/l

Contains 10 mmol/l chlorine

Does not contain magnesium

Does not contain calcium

In a patient during the recovery period after drowning in sea water, clinical manifestations are very likely

Intrapulmonary shunting and metabolic acidosis

Pulmonary edema

Electrolyte disturbances

Everything is true

The cause of syncope may be

Aortic valve insufficiency

Hypercapnia

Everything is true

Decompression sickness

Causes avascular necrosis of bone

Caused by O2 deficiency in the alveoli

Treated by inhaling a mixture of O2 and helium

Develops within a day after decompression

It can be avoided if helium is added to the inhaled gas mixture

Treatment of a patient with acute left ventricular failure includes

Breathing or mechanical ventilation with constant high blood pressure

Nitroglycerin infusion

Phosphodiesterase inhibitors, furosemide

All answers are correct

If signs of digoxin toxicity develop, treatment includes intravenous administration.

Verapamil

Lidocaine

All answers are correct

Swollen (stretched) neck veins in a standing position are observed when

Cardiac tamponade

Tension pneumothorax

Pulmonary embolism

All answers are correct

Hypotension in anaphylactic shock develops due to

Increased vascular permeability and loss of intravascular fluid volume

Loss of sympathetic tone

Prostaglandin release

Bradycardia

All of the above

A satisfactory oxygen capacity of the blood is ensured by a hematocrit, not lower than

Intravenous administration of morphine for cardiogenic pulmonary edema can achieve the following positive effects:

Venodilation and decentralization of blood circulation

Sedation, decreased respiratory rate

Unloading of the pulmonary circulation

All of the above are true

Vasodilators that act primarily on arterioles and reduce afterload include:

Ganglioblockers

Nitroprusside

The leading symptom for the diagnosis of circulatory arrest is:

Wide pupils that do not respond to light

Lack of consciousness

Lack of breathing

Absence of carotid pulse

The most pronounced positive inotropic effect in cardiogenic shock is observed when administered:

Norepinephrine

Dopamine

Digoxin

Izadrina

Ephedrine

The easiest way to eliminate pain during an emergency call for acute myocardial infarction is:

Administration of narcotic and non-narcotic analgesics

Epidural analgesia

Inhalation of nitrous oxide, xenon with O2 (1:1)

The cardiotoxic effect of hyperkalemia is stopped by using:

Adrenaline hydrochloride

Caffeine, ephedrine hydrochloride

Calcium preparations (Ca chloride, Ca gluconate)

10% glucose solution

Corticosteroids

In acute respiratory distress syndrome in adults,

Increased alveolar ventilation

Decreased alveolar-arterial PO2 gradient

Decreased pulmonary surfactant activity

Increased compliance of the lungs

Reduced airway resistance

For acute respiratory distress syndrome in adults

Total pulmonary water is reduced

Functional residual capacity increased

Hypoxemia responds to increased FiO2

The cause may be kidney failure

Pulmonary arterial pressure is increased

An increase in PaCO2 can be expected with

Massive pulmonary embolism

Moderate asthmatic attack

Kidney failure

Diabetic coma

Alveolar hypoventilation often develops in patients

When ICP increases

Emphysema and asthma

In the presence of metabolic alkalosis

All answers are correct

Positive end expiratory pressure (PEEP) reduces

Intrathoracic blood volume

Functional residual capacity

Intracranial pressure

Pulmonary capillary wedge pressure (wedge)

An attack of bronchial asthma is accompanied by:

Reducing the volume and rate of forced expiration

Increasing residual volume

Increased resistance to exhalation

All answers are correct

The reason for a significant decrease in blood oxygen saturation when opening the pleural cavity on one side is:

Forced position of the patient

Decrease in % oxygen in inspired air

Effect of anesthetic

Venous shunt in a collapsed lung

Pathological reflexes from the wound

In severe chest injuries, gas exchange is impaired due to all of the following reasons, except:

Circulatory disorders in the microcirculation system

Obstruction of the tracheobronchial tree

Chest frame disorders

Fat embolism of pulmonary vessels

Disturbances of the central mechanisms of respiratory regulation

Newborns with respiratory distress syndrome have

Decreased pulmonary blood flow

Left-to-right cardiac shunt

Normal alveolar surfactant activity

Metabolic alkalosis

All listed violations

For a child on mechanical ventilation with normal warming and humidification of the gas mixture, the volume of daily infusion should be reduced

The main sign of the severity of a traumatic brain injury in a child is

Severity of bone-traumatic injuries

Degree of loss of consciousness

Severity of meningeal syndrome

All answers are correct

Decongestant therapy for traumatic brain injury in children is indicated because it prevents

Hematoma growth

Development of cerebral edema

Increased intracranial pressure

All answers are correct

Acute stenotic tracheobronchitis in children is characterized by:

2) extended exhalation

3) retraction of the intercostal spaces during inspiration

Everything is true

1 and 3 are correct

For grade III croup, the duration of steam oxygen inhalation should be:

Before a productive cough appears

The frequent development of respiratory distress syndrome in premature infants is mainly due to:

Smaller alveolar diameter than in adults

Initial surfactant deficiency

Fewer alveoli

Hypovolemia

All answers are correct

The PO2 value in arterialized capillary blood in a healthy child under 1.5 years of age is:

86 mmHg Art.

92 mmHg Art.

95 mmHg Art.

98 mmHg Art.

The normal breathing rate in newborns is

16 per minute

24 per minute

30 per minute

40 per minute

50 per minute

A child's tidal volume is approximately

11-12 ml/kg

The percentage of fetal hemoglobin in newborns is

The set (initial) value of peak pressure at the start of mechanical ventilation in a full-term newborn should be considered

10-15 cm water. Art.

20-25 cm water. Art.

25-35 cm water. Art.

30-40 cm water. Art.

40-50 cm water. Art.

The set (initial) respiratory rate at the beginning of mechanical ventilation of a newborn should be considered

15-25 per minute

30-40 per minute

40-60 per minute

50-70 per minute

70-80 per minute

The optimal PEEP value during the transfer of a newborn from mechanical ventilation to spontaneous breathing is considered

2-3 cm here. Art.

5 cm water. Art.

5-10 cm water. Art.

10 cm water. Art.

10-15 cm water. Art.

The optimal temperature for heating the insufflated gas mixture during mechanical ventilation in children with a normal condition of the mucous membrane of the tracheobronchial tree is

The minimum gas flow through the patient circuit during mechanical ventilation of a newborn with a time-cycling constant-flow pressure-controlled ventilator is

The normal daily water requirement for a healthy newborn at 15 days of age is

The minimum hematocrit value in a newborn, at which blood transfusion is not required even after blood loss, is

The average amount of blood relative to body weight in a newborn in the first day of life is

Spinal puncture is the first-priority diagnostic measure in children

If intracranial hemorrhage is suspected

With convulsive status

With long-term cerebral edema

If you suspect meningitis

All answers are correct

The most common cause of seizure syndrome in young children is

Purulent meningitis

Epilepsy

Acute poisoning

Encephalic response to viral infections

Lead to the development of generalized seizures in children

Epilepsy

Encephalitis

Brain hemorrhage

Acute poisoning

Intubation should be replaced by tracheostomy through

The decision is made individually

The most effective detoxification method for most acute poisonings in children is

Forced diuresis

Exchange blood transfusion

Peritoneal dialysis

Hemosorption

The most appropriate treatment for carbon monoxide poisoning in children is

Exchange blood transfusion

Oxygen inhalation

Hyperbaric oxygenation

Hemosorption

The most characteristic symptoms of poisoning with atropine-like substances include

Salivation, bronchospasm, constriction of pupils

Depression of consciousness, constriction of pupils

Skin hyperemia, hallucinations, dilated pupils

Tonic-clonic seizures

Gastric lavage in an unconscious child with poisoning is permissible:

Lying on your side with your head down

In the supine position

After identifying the poison

After tracheal intubation

The shunt through the ductus arteriosus in a newborn in the first hours of life is

Has the strongest pulmonary vasodilating effect

Nitroprusside

Ftorotan

Nitric oxide

Tolazoline

Magnesium sulfate

In case of poisoning with an unknown poison, it should be administered as an antidote.

Do not enter

Unithiol, chromosmon, atropine

Unithiol is used as an antidote for poisoning

Insulin

Amitriptyline

Ethylene glycol, methyl alcohol

Heavy metals

When bitten by snakes of the asp family (cobra), the following develop:

Severe tissue swelling, lymphangitis, lymphadenitis

Hemolysis, thrombohemorrhagic syndrome

Muscle paralysis, breathing problems

All answers are correct

Has the greatest analgesic activity:

Thiopental

Calypsol

Diprivan

Sombrevin

Hexenal

Alpha blockers include:

Novodrin

Tropaphen

Norepinephrine causes:

Arterial spasm and varicose veins

Dilatation of arteries and spasm of veins

Dilatation of arteries and veins

Spasm of arteries and veins

Dilatation of arteries in certain areas

The greatest vasoconstrictor effect has:

Novocaine

Lidocaine

Beta-2 adrenergic agonists cause

Hypokalemia

Bronchoconstriction

Increased motility of the gastrointestinal tract

Increased contractions of the pregnant uterus

Nitroglycerin infusion increases

Intracranial pressure

Oxygen consumption by the brain decreases under the influence of

Thiopentone and propofol (diprivan)

Nimodipina