What causes breathing problems after a stroke and how to deal with it. Ventilator. Devices for artificial lung ventilation. Medical equipment Artificial ventilation after surgery

Artificial ventilation is used not only in case of sudden cessation of blood circulation, but also in other terminal conditions, when the activity of the heart is preserved, but the function of external respiration is sharply impaired (mechanical asphyxia, extensive trauma to the chest, brain, acute poisoning, severe arterial hypotension, areactive cardiogenic shock , status asthmaticus and other conditions in which metabolic and gas acidosis progresses).

Before you begin to restore breathing, it is advisable to make sure that the airways are clear. To do this, it is necessary to open the patient’s mouth (remove dentures) and use your fingers, a curved clamp and a gauze pad to remove food debris and other visible foreign objects.

If possible, aspiration of the contents is used using an electric suction through a wide lumen of a tube inserted directly into the oral cavity, and then through a nasal catheter. In cases of regurgitation and aspiration of gastric contents, it is necessary to thoroughly clean the oral cavity, since even minimal reflux into the bronchial tree causes severe post-resuscitation complications (Mendelssohn syndrome).

Patients with acute myocardial infarction should limit themselves in food, since overeating, especially in the first day of the disease, is often the direct cause of sudden cessation of blood circulation. Carrying out resuscitation measures in these cases is accompanied by regurgitation and aspiration of gastric contents. To prevent this formidable complication, you need to give the patient a slightly elevated position, raising the head end of the bed, or create a Trendelenburg position. In the first case, the danger of reflux of stomach contents into the trachea is reduced, although during mechanical ventilation a certain part of the inhaled air enters the stomach, its stretching occurs, and with indirect cardiac massage, regurgitation sooner or later occurs. In the Trendelenburg position, it is possible to evacuate the leaking stomach contents using an electric suction followed by insertion of a probe into the stomach. Carrying out these manipulations requires certain time and appropriate skills. Therefore, you first need to slightly raise the head end, and then insert a probe to remove the stomach contents.

The applied method of strong pressure on the epigastric region of the patient to prevent overdistension of the stomach can cause evacuation of air and stomach contents, followed by immediate aspiration.

It is customary to start mechanical ventilation with the patient lying on his back with his head thrown back. This promotes complete opening of the upper respiratory tract, as the root of the tongue extends from the back wall of the pharynx. If there is no ventilator at the scene, you should immediately begin mouth-to-mouth or mouth-to-nose breathing. The choice of mechanical ventilation technique is mainly determined by muscle relaxation and patency of the corresponding part of the upper respiratory tract. With sufficient muscle relaxation and a free (passable for air) oral cavity, it is better to breathe mouth to mouth. To do this, the resuscitator, tilting the patient's head back, pushes the lower jaw forward with one hand, and tightly closes the victim's nose with the index and thumb of the other hand. After a deep breath, the resuscitator, pressing his mouth tightly to the patient’s half-open mouth, makes a forced exhalation (within 1 s). In this case, the patient’s chest rises freely and easily, and after opening the mouth and nose, passive exhalation is carried out with the typical sound of exhaled air.

In some cases, it is necessary to perform mechanical ventilation in the presence of signs of spasm of the masticatory muscles (in the first seconds after a sudden stop of blood circulation). It is not advisable to spend time inserting a mouth dilator, as this is not always possible. Mouth-to-nose ventilation should be started. As with mouth-to-mouth breathing, the patient’s head is thrown back and, having previously clasped the area of ​​the patient’s lower nasal passages with his lips, a deep exhalation is made.

At this time, the thumb or index finger of the resuscitator’s hand, supporting the chin, covers the victim’s mouth. Passive exhalation is carried out mainly through the patient’s mouth. Typically, when breathing mouth to mouth or mouth to nose, a gauze pad or handkerchief is used. They, as a rule, interfere with mechanical ventilation, as they quickly become wet, become knocked down and prevent the passage of air into the patient’s upper respiratory tract.

In the clinic, various air tubes and masks are widely used for mechanical ventilation. It is most physiological to use an S-shaped tube for this purpose, which is inserted into the oral cavity above the tongue before entering the larynx. The patient's head is tilted back, an S-shaped tube is inserted 8-12 cm with a bend towards the pharynx and fixed in this position with a special cup-shaped flange. The latter, located in the middle of the tube, tightly presses the patient’s lips to it and ensures adequate ventilation of the lungs. The resuscitator is located behind the patient’s head, with the little fingers and ring fingers of both hands he pushes the lower jaw forward, with his index fingers he tightly presses the flange of the S-shaped tube, and with his thumbs he closes the patient’s nose. The doctor exhales deeply into the mouthpiece of the tube, after which an excursion of the patient's chest is noted. If, when inhaling into the patient, there is a feeling of resistance or only the epigastric region is raised, it is necessary to tighten the tube slightly, since perhaps the epiglottis is wedged above the entrance to the larynx or the distal end of the tube is located above the entrance to the esophagus.

In this case, with continued ventilation, the possibility of regurgitation of the stomach contents cannot be excluded.

It is easier and more reliable in emergency situations to use a conventional anesthesia-breathing mask, when the exhaled air of the resuscitator is blown through its fitting. The mask is hermetically fixed to the victim’s face, throwing back the head in the same way, pushing out the lower jaw, as when breathing through an S-shaped tube. This method is reminiscent of mouth-to-nose ventilation, since when the anesthesia-breathing mask is tightly fixed, the victim’s mouth is usually closed. With a certain skill, the mask can be positioned so that the oral cavity opens slightly: for this, the patient’s lower jaw is pushed forward. For better ventilation of the lungs using an anesthesia-breathing mask, you can first introduce an oropharyngeal airway; then breathing is carried out through the victim’s mouth and nose.

It must be remembered that with all methods of expiratory ventilation based on blowing resuscitator air into the victim, the oxygen concentration in the exhaled air should be at least 17-18 vol%. If resuscitation measures are carried out by one person, then with an increase in his physical activity, the oxygen concentration in the exhaled air drops below 16 vol% and, of course, the oxygenation of the patient’s blood sharply decreases. In addition, although when saving the life of a patient, hygienic precautions during mechanical ventilation using the mouth-to-mouth or mouth-to-nose method fade into the background, they cannot be neglected, especially if resuscitation of infectious patients is carried out. For these purposes, any department of a medical institution must have devices for manual ventilation. Such devices allow ventilation through an anesthesia-breathing mask (as well as through an endotracheal tube) with ambient air or oxygen from a centralized oxygen system or from a portable oxygen cylinder to the suction valve of a reservoir tank. By adjusting the oxygen supply, you can achieve from 30 to 100% of its concentration in the inhaled air. The use of devices for manual ventilation makes it possible to reliably fix the anesthesia-breathing mask to the patient’s face, since active inhalation into the patient and his passive exhalation are carried out through a non-reversible breathing valve. The use of such breathing apparatus for resuscitation requires certain skills. The patient’s head is tilted back, the lower jaw is pushed forward with the little finger and held by the chin with the ring and middle fingers, the mask is fixed with one hand, holding it by the fitting with the thumb and forefinger; With the other hand, the resuscitator squeezes the breathing bellows. It is best to choose a position behind the patient's head.

In some cases, especially in the elderly with no teeth and atrophied alveolar processes of the jaws, it is not possible to achieve a tight seal between the anesthesia-respiratory mask and the victim’s face. In such a situation, it is advisable to use an oropharyngeal airway or perform mechanical ventilation after sealing the mask only with the patient’s nose with the oral cavity tightly closed. Naturally, in the latter case, a smaller anesthesia-breathing mask is selected, and its sealed rim (obturator) is half filled with air. All this does not exclude errors in the implementation of mechanical ventilation and requires preliminary training of medical personnel on special mannequins for cardiopulmonary resuscitation. Thus, with their help, you can practice basic resuscitation measures and, most importantly, learn to determine the patency of the airways with sufficient chest excursion, and estimate the amount of inhaled air. For adult victims, the required tidal volume ranges from 500 to 1000 ml. If air is inflated excessively, lung rupture is possible, most often in cases of emphysema, air entering the stomach, followed by regurgitation and aspiration of stomach contents. True, in modern manual ventilators there is a safety valve that releases excess air into the atmosphere. However, this is also possible with insufficient ventilation of the lungs due to obstruction of the airways. To avoid this, constant monitoring of chest excursion or auscultation of breath sounds is necessary (necessarily on both sides).

In emergency situations, when the patient’s life depends on a few minutes, it is natural to strive to provide assistance as quickly and efficiently as possible. This sometimes entails sudden and unjustified movements. Thus, throwing back the patient’s head too vigorously can lead to impaired cerebral circulation, especially in patients with inflammatory diseases of the brain or traumatic brain injury. Excessive air injection, as mentioned above, can result in lung rupture and pneumothorax, and forced mechanical ventilation in the presence of foreign bodies in the oral cavity can contribute to their dislocation into the bronchial tree. In such cases, even if it is possible to restore cardiac activity and breathing, the patient may die from complications associated with resuscitation (lung rupture, hemo- and pneumothorax, aspiration of gastric contents, aspiration pneumonia, Mendelssohn syndrome).

The most adequate way to perform mechanical ventilation is after endotracheal intubation. At the same time, there are indications and contraindications for performing this manipulation in case of sudden cessation of blood circulation. It is generally accepted that in the early stages of cardiopulmonary resuscitation one should not waste time on this procedure: during intubation, breathing stops, and if it is technically difficult to perform (short neck in the victim, stiffness in the cervical spine), then due to worsening hypoxia death may occur. However, if for a number of reasons, in particular due to the presence of foreign bodies and vomit in the airways, mechanical ventilation cannot be performed, endotracheal intubation becomes extremely necessary. In this case, with the help of a laryngoscope, visual control and thorough evacuation of vomit and other foreign bodies from the oral cavity are carried out. In addition, the introduction of an endotracheal tube into the trachea makes it possible to establish adequate mechanical ventilation, followed by aspiration of the contents of the bronchial tree through the tube and appropriate pathogenetic treatment. It is advisable to insert an endotracheal tube in cases where resuscitation lasts more than 20-30 minutes or when cardiac activity has been restored, but breathing is severely impaired or inadequate. Simultaneously with endotracheal intubation, a gastric tube is inserted into the stomach cavity. For this purpose, under the control of a laryngoscope, an endotracheal tube is first inserted into the esophagus, and a thin gastric tube is inserted through it into the stomach; then the endotracheal tube is removed, and the proximal end of the gastric tube is brought out through the nasal passage using a nasal catheter.

Endotracheal intubation is best performed after preliminary mechanical ventilation using a manual breathing apparatus with 100% oxygen supply. For intubation, it is necessary to tilt the patient's head back so that the pharynx and trachea form a straight line, the so-called "classic Jackson position". It is more convenient to place the patient in the “improved Jackson position”, in which the head is thrown back, but raised above the level of the bed by 8-10 cm. Having opened the patient’s mouth with the index finger and thumb of the right hand, with the left hand, gradually pushing the tongue with the instrument slightly to the left and up from the blade, A laryngoscope is inserted into the oral cavity. It is best to use a curved laryngoscope blade (McIntosh type), placing its end between the anterior wall of the pharynx and the base of the epiglottis. By lifting the epiglottis by pressing the end of the blade on the anterior wall of the pharynx at the site of the glosso-epiglossal fold, the glottis is made visible. Sometimes this requires some external pressure on the anterior wall of the larynx. With the right hand, under visual control, an endotracheal tube is inserted into the trachea through the glottis. In intensive care settings, it is advisable to use an endotracheal tube with an inflatable cuff to prevent the flow of stomach contents from the oral cavity into the trachea. The endotracheal tube should not be inserted beyond the glottis beyond the end of the inflatable cuff.

With the correct placement of the tube in the trachea, both halves of the chest rise evenly during breathing; inhalation and exhalation do not cause a feeling of resistance: during auscultation over the lungs, breathing is carried out evenly on both sides. If the endotracheal tube is mistakenly inserted into the esophagus, then with each breath the epigastric region rises, there are no breath sounds during auscultation of the lungs, and exhalation is difficult or absent.

Often the endotracheal tube is passed into the right bronchus, obstructing it, then breathing is not heard on the left, and the opposite scenario for the development of such a complication cannot be ruled out. Sometimes, if the cuff is overinflated, it can cover the opening of the endotracheal tube.

At this time, with each inhalation, an additional amount of air enters the lungs, and exhalation is sharply difficult. Therefore, when inflating the cuff, it is necessary to focus on the control balloon, which is connected to the obturator cuff.

As already indicated, in some cases endotracheal intubation is technically difficult. This is especially difficult if the patient has a short, thick neck and limited mobility in the cervical spine, since with direct laryngoscopy only part of the glottis is visible. In such cases, it is necessary to insert a metal guidewire (with an olive at its distal end) into the endotracheal tube and bend the tube more sharply, allowing it to be inserted into the trachea.

To avoid perforation of the trachea with a metal conductor, the endotracheal tube with the conductor is inserted a short distance (2-3 cm) behind the glottis and the conductor is immediately removed, and the tube is passed into the patient’s trachea with gentle translational movements.

Endotracheal intubation can also be performed blindly, with the index and middle fingers of the left hand inserted deep into the root of the tongue, the middle finger pushing the epiglottis forward, and the index finger identifying the entrance to the esophagus. The endotracheal tube is passed into the trachea between the index and middle fingers.

It should be noted that endotracheal intubation can be performed under conditions of good muscle relaxation, which occurs 20-30 s after cardiac arrest. In case of trismus (spasm) of the masticatory muscles, when it is difficult to open the jaws and place the laryngoscope blade between the teeth, conventional tracheal intubation can be performed after preliminary administration of muscle relaxants, which is not entirely desirable (prolonged cessation of breathing due to hypoxia, difficult restoration of consciousness, further depression of cardiac activity) , or try to insert an endotracheal tube into the fuck through the nose. A smooth tube without a cuff with a pronounced bend, lubricated with sterile petroleum jelly, is inserted through the nasal passage towards the trachea under visual control during direct laryngoscopy using guide intubation forceps or forceps.

If direct laryngoscopy is not possible, you should try to insert the endotracheal tube into the trachea through the nose, using as a control the appearance of respiratory sounds in the lungs when air is blown into them.

Thus, during cardiopulmonary resuscitation, all methods of ventilation can be successfully used. Naturally, expiratory methods of ventilation such as mouth-to-mouth or mouth-to-nose breathing should be used only if there are no manual ventilators at the scene.

Every doctor should be familiar with the technique of endotracheal intubation, since in some cases only the insertion of an endotracheal tube into the trachea can provide adequate mechanical ventilation and prevent serious complications associated with regurgitation and aspiration of gastric contents.

For prolonged mechanical ventilation, volumetric respirators of the RO-2, RO-5, RO-6 types are used. As a rule, mechanical ventilation is performed through an endotracheal tube. The ventilation mode is selected depending on the partial tension of carbon dioxide and oxygen in the arterial blood; Mechanical ventilation is carried out in the mode of moderate hyperventilation. To synchronize the operation of the respirator with the patient’s spontaneous breathing, morphine hydrochloride (1 ml of 1% solution), seduxen (1-2 ml of 0.5% solution), and sodium hydroxybutyrate (10-20 ml of 20% solution) are used. True, it is not always possible to achieve the desired effect. Before administering muscle relaxants, ensure that the airway is patent. And only in case of sudden agitation of the patient (not associated with hypoxia due to errors in mechanical ventilation), when narcotic drugs do not lead to the switching off of spontaneous breathing, short-acting muscle relaxants (ditilin 1-2 mg/kg body weight) can be used. Tubocurarine and other non-depolarizing muscle relaxants are dangerous to use due to the possibility of a further decrease in blood pressure.

Prof. A.I. Gritsyuk

“In what cases is artificial ventilation of the lungs carried out, methods of mechanical ventilation” section

Page 29 of 43

A patient needs mechanical ventilation only as long as his spontaneous breathing is insufficient or is accompanied by too much energy consumption. Unjustified prolongation of artificial respiration can bring nothing but harm. However, deciding on the timeliness of stopping mechanical ventilation, especially long-term ventilation, is not always easy. Perhaps the second most common mistake when performing mechanical ventilation in intensive care practice is premature shutdown of the respirator. This can easily cause re-development of hypoxia and negate all previous efforts. Here is an observation.
A 41-year-old patient underwent surgery for a tumor of the middle lobe of the right lung. During the lobectomy, massive bleeding occurred and clinical death occurred. Cardiac activity was restored by direct cardiac massage after 4-5 minutes. After the end of the operation, transfusion of 1500 ml of blood and 1750 ml of plasma substitutes, the patient with stable hemodynamics was transferred to the postoperative intensive care unit, where mechanical ventilation was continued. After 7 hours, consciousness was restored, a reaction to the endotracheal tube appeared, and therefore mechanical ventilation was stopped and the trachea was extubated. Respiratory functions were not determined by gas analysis and blood CBS was not performed.
4 hours after extubation, the patient stopped answering questions and responded poorly to calls. On examination, the pulse is 132 per minute, blood pressure is 140/60 mmHg. Art., capillary blood PO2 60 mm Hg. Art., РсО2 38 mm Hg. Art. The trachea was re-intubated and mechanical ventilation was resumed. The condition improved somewhat, the tachycardia decreased, but there was no complete restoration of consciousness.
After 2 days, the patient follows simple instructions, fixes his gaze, sometimes shows signs of understanding speech addressed to him and recognizes those around him. Hemodynamics are stable, breathing in the lungs on the right is weakened, and the X-ray shows signs of incipient right-sided lower lobe pneumonia. When the respirator is turned off, spontaneous breathing is rhythmic, 18 per minute, “medium depth” (?). During mechanical ventilation with (FiO2 = 0.6) PO2 of capillary blood is 95 mm Hg, 15 minutes after switching off - 70 mm Hg. Art. Under these conditions, the trachea was extubated again. After 2 hours, the medical history noted: “Spontaneous breathing is adequate.” However, all signs of consciousness gradually disappeared, which was regarded as cerebral edema. Dehydration therapy (mannitol, Lasix) did not improve the condition. 11 hours after repeated cessation of mechanical ventilation, a tracheostomy was performed and artificial respiration was resumed. It was not possible to achieve an improvement in the condition. On the 12th day after the operation, the patient died.
Pathological examination: edema and swelling of the brain, bilateral focal bronchopneumonia, fibrinous pleurisy on the right.
When deciding on the possibility of transferring a patient to spontaneous breathing, many authors consider monitoring clinical symptoms and blood gases to be the main thing. There is an opinion that if the respiratory rate does not exceed 30 per minute, and PaO2 for 1 hour does not exceed 35-40 mm Hg. Art., then mechanical ventilation can be stopped. However, a number of researchers believe that after switching off the respirator, post-hyperventilation hypoxia may be observed and, in general, PaO2 in the first hours after stopping mechanical ventilation is too inconsistent and variable to serve as a reliable criterion for the adequacy of spontaneous breathing. According to E.V. Vikhrov (1983), the absence of hypercapnia during spontaneous breathing cannot serve as a basis for complete cessation of mechanical ventilation.
We consider it necessary to emphasize that stopping mechanical ventilation is a very important moment. After prolonged artificial respiration, disconnection of the respirator can cause adverse hemodynamic changes - a decrease in cardiac output, an increase in vascular resistance in the pulmonary circulation and an increase in right-to-left shunting in the lungs. During the transition to independent breathing, the patient needs not less, but perhaps even more attention and care.
Ventilation can be stopped only if there is significant regression of the underlying pathological process that caused breathing problems. It is necessary to eliminate hypovolemia and gross metabolic disorders.
If the duration of mechanical ventilation is no more than 24 hours, then it can most often be stopped immediately. The main conditions under which you can try to turn off the respirator are:
restoration of clear consciousness;
stable hemodynamics for at least 2 hours, pulse less than 120 per minute, urine output rate at least 50 ml/h without the use of diuretics;
absence of severe anemia (hemoglobin content not less than 90 g/l), hypokalemia (plasma potassium not less than 3.5 mmol/l) metabolic acidosis (BE not less than -4 mmol/l).
Before turning off the respirator, you must once again count the pulse, measure blood pressure, determine gases and blood oxygen levels. Immediately after stopping mechanical ventilation, after 5, 10 and 20 minutes of spontaneous breathing, the pulse and number of respirations should be determined again, blood pressure, MOD and vital capacity should be measured. Increasing tachycardia and arterial hypertension, a progressive increase in MOD, respiration more than 30 per minute, vital capacity below 15 cm3/kg are contraindications to continued spontaneous breathing. If the condition remains stable, does not worsen, and vital capacity exceeds 15 cm3/kg, observation should be continued. After 30 and 60 minutes, it is necessary to repeat the analysis of gases and blood CBS. Capillary blood PO2 is below 75 mmHg. Art. (under conditions of oxygen inhalation) and a progressive decrease in PcO2, as well as increasing metabolic acidosis, serve as indications for the resumption of mechanical ventilation. Re-monitoring of blood gases and CBS, external respiration indicators is mandatory after 3; 6 and 9 hours after tracheal extubation. After stopping mechanical ventilation, it is useful to allow the patient to breathe oxygen for 11/2-2 hours with an exhalation resistance of 5-8 cm of water. Art. using a special mask or some other device. We must not forget that the appearance of well-being in terms of breathing does not necessarily mean the absence of respiratory failure and hidden hypoxia.
When mechanical ventilation lasts for several days, stopping it immediately is most often impractical. The conditions under which the transition to spontaneous breathing can begin, along with those listed above, are:
absence of inflammatory changes in the lungs (or their significant regression), septic complications, hyperthermia;
absence of hypercoagulation syndrome;
good tolerance by patients to short-term cessation of mechanical ventilation (when changing body position, suction, changing the tracheostomy cannula);
PaO2 not lower than 80 mm Hg. Art. at Fi0, no more than 0.3 during the day;
restoration of the cough reflex and cough impulse.
A valuable method for judging the adequacy of spontaneous breathing after cessation of mechanical ventilation is electroencephalography. G.V. Alekseeva (1984) found that when the respirator is turned off prematurely, despite the patient’s clear consciousness and the absence of clinical signs of respiratory failure, the EEG begins to register a flattening of the alpha rhythm after 10-15 minutes, and beta activity may appear. If mechanical ventilation is not resumed, then after 40-60 minutes PaO2 decreases and signs of respiratory failure develop. In the most severe cases, immediately after the flattening of the alpha rhythm, slow waves appear in the theta rhythm range. Following this, a disturbance of consciousness may occur, leading to coma. When mechanical ventilation is resumed, consciousness and the alpha rhythm on the EEG are quickly restored. The appearance of a delta rhythm should be considered especially unfavorable, which is a harbinger of rapidly occurring respiratory decompensation and loss of consciousness. Thus, we can assume that changes in the EEG are an early indicator of tension and exhaustion of compensatory mechanisms, and a discrepancy between the patient’s capabilities and the increased work of breathing.
Before stopping long-term mechanical ventilation, Fi02 should be gradually reduced and psychological preparation of the patient should be carried out. During the period of cessation of artificial respiration, the patient’s condition is monitored as described above, but along with the listed tests, D(A-a)O2 studies are of great importance: it should be no more than 350 mm Hg. Art. when breathing 100% oxygen and Vd/Vt no more than 0.5. When trying to inhale from a confined space, the patient must create a vacuum of at least -30 cm of water column. (Table 9).
Even with good clinical and instrumental indicators, the first period of spontaneous breathing should not exceed 1.5-2 hours, after which mechanical ventilation should be resumed for 4-5 hours and a break taken again. You can start turning off the respirator only in the morning and afternoon hours. At night, mechanical ventilation should be resumed, and the next day it should be interrupted again under the control described above.

Criterion

In conditions of mechanical ventilation

After disconnecting the respirator

Clinical
signs

Clear consciousness, stable blood pressure, pulse less than 100 per minute, diuresis of at least 50 ml/h, absence of pneumonia, sepsis, hyperthermia, restoration of coughing

Respiratory rate no more than 30 per minute, no progressive tachycardia, arterial hypertension and complaints of lack of air

Laboratory
data

PO2 of capillary blood is not lower than 75 mm Hg. Art., РсО2 does not tend to decrease, metabolic acidosis does not increase

Functions of respiration and gas exchange

MOP does not increase, vital capacity is more than 15 cm3/kg, forced expiratory volume is more than 10 cm3/kg, vacuum when inhaling from a confined space is more than -30 cm of water. Art., Vp/Vx less than 0.5, D(A-a)o.. at Fi0 = 1.0 no more than 300 mm Hg. Art.

By increasing and increasing the periods of spontaneous breathing, mechanical ventilation is stopped for the entire day, and then for the whole day. After prolonged mechanical ventilation (more than 6-7 days), the period of transition to independent breathing usually lasts 2-4 days.
The transition to spontaneous breathing can be facilitated by using the intermittent mandatory ventilation (IPPV) technique described in Chapter III. PPVL is especially indicated for patients who have undergone long-term mechanical ventilation in the PEEP mode.
When using a RO-6 respirator for PPVL, it is recommended to start with a forced breath rate of about 20 per minute (key “2c”). Then, every 20-30 minutes, forceful breaths are reduced to 3-4 per minute, all the time maintaining a positive pressure of at least 5 cm of water in the respiratory tract. Art. Such sessions of PPVL with a constant decrease in instrumental inhalations usually take 3-31/2 hours; they can be repeated 2-3 times a day.
As studies have shown [Vikhrov E.V., Kassil V.L., 1984], PPVL facilitates the patient’s adaptation to independent breathing and prevents the development of decompensation. During the transition from mechanical ventilation to PPVL, PasO2 increases to subnormal values, good oxygenation of arterial blood is maintained without increasing energy costs. Similar data were obtained by R. G. Hooper and M. Browning (1985). As a rule, patients prepared to stop mechanical ventilation subjectively tolerate PPV sessions well. After carrying out PPVL with the most infrequent mode of forced breaths for 1 - 11/2 hours, you can completely turn off the respirator under the control described above. The next day, it is also advisable to begin the next cessation of mechanical ventilation with a PPV session, but forced breaths can be reduced much faster - every 10-15 minutes. If PPVL is accompanied by a deterioration in the patient’s condition and reducing the frequency of forced breaths is impossible, then the patient is not ready to stop mechanical ventilation.
In the first 2-3 days, some patients do not tolerate prolongation of periods when the respirator is turned off by more than 30-40 minutes, not because of a deterioration in their condition, but for purely subjective reasons. In such cases, we do not recommend immediately extending mechanical ventilation breaks. It is better to increase their frequency up to 8-10 times a day, and then gradually and unnoticed by the patient to increase the time of spontaneous breathing.
After prolonged mechanical ventilation (more than 4-6 weeks), some patients become accustomed not so much to hypocapnia as to constant mechanical stretching of the lungs. In this regard, a decrease in tidal volume causes them to feel a lack of air even at a relatively low Raso, and the cessation of mechanical ventilation leads to debilitating hyperventilation. In such situations, L. M. Popova (1983), K. Suwa and N. N. Bendixen (1968) recommend increasing the dead space of the respirator. Indeed, by gradually increasing it from 50 to 200 cm3, it is possible to achieve an increase in PaO2 to 35-38 mm Hg. Art., after which patients switch to independent breathing much more easily. An increase in the dead space of the device is achieved by connecting additional sections of hose of increasing length, and therefore volume, between the tee connecting the inhalation and exhalation hoses and the tracheostomy cannula adapter.

Nevertheless, the patient’s complaints of fatigue and a feeling of lack of air should be treated carefully and the process of stopping mechanical ventilation should not be forced.
If a decrease in Pco and a moderate decrease in Po of capillary blood during the first shutdown of the respirator are not accompanied by any clinical signs of deterioration of the patient’s condition, then we recommend not to rush into resuming mechanical ventilation, but to repeat the study after 1* /2-2 hours. Often during this time adaptation to new living conditions occurs and external respiration functions improve. But if, while feeling well, vital capacity decreases, then it is necessary to resume mechanical ventilation.
It should be borne in mind that turning off a respirator with a humidifier and a warmer of inhaled air can dry out and cool the mucous membrane of the respiratory tract and impair their patency. During spontaneous breathing, it is recommended to supply oxygen to the opening of the tracheostomy cannula through a steam inhaler or UDS-1P humidifier. Decannulation should also not be over-delayed. The question about it can be raised after the patient has spent a day (including the night) without mechanical ventilation. A prerequisite for decannulation is restoration of the act of swallowing1. Before removing the cannula from the trachea, the patient should be examined by an otolaryngologist.
*T. V. Geironimus (1975) recommends giving the patient water colored with methylene blue, and then checking the contents of the trachea for the presence of dye.
If mechanical ventilation lasted more than 5 days, then it is advisable to carry out decannulation in several stages: 1) replace the cannula with an inflatable cuff with a plastic one without a cuff and of a smaller diameter; 2) if the patient’s condition has not worsened, then the next day replace this tube with a cannula of minimal diameter; 3) on the 2nd day, remove the cannula and tighten the skin wound with an adhesive plaster. The patch must be changed at least 3-4 times a day.
During the process of replacing cannulas and after decannulation, the patient should also be under the supervision of an otolaryngologist. After the tube is completely removed from the trachea, the patient should be taught to talk and cough while pressing down on the bandage with a finger. The wound after tracheostomy quickly heals by secondary intention.
The doctor’s desire to stop mechanical ventilation as soon as possible is understandable, but not always justified. This issue should be resolved on the basis of objective tests, which are quite accessible in a modern intensive care unit. To avoid premature shutdown of the respirator with all its dangerous consequences, it is necessary to take into account a set of parameters and their dynamics. The more severe the patient’s condition before the start of mechanical ventilation and the longer the period of hypoxia, the slower the body’s adaptation to independent breathing occurs. Sometimes stopping mechanical ventilation takes significantly longer than continuous respiratory therapy. The following observation illustrates this point well.
A 50-year-old patient was admitted to the intensive care unit on October 17, 1974 with a diagnosis of diffuse pneumosclerosis with the development of bronchiectasis, cor pulmonale. He has suffered from bronchial asthma for many years. On admission: consciousness is preserved, complains of lack of air. Severe cyanosis of the skin, acrocyanosis. Breathing 40 per minute, shallow. Blood pressure 160/110 mm Hg, pulse 130 per minute. In the lungs, breathing is weakened in all parts, there is a lot of dry and wet rales. The radiograph shows pulmonary emphysema, pneumosclerosis, congestive pulmonary pattern, residual effects of pulmonary edema Pco, capillary blood 71.5-68.9 mm Hg. Art.
On the 2nd day from the moment of admission, despite intensive therapy, the condition worsened: severe lethargy appeared, blood pressure increased to 190/110 mm Hg. Art., РсО2 135 mm Hg. Art. A tracheostomy was performed and mechanical ventilation was started. After a few hours, consciousness began to recover, blood pressure dropped to 140/80 mm Hg, PcO2 68 mm Hg. Over the next 5 days, the condition gradually improved significantly. РсО2 decreased to 34-47 mm Hg. Art. Fi0 was reduced from 1.0 to 0.4. On
On the first day, a trial shutdown of the respirator was performed. After 20 minutes, the patient began to complain of a feeling of lack of air, the pulse increased from 76 to 108 per minute, blood pressure increased from 140/70 to 165/100 mm Hg. Art. Ventilation was resumed and the attempt was repeated the next day. However, after 30 minutes, tachycardia developed again, breathing increased to 34 per minute, Pco7 decreased from 39 to 30 mm Hg. Art. Starting from the 9th day after the start of mechanical ventilation, the patient was allowed to breathe on his own for 30-40 minutes 3-4 times a day. Only on the 20th day were the periods of spontaneous breathing able to be extended to 1 1/2-2 hours. The period of stopping mechanical ventilation took 26 days. The patient was discharged on February 16, 1975.
This observation once again shows that stopping mechanical ventilation is a complex process that requires patience and exceptional attention to the patient from the doctor and nursing staff. We consider it necessary to remind about this, because by the time mechanical ventilation is stopped, the patient’s condition improves significantly compared to the moment mechanical ventilation began. It is easy to feel unjustifiably confident that nothing will happen. However, this is true: deterioration during the period of stopping mechanical ventilation can negate the multi-day efforts of the entire team and cause a number of life-threatening complications for the patient.

This information is intended for healthcare and pharmaceutical professionals. Patients should not use this information as medical advice or recommendations.

Types of artificial ventilation

1. What is artificial ventilation?

Artificial pulmonary ventilation (ALV) is a form of ventilation designed to solve the task that the respiratory muscles normally perform. The task includes providing oxygenation and ventilation (removal of carbon dioxide) to the patient. There are two main types of ventilation: positive pressure ventilation and negative pressure ventilation. Positive pressure ventilation can be invasive (via an endotracheal tube) or non-invasive (via a face mask). Ventilation with phase switching by volume and pressure is also possible (see question 4). The many different modes of mechanical ventilation include controlled artificial ventilation (CMV in the English abbreviation - ed.), assisted artificial ventilation (ACV in the English abbreviation), intermittent mandatory (mandatory) ventilation (IMV in the English abbreviation), synchronized intermittent mandatory ventilation (SIMV). ), pressure controlled ventilation (PCV), pressure support ventilation (PSV), inverted inspiratory ratio ventilation (IRV), pressure relief ventilation (PRV in its English acronym) and high-frequency modes.

It is important to distinguish between endotracheal intubation and mechanical ventilation, since one does not necessarily imply the other. For example, a patient may require endotracheal intubation to ensure airway patency, but still be able to independently maintain ventilation through an endotracheal tube without the aid of a ventilator.

2. What are the indications for mechanical ventilation?

Mechanical ventilation is indicated for many disorders. At the same time, in many cases the indications are not strictly defined. The main reasons for the use of mechanical ventilation include the inability to obtain sufficient oxygenation and loss of adequate alveolar ventilation, which may be associated either with primary parenchymal lung disease (for example, with pneumonia or pulmonary edema) or with systemic processes that indirectly affect lung function (as occurs with sepsis or dysfunction of the central nervous system). In addition, general anesthesia often involves mechanical ventilation, because many drugs have a depressant effect on breathing, and muscle relaxants cause paralysis of the respiratory muscles. The main task of mechanical ventilation in conditions of respiratory failure is to maintain gas exchange until the pathological process that caused this failure is eliminated.

3. What is non-invasive ventilation and what are the indications for it?

Noninvasive ventilation can be performed in either a negative or positive pressure mode. Negative pressure ventilation (usually using an iron lung or cuirass respirator) is rarely used in patients with neuromuscular disorders or chronic diaphragm fatigue due to chronic obstructive pulmonary disease (COPD). The respirator shell wraps around the torso below the neck, and the negative pressure created under the shell leads to a pressure gradient and gas flow from the upper respiratory tract to the lungs. Exhalation occurs passively. This mode of ventilation allows you to avoid tracheal intubation and avoid problems associated with it. The upper airway should be kept clear, but this makes it vulnerable to aspiration. Due to stagnation of blood in the internal organs, hypotension may occur.

Non-invasive positive pressure ventilation (NIPPV) can be performed in several modes, including continuous positive pressure (CPAP), bi-level positive pressure (BiPAP), pressure-assisted mask ventilation, or a combination of these ventilation methods. This type of ventilation can be used in those patients who do not want tracheal intubation - patients with end-stage disease or with certain types of respiratory failure (for example, exacerbation of COPD with hypercapnia). In patients with end-stage disease who have respiratory disorders, NIPPV is a reliable, effective and more comfortable means of supporting ventilation compared to other methods. The method is not so complicated and allows the patient to maintain independence and verbal contact; There is less stress associated with ending non-invasive ventilation when indicated.

4. Describe the most common modes of ventilation: CMV, ACV, IMV.

These three modes, with conventional volume switching, essentially represent three different ways the respirator can respond. With CMV, the patient's ventilation is entirely controlled using a preset tidal volume (TIV) and a set respiratory rate (RR). CMV is used in patients who have completely lost the ability to attempt breathing, which is particularly the case during general anesthesia with central respiratory depression or muscle relaxant-induced muscle paralysis. The ACV (IVL) mode allows the patient to induce artificial inspiration (which is why it contains the word “auxiliary”), after which the specified tidal volume is supplied. If for some reason bradypnea or apnea develops, the respirator switches to a backup controlled ventilation mode. The IMV mode, originally proposed as a means of weaning off a respirator, allows the patient to breathe spontaneously through the breathing circuit of the device. The respirator performs mechanical ventilation with established DO and RR. The SIMV mode eliminates mechanical breaths during ongoing spontaneous breathing.

The debate surrounding the advantages and disadvantages of ACV and IMV continues to be heated. Theoretically, since not every breath is a positive pressure, IMV can reduce mean airway pressure (Paw) and thus reduce the likelihood of barotrauma. In addition, with IMV, it is easier to synchronize the patient with the respirator. It is possible that ACV more often causes respiratory alkalosis, since the patient, even experiencing tachypnea, receives the full set DO with each breath. Any type of ventilation requires a certain work of breathing from the patient (usually greater with IMV). In patients with acute respiratory failure (ARF), it is advisable to minimize the work of breathing at the initial stage and until the pathological process underlying the respiratory disorder begins to regress. Usually in such cases it is necessary to provide sedation, occasionally muscle relaxation and CMV.

5. What are the initial settings of the respirator for ARF? What problems are solved using these settings?

Most patients with ARF require complete replacement ventilation. The main objectives are to ensure saturation of arterial blood with oxygen and to prevent complications associated with artificial ventilation. Complications may occur due to increased airway pressure or prolonged exposure to elevated inspiratory oxygen (FiO2) concentrations (see below).

Most often they start with the mode VIVL, guaranteeing the supply of a given volume. However, pressocyclic regimens are becoming increasingly popular.

Must select FiO2. Typically start at 1.0 and slowly decrease to the minimum concentration tolerated by the patient. Long-term exposure to high FiO2 values ​​(> 60-70%) may result in oxygen toxicity.

Tidal volume is selected taking into account body weight and pathophysiological mechanisms of lung damage. Currently, a volume setting of 10–12 ml/kg body weight is considered acceptable. However, in conditions like acute respiratory distress syndrome (ARDS), lung capacity decreases. Since high values ​​of pressure and volume can worsen the course of the underlying disease, smaller volumes are used - in the range of 6–10 ml/kg.

Breathing rate(RR), as a rule, is set in the range of 10 – 20 breaths per minute. For patients requiring large amounts of minute ventilation, a respiratory rate of 20 to 30 breaths per minute may be required. At a rate > 25, carbon dioxide (CO2) removal is not significantly improved, and a respiratory rate > 30 predisposes to gas trapping due to reduced expiratory time.

Positive end-expiratory pressure (PEEP; see question 6) is usually set low initially (eg, 5 cmH2O) and can be gradually increased as needed to improve oxygenation. Low PEEP values ​​in most cases of acute lung injury help maintain the airiness of the alveoli, which are prone to collapse. Current evidence suggests that a low PEEP avoids the effects of opposing forces that occur during repeated opening and collapse of the alveoli. The effects of such forces can worsen lung damage.

Inspiratory flow rate, inflation curve shape, and inspiratory/expiratory (I/E) ratio are often set by the respiratory therapist, but the meaning of these settings should also be understood by the critical care physician. Peak inspiratory flow rate determines the maximum rate of inflation produced by the respirator during the inspiratory phase. At the initial stage, a flow of 50–80 l/min is usually considered satisfactory. The I/E ratio depends on the set minute volume and flow. Moreover, if the inhalation time is determined by the flow and DO, then the exhalation time is determined by the flow and breathing frequency. In most situations, an I:E ratio of 1/2 to 1/3 is justified. However, patients with COPD may require even longer expiratory times to achieve adequate exhalation.

A decrease in I:E can be achieved by increasing the inflation rate. However, high inspiratory flow rates can increase airway pressure and sometimes impair gas distribution. With a slower flow, it is possible to reduce airway pressure and improve gas distribution due to an increase in I:E. An increased (or “reversed” as discussed below) I:E ratio increases Paw and also increases cardiovascular side effects. A shortened expiratory time is poorly tolerated in obstructive airway diseases. Additionally, the type or shape of the inflation curve has little effect on ventilation. A constant flow (rectangular curve shape) provides inflation at a set volumetric speed. Selecting a downward or upward inflation curve can result in improved gas distribution as airway pressure increases. Pause on inhalation, slow exhalation and periodic double-volume breaths - all this can also be set.

6. Explain what PEEP is. How to choose the optimal PEEP level?

PEEP is additionally set for many types and modes of ventilation. In this case, the pressure in the airways at the end of expiration remains above atmospheric pressure. PEEP is aimed at preventing the collapse of the alveoli, as well as restoring the lumen of alveoli that have collapsed in a state of acute lung damage. Functional residual capacity (FRC) and oxygenation increase. Initially, PEEP is set at approximately 5 cmH2O, and is increased to maximum values ​​- 15–20 cmH2O - in small portions. High PEEP levels can negatively affect cardiac output (see question 8). Optimal PEEP provides the best arterial oxygenation with the least reduction in cardiac output and acceptable airway pressure. Optimal PEEP also corresponds to the level of best straightening of collapsed alveoli, which can be quickly established at the patient’s bedside, increasing PEEP to the degree of pneumatization of the lungs when their compliance (see question 14) begins to fall.

Monitoring airway pressure after each increase in PEEP is easy. Airway pressure should increase only in proportion to the set PEEP. If the pressure in the airways begins to increase faster than the set PEEP values, this will indicate overdistension of the alveoli and exceeding the level of optimal opening of the collapsed alveoli. Continuous positive pressure (CPP) is a form of PEEP delivered by a breathing circuit while the patient is breathing spontaneously.

7. What is internal or auto-PEEP?

First described by Pepe and Marini in 1982, internal PEEP (PEEP) refers to the development of positive pressure and gas movement within the alveoli at end expiration in the absence of artificially generated external PEEP (PEEP). Normally, the volume of the lungs at the end of expiration (FRC) depends on the result of the confrontation between the elastic traction of the lungs and the elasticity of the chest wall. The balancing of these forces under normal conditions results in no pressure gradient or airflow at end expiration. PEEP occurs due to two main reasons. If the RR is too high or the expiratory time is too short, mechanical ventilation leaves insufficient time for the healthy lungs to complete exhalation before the next respiratory cycle begins. This leads to the accumulation of air in the lungs and the appearance of positive pressure at the end of exhalation. Therefore, patients ventilated with high minute volume (eg, sepsis, trauma) or with a high I/E ratio are at risk of developing PEEP. A small bore endotracheal tube may also obstruct expiration, promoting PEEP. Another main mechanism for the development of PDCV is associated with damage to the lungs themselves.

Patients with increased airway resistance and lung compliance (eg, asthma, COPD) are at high risk of PEEP. Due to airway obstruction and associated difficulty in expiration, such patients tend to experience PEEP during both spontaneous breathing and mechanical ventilation. PDKVn has the same side effects as PDKVn, but requires greater vigilance. If the respirator, as is usually the case, has an outlet open to the atmosphere, then the only way to detect and measure PEEP is to close the exhalation outlet while airway pressure is monitored. This procedure should become routine, especially for high-risk patients. The treatment approach is based on etiology. Changing the respirator parameters (such as reducing the RR or increasing the inflation rate with a decrease in I/E) can create conditions for full exhalation. In addition, treatment of the underlying pathological process (for example, with bronchodilators) may help. In patients with limited expiratory flow due to obstructive airway lesions, a positive effect was achieved by using PEEP, which ensured a reduction in gas trapping. Theoretically, PEEP can act as an airway spacer to allow full exhalation. However, since PEEP is added to PEEP, severe disturbances in hemodynamics and gas exchange may occur.

8. What are the side effects of PEEP and PEEP?

Barotrauma - due to overstretching of the alveoli.
Decreased cardiac output, which may be due to several mechanisms. PEEP increases intrathoracic pressure, causing an increase in transmural pressure in the right atrium and a decrease in venous return. In addition, PEEP leads to an increase in pressure in the pulmonary artery, which makes it difficult for blood to eject from the right ventricle. A consequence of right ventricular dilatation may be prolapse of the interventricular septum into the cavity of the left ventricle, preventing the filling of the latter and contributing to a decrease in cardiac output. All this will manifest itself as hypotension, especially severe in patients with hypovolemia.

In routine practice, emergency endotracheal intubation is performed in patients with COPD and respiratory failure. Such patients remain in serious condition, usually for several days, during which they eat poorly and do not replenish fluid loss. After intubation, patients' lungs are vigorously inflated to improve oxygenation and ventilation. Auto-PEEP increases rapidly, and in conditions of hypovolemia, severe hypotension occurs. Treatment (if preventive measures are unsuccessful) includes intensive infusions, provision of conditions for longer expiration and elimination of bronchospasm.
During PEEP, erroneous assessment of cardiac filling parameters (in particular, central venous pressure or pulmonary artery occlusion pressure) is also possible. Pressure transmitted from the alveoli to the pulmonary vessels can lead to a false increase in these indicators. The more pliable the lungs are, the more pressure is transmitted. The correction can be made using a rule of thumb: from the measured value of pulmonary capillary wedge pressure (PCWP), one must subtract half of the PEEP value exceeding 5 cm H2O.
Overdistension of the alveoli by excessive PEEP reduces blood flow in these alveoli, increasing dead space (MD/DO).
PEEP can increase the work of breathing (in triggered modes of ventilation or during spontaneous breathing through the respirator circuit), since the patient will have to create greater negative pressure to turn on the respirator.
Other side effects include increased intracranial pressure (ICP) and fluid retention.

9. Describe the types of pressure-limited ventilation.

The ability to provide pressure-limited ventilation—either triggered (pressure-assisted ventilation) or forced-mode (pressure-controlled ventilation)—has only appeared on most adult respirators in recent years. For neonatal ventilation, the use of pressure-limited modes is routine practice. In pressure support ventilation (PSV), the patient begins to inhale, which causes the respirator to deliver gas to a predetermined - designed to increase DO - pressure. The rescue breath ends when the inspiratory flow falls below a preset level, usually below 25% of the maximum value. Note that the pressure is maintained until the flow is minimal. Such flow characteristics correspond well to the patient’s external breathing requirements, resulting in the mode being tolerated with greater comfort. This mode of spontaneous ventilation can be used in patients in a terminal condition to reduce the work of breathing spent on overcoming the resistance of the respiratory circuit and increasing DO. Pressure support can be used in conjunction with the IMV mode or independently, with or without PEEP or NPP. In addition, PSV has been shown to accelerate the recovery of spontaneous breathing after mechanical ventilation.

In pressure controlled ventilation (PCV), the inspiratory phase stops once a preset maximum pressure is reached. Tidal volume depends on airway resistance and lung compliance. PCV can be used alone or in combination with other regimens, such as IRV (see question 10). The characteristic flow of PCV (high initial flow followed by a fall) likely has properties that improve lung compliance and gas distribution. It has been suggested that PCV can be used as a safe and patient-friendly initial mode of ventilation in patients with acute hypoxic respiratory failure. Currently, respirators have begun to enter the market that provide a minimum guaranteed volume in a pressure-controlled mode.

10. Does the inverse ratio of inhalation and exhalation matter when ventilating a patient?

A type of ventilation, referred to by the acronym IRV, has been used with some success in patients with SLP. The mode itself is perceived ambiguously, since it involves prolonging the inspiratory time beyond the usual maximum - 50% of the time of the respiratory cycle with pressocyclic or volumetric ventilation. As inspiratory time increases, the I/E ratio becomes inverted (eg, 1/1, 1.5/1, 2/1, 3/1). Most critical care physicians do not recommend exceeding a 2/1 ratio due to possible hemodynamic deterioration and the risk of barotrauma. Although prolongation of inspiratory time has been shown to improve oxygenation, no prospective randomized trials have been performed on this topic. The improvement in oxygenation can be explained by several factors: an increase in average Paw (without an increase in peak Paw), the opening - as a result of a slowdown in inspiratory flow and the development of PEEP - of additional alveoli with a greater inspiratory time constant.

Slower inspiratory flow may reduce the likelihood of developing barotrauma and volotrauma. However, in patients with airway obstruction (eg, COPD or asthma), due to the enhancement of PEEP, this regimen may have a negative effect. Considering that patients often experience discomfort during mechanical ventilation, deep sedation or muscle relaxation may be required. Ultimately, despite the lack of irrefutably proven advantages of the method, it should be recognized that mechanical ventilation may have independent significance in the treatment of advanced forms of SLP.

11. Does mechanical ventilation affect various body systems other than the cardiovascular system?

Yes. Increased intrathoracic pressure can cause or contribute to a rise in ICP. As a result of prolonged nasotracheal intubation, sinusitis may develop. A constant threat to patients on artificial ventilation is the possibility of developing hospital-acquired pneumonia. Gastrointestinal bleeding from stress ulcers is quite common, which requires preventive therapy. Increased vasopressin production and decreased natriuretic hormone levels can lead to water and salt retention. Immobile critically ill patients are at constant risk of thromboembolic complications, so preventive measures are appropriate. Many patients require sedation and, in some cases, muscle relaxation (see question 17).

12. What is controlled hypoventilation with acceptable hypercapnia?

Controlled hypoventilation is a method that has found application in patients who require such mechanical ventilation that could prevent overdistension of the alveoli and possible damage to the alveolar-capillary membrane. Current evidence suggests that high volumes and pressures may cause or predispose to lung injury due to alveolar overdistension. Controlled hypoventilation (or tolerant hypercapnia) implements a strategy of safe, pressure-limited ventilation that prioritizes lung inflation pressure rather than pCO2 levels. Conducted in this regard, studies of patients with SOLP and status asthmaticus showed a decrease in the frequency of barotrauma, the number of days requiring intensive care, and mortality. To maintain peak Paw below 35–40 cmH2O and static Paw below 30 cmH2O, DO is set to approximately 6–10 ml/kg. A small DO is justified in the case of SOLP - when the lungs are affected inhomogeneously and only a small volume of them is able to be ventilated. Gattioni et al. described three zones in the affected lungs: a zone of atelectatic alveoli, a zone of collapsed but still capable of opening alveoli, and a small zone (25–30% of the volume of healthy lungs) of alveoli capable of ventilating. The traditionally set DO, which significantly exceeds the volume of the lungs available for ventilation, can cause overstretching of healthy alveoli and thereby aggravate acute lung injury. The term “child’s lungs” was proposed precisely due to the fact that only a small part of the lung volume is capable of ventilation. A gradual rise in pCO2 to a level of 80–100 mm Hg is quite acceptable. A decrease in pH below 7.20–7.25 can be eliminated by introducing buffer solutions. Another option is to wait until the normally functioning kidneys compensate for the hypercapnia by retaining bicarbonate. Tolerable hypercapnia is usually well tolerated. Possible adverse effects include cerebral vasodilation, which increases ICP. Indeed, intracranial hypertension is the only absolute contraindication for tolerable hypercapnia. In addition, increased sympathetic tone, pulmonary vasoconstriction, and cardiac arrhythmias may occur with permissible hypercapnia, although these rarely become dangerous. In patients with underlying ventricular dysfunction, depression of cardiac contractility may be significant.

13. What other methods are used to control pCO2?

There are several alternative methods for controlling pCO2. Reduced CO2 production can be achieved by deep sedation, muscle relaxation, cooling (avoiding hypothermia, of course) and reducing carbohydrate intake. A simple method of increasing CO2 clearance is tracheal gas insufflation (TIG). In this case, a small catheter (as for suction) is inserted through the endotracheal tube, passing it to the level of the tracheal bifurcation. A mixture of oxygen and nitrogen is supplied through this catheter at a rate of 4–6 L/min. This leads to the flushing out of dead space gas while minute ventilation and airway pressure remain unchanged. The average reduction in pCO2 is 15%. This method is well suited to the category of patients with head trauma in whom controlled hypoventilation can be usefully applied. In rare cases, an extracorporeal method of CO2 removal is used.

14. What is lung compliance? How to determine it?

Compliance is a measure of stretchability. It is expressed through the dependence of the change in volume on a given change in pressure and for the lungs is calculated using the formula: DO/(Paw - PEEP). Static extensibility is 70–100 ml/cm water column. With SOLP it is less than 40–50 ml/cm water column. Compliance is an integral indicator that does not reflect regional differences in SOLP - a condition in which affected areas alternate with relatively healthy ones. The nature of changes in lung compliance serves as a useful guide in determining the dynamics of ARF in a particular patient.

15. Is ventilation in the prone position the method of choice in patients with persistent hypoxia?

Studies have shown that the prone position significantly improves oxygenation in most patients with SLP. This may be due to improved ventilation-perfusion relationships in the lungs. However, due to the increasing complexity of nursing care, ventilation in the prone position has not become common practice.

16. What approach do patients “struggling with a respirator” require?

Agitation, respiratory distress or respiratory distress must be taken seriously as a number of causes are life-threatening. In order to avoid irreversible deterioration of the patient’s condition, it is necessary to quickly determine the diagnosis. To do this, first, possible causes related to the respirator (device, circuit, and endotracheal tube) and causes related to the patient's condition are analyzed separately. Causes related to the patient's condition include hypoxemia, airway obstruction with sputum or mucus, pneumothorax, bronchospasm, infectious processes like pneumonia or sepsis, pulmonary embolism, myocardial ischemia, gastrointestinal bleeding, increasing PEEP and anxiety.

Respirator-related causes include circuit leakage or depressurization, inadequate ventilation volume or insufficient FiO2, endotracheal tube problems including extubation, tube obstruction, cuff rupture or deformation, and incorrect trigger sensitivity or inspiratory flow rate settings. Until the situation can be fully resolved, it is necessary to manually ventilate the patient with 100% oxygen. Auscultate the lungs and check vital signs (including pulse oximetry and end-tidal CO2) without delay. If time permits, arterial blood gas analysis and chest x-ray should be performed.

To monitor the patency of the endotracheal tube and remove sputum and mucus plugs, rapid passage of a suction catheter through the tube is acceptable. If pneumothorax with hemodynamic disturbances is suspected, decompression should be performed immediately, without waiting for a chest x-ray. In case of adequate oxygenation and ventilation of the patient, as well as stable hemodynamics, a more thorough analysis of the situation is possible, and, if necessary, sedation of the patient.

17. Should muscle relaxation be used to improve mechanical ventilation conditions?

Muscle relaxation is widely used to facilitate mechanical ventilation. This contributes to a moderate improvement in oxygenation, reduces peak Paw and provides better patient-respirator interaction. And in such specific situations as intracranial hypertension or ventilation in unusual modes (for example, mechanical ventilation or extracorporeal method), muscle relaxation can be even more beneficial. Disadvantages of muscle relaxation include loss of neurological examination, loss of cough, the possibility of inadvertent muscle relaxation of the conscious patient, numerous problems associated with drug-electrolyte interactions, and the possibility of prolonged block.

Additionally, there is no scientific evidence that muscle relaxation improves outcomes in critically ill patients. The use of muscle relaxants should be carefully considered. Until the patient is adequately sedated, muscle relaxation should be excluded. If muscle relaxation seems absolutely indicated, it should be carried out only after the final weighing of all the pros and cons. To avoid prolonged block, the use of muscle relaxation should be limited to 24–48 hours whenever possible.

18. Is there really any benefit from separate ventilation?

Separate ventilation of the lungs (RIVL) is the ventilation of each lung independently of each other, usually using a double-lumen tube and two respirators. Initially arose with the aim of improving the conditions for thoracic operations, RIVL was extended to some cases in intensive care practice. Here, patients with unilateral lung disease may be candidates for separate ventilation. This type of ventilation has been shown to improve oxygenation in patients with unilateral pneumonia, edema and contusions of the lungs.

Protecting the healthy lung from the contents of the affected lung, achieved by isolating each of them, can be life-saving for patients with massive bleeding or lung abscess. In addition, RIVL may be useful in patients with bronchopleural fistula. For each lung, individual ventilation parameters can be set, including the values ​​of DO, flow rate, PEEP and NAP. There is no need to synchronize the operation of two respirators, since, as practice shows, hemodynamic stability is better achieved when they operate asynchronously.

More than one ventilator works, helping a person overcome critical moments of the disease.

Breath is life

Try holding your breath while looking at the stopwatch. An untrained person will be able not to breathe for no more than 1 minute, then a deep breath takes place. Record holders last more than 15 minutes, but this is the result of ten years of training.

We cannot hold our breath because oxidative processes in our body never stop - while we are alive, of course. Carbon dioxide constantly accumulates and needs to be removed. Oxygen is constantly required, without it life itself is impossible.

What were the first breathing apparatuses?

The first ventilator mimicked the movement of the chest by raising the ribs and expanding the chest. It was called a “cuirass” and was worn over the chest. Negative air pressure was created, that is, air was involuntarily sucked into the respiratory tract. There are no statistics available on how effective it was.

Then, for centuries, devices similar to blacksmith's bellows were used. Atmospheric air was blown in and the pressure was adjusted by eye. There were frequent cases of lung rupture due to excessive pressure of the supplied air.

Modern medical devices work differently.

A mixture of oxygen and atmospheric air is blown into the lungs. The pressure of the mixture is not much higher than the pulmonary pressure. This method is somewhat contrary to physiology, but its effectiveness is very high: all people connected to the device breathe - therefore, live.

How do modern devices work?

Each ventilator has control and execution units. The control unit is a keyboard and a screen on which all indicators are visible. The devices of earlier models are simpler; there is a simple transparent tube inside which the cannula moves. The movements of the cannula reflect the respiratory rate. There is also a pressure gauge on which you can see the pressure of the injected mixture.

An execution unit is a set of devices. First of all, it is a high-pressure chamber for mixing pure oxygen with other gases. Oxygen can be supplied to the chamber from a central gas pipeline or a cylinder. A centralized oxygen supply is installed in large clinics where there are oxygen stations. Everyone else is content with cylinders, but this does not change the quality.

There must be a gas mixture supply speed regulator. This is a screw that changes the diameter of the tube supplying oxygen.

Good devices also have a chamber for mixing and warming gases. There is also a bacterial filter and a humidifier.

A breathing circuit is designed for the patient, supplying an oxygen-enriched gas mixture and removing carbon dioxide.

How is the device connected to the patient?

It depends on the person's condition. Patients who have difficulty swallowing and speaking can receive life-giving oxygen through a mask. The device can temporarily “breathe” instead of a person in case of a heart attack, injury or malignant tumor.

For unconscious people, a tube is inserted into the trachea - they are intubated or a tracheostomy is performed. The same is done for people who are conscious but have bulbar palsy; such patients cannot swallow or speak independently. In all these cases, a ventilator is the only way to survive.

Additional medical devices

To perform intubation, various medical devices are used: a laryngoscope with autonomous lighting and the manipulation is performed only by a doctor with sufficient experience. First, a laryngoscope is inserted - a device that pushes back the epiglottis and spreads it apart. When the doctor clearly sees what is in the trachea, the tube itself is inserted through the laryngoscope. To fix the tube, the cuff at its end is inflated with air.

The tube is inserted through the mouth or nose, but through the mouth is more convenient.

Medical equipment for life support

A defibrillator helps restore heart rhythm and effective blood circulation. Cardiology ambulance teams and intensive care units are required to be equipped with them.

An objective assessment of the body’s health is impossible without a variety of analyzers: hematological, biochemical, homeostasis and biological fluid analyzers.

Medical technology allows you to study all the necessary parameters and select adequate treatment in each specific case.

Devices for rescue teams

A disaster, natural disaster or accident can happen at any time and to anyone. A person in critical condition can be saved if resuscitation equipment is available. The vehicles of the rescue teams of the Ministry of Emergency Situations, disaster medicine and cardiac ambulances must have a portable ventilator, which allows the victims to be transported alive to hospital hospitals.

Portable devices differ from stationary ones only in size and number of modes. Pure oxygen is in cylinders, the number of which can be as large as desired.

Modes of use of a portable device must include forced and auxiliary ventilation.

Emergency medical equipment

Certain standards, as well as medical equipment and instruments for emergency care, have been adopted throughout the world. So, the car must have a high roof so that employees can stand up to their full height to provide assistance. A transport ventilator, pulse oximeters, infusers for dosed administration of drugs, catheters for large vessels, sets for conicotomy, intracardiac stimulation and spinal puncture are required.

The equipment of the emergency vehicle and the actions of medical personnel must preserve the person’s life until hospitalization.

The born baby must live

The birth of a person is not only the main and exciting event in the family, but also a dangerous period. During childbirth, the child is exposed to extreme stress, and often only an experienced neonatologist can revive newborns, since the body of a newly born child has specific characteristics.

Immediately after birth, the doctor evaluates 4 criteria:

  • independent breathing;
  • heart rate;
  • independence of movement;
  • pulsation of the umbilical cord.

If a child shows at least one sign of life, then the probability of his survival is very high.

Newborn revival

Artificial ventilation of the lungs of newborns has its own characteristics: the frequency of respiratory movements is in the range from 40 to 60 (in an adult at rest up to 20), unopened areas may remain in the lungs, and is only 120-140 ml.

Because of these features, the use of adult devices to revive newborns is impossible. Therefore, the very principle of breathing restoration is different, namely high-frequency jet ventilation.

Any ventilator for newborns is designed to deliver 100 to 200 ml of respiratory mixture into the patient’s respiratory tract at a frequency of more than 60 cycles/minute. The mixture is supplied through a mask; intubation is not used in the vast majority of cases.

The advantage of this method is that negative pressure is maintained in the chest. This is very important for later life, because the normal physiology of all respiratory organs is preserved. The incoming arterial blood is maximally enriched with oxygen, which increases survival.

Modern devices are highly sensitive; they perform synchronization and constant adaptation functions. Thus, spontaneous breathing and the best ventilation mode are supported by a ventilator. The instructions for the device teach you to measure the slightest tidal volume so as not to suppress the spontaneous breathing of the newborn. This makes it possible to adjust the operation of the device to a specific child, catch his own rhythm of life and help him adapt to the external environment.

Everyone is well aware that breathing is a vital physiological process. On average, you can live up to 7 minutes without breathing, after which loss of consciousness, coma and death occur. If a person is unable to breathe on his own, he is transferred to artificial ventilation. Ventilators are used only when indicated.

What is artificial pulmonary ventilation (ALV)? This is a set of measures that provide mechanical support for respiratory function. The ventilator, intended for patients in intensive care units and intensive care units, allows gas mixtures that are necessary for the life support of the body to be injected into the respiratory system. Gas mixtures enter the lungs under positive pressure.

Artificial ventilation is a last resort measure to help prolong the life of a seriously ill patient (for example, in a coma).

Indications

To use a ventilator, there must be objective evidence. We list the main pathological conditions for which a ventilator should be used:

  • Stopping breathing (apnea).
  • Acute respiratory failure.
  • High risk of developing acute respiratory failure.
  • Severe deficiency of oxygen saturation in the body.

Similar conditions may occur in the following cases:

  • Traumatic brain injuries.
  • Coma.
  • Overdose of pharmacological drugs (sedatives, narcotics, etc.).
  • Severe chronic lung diseases.
  • Bronchospasm.
  • Peripheral neuropathies.
  • Hypothyroidism.
  • Serious damage to the brain and/or spinal cord.
  • Respiratory muscle dysfunction, etc.

Ventilators

What is a ventilator? According to generally accepted terminology, ventilators belong to the category of special medical equipment that provides forced supply of oxygen and compressed air to the human respiratory system and removal of carbon dioxide. Main types of mechanical ventilation:

  • Invasive artificial air ventilation. To carry it out, an endotracheal or tracheostomy tube is used, which is inserted into the respiratory tract.
  • Non-invasive artificial air ventilation. This is done through a respiratory mask.

Taking into account the features of the drive and control, ventilators are divided into the following types:

  • Electrically driven.
  • Pneumatic.
  • With manual drive.

Before use, the ventilator and auxiliary equipment must undergo the necessary certification.

The influence of mechanical ventilation on organs and systems

Mechanical ventilators can have both beneficial and adverse physiological effects on the body. Mechanical ventilation affects the functioning of the following organs:

  • Lungs.
  • Heart.
  • Kidneys.
  • Stomach.
  • Liver.
  • Nervous system.

When performing artificial ventilation, a decrease in cardiac output is possible, which, as a rule, provokes a drop in blood pressure and a lack of oxygen in the tissues (hypoxia). In addition, a decrease in cardiac output affects the functioning of the kidneys, which is expressed in a decrease in daily diuresis (the volume of urine excreted).

If the patient is in a coma due to a traumatic brain injury, then artificial ventilation can lead to increased intracranial pressure. This pathological condition is explained by the fact that venous outflow decreases, blood volume increases and pressure in the head increases. Maintaining a lower average pressure in the respiratory system reduces the risk of increased intracranial pressure.


In most cases, the ventilator is connected using an endotracheal or tracheostomy tube. It has been clinically established that their use increases the risk of a number of pathological conditions:

  • Edema of the larynx.
  • Injuries to the mucous membrane of the respiratory tract.
  • Infection of the trachea, bronchi and lungs.
  • Atrophy of the mucous membrane (drying).

The artificial respiration device is used exclusively for indications.

Possible complications

It has been noted that mechanical ventilation, to one degree or another, negatively affects the condition of the lungs, especially after prolonged use of mechanical support of respiratory function (for example, in coma). Patients quite often encounter complications such as:

  • Atelectasis.
  • Barotrauma.
  • Acute lung injury.
  • Pneumonia.

Ventilation of the lungs (artificial) often leads to atelectasis. The cause may be either a decrease in lung volume or blockage of the airways with mucus. To prevent the development of atelectasis, it is necessary to effectively maintain proper pulmonary volume and regularly clear the airways from the accumulation of sputum, using sanative bronchoscopy.


If the lung is damaged as a result of overstretching of the alveoli associated with improper use of the type and type of mechanical ventilation, then we are talking about barotrauma. Against the background of this pathological condition, emphysema and pneumothorax (air entering the pleural cavity) may develop. At the same time, the occurrence of acute lung injury occurs due to excessive stretching of the alveoli, which is observed due to the large volume of inspiration. Therefore, it is extremely important to correctly configure the parameters of the ventilator.

Another fairly common problem in patients on mechanical ventilation is the development of hospital-acquired pneumonia. Gram-negative bacteria are usually the causative agents of pneumonia. Recent studies show that the pathogenic microflora responsible for the development of pneumonia enters the respiratory tract from the digestive system and oropharynx of the patient himself. It turns out that regular antiseptic treatment of tubes is practically of no importance in terms of preventing ventilation pneumonia. It is necessary to ensure that secretions from the oropharynx and gastric contents do not enter the respiratory tract. If there are no contraindications, it is advisable to keep the head end of the bed in an elevated position.

Mechanical ventilation in the postoperative period

Some patients require artificial ventilation for the first few days after certain surgical interventions to maintain breathing. This mainly concerns thoracic and cardiac operations. We list the indications for connecting to a ventilator after various operations:

  • Apnea associated with the continued effect of anesthetic drugs used during surgery.
  • The need to reduce the load on the heart and respiratory system.
  • The presence of concomitant lung disease, which reduces the functional state of the cardiopulmonary system.

In the postoperative period, it is necessary to carefully monitor the patient’s condition and transfer him to independent breathing as quickly as possible. They monitor gas exchange parameters, monitor the state of consciousness, evaluate pulmonary ventilation and the ability to breathe independently. In addition, it is advisable to monitor fluid balance and central venous pressure. It is worth noting that in most situations, postoperative patients quickly return to spontaneous breathing.

Each type of ventilation has its own application characteristics.

Long-term mechanical ventilation

For a certain category of patients, prolonged artificial ventilation may be necessary, which has its own characteristics and differences from standard mechanical ventilation performed in the intensive care unit. In some cases, mechanical ventilation is even performed at home, which significantly improves the patient’s quality of life. Patients with neuromuscular lesions are considered ideal candidates for home mechanical ventilation.

However, these patients must have a stable general condition. Particular attention is paid to the functional state of the heart and kidneys, as well as metabolism and nutritional status. In addition, support from loved ones, the ability to self-care and a sufficient financial situation are of no small importance. Without the necessary resources, successful mechanical ventilation at home can be very difficult.

Restoring breathing

The final goal of mechanical ventilation is to restore spontaneous breathing in the patient. In approximately 70% of cases, after eliminating the causes that required artificial ventilation, it is possible to successfully disconnect the person from the device. Some patients need to restore breathing for some time before being completely removed from the ventilator. In extremely rare situations, the patient is left on a lifelong connection to a respirator.

Criteria for the patient’s readiness to breathe independently:

  • Reducing the severity of respiratory failure.
  • Normalization of basic respiratory parameters (for example, partial oxygen tension in arterial blood).
  • Adequate functioning of the respiratory center.
  • Stable hemodynamics (blood movement through the vessels).
  • Normalization of electrolyte balance indicators.
  • Optimal nutritional status.
  • There are no serious problems with the functioning of other organs.

If vital organs and systems are functioning optimally, then disconnection from the ventilator is successful. Before shutdown, heart rhythm disturbances are eliminated and water and electrolyte balance is stabilized. It is also necessary to normalize body temperature. It should be noted that disruption of the kidneys, liver and digestive system can negatively affect the restoration of independent breathing.

The pathological condition of the patient (trauma, coma, damage to the respiratory muscles, etc.) plays a decisive role in choosing the appropriate type of mechanical ventilation.