Artificial ventilation. Negative effects of mechanical ventilation

08.05.2011 44341

Once, at one of the professional medical forums, the question of mechanical ventilation modes was raised. The idea arose to write about this “in a simple and accessible way,” i.e. so as not to confuse the reader in the abundance of abbreviations of modes and names of ventilation methods.

Moreover, they are all very similar to each other in essence and are nothing more than a commercial move by manufacturers of breathing equipment.

Modernization of the equipment of EMS machines has led to the appearance of modern respirators in them (for example, the Dreger “Karina” device), which allow mechanical ventilation at a high level, using a wide variety of modes. However, the orientation of EMS workers in these modes is often difficult and this article is intended to help solve this problem to some extent.

I will not dwell on outdated modes; I will only write about what is relevant today, so that after reading you will have a foundation on which further knowledge in this area will be superimposed.

So, what is a ventilator mode? To put it simply, the ventilation mode is an algorithm for controlling the flow in the breathing circuit. The flow can be controlled using mechanics - fur (old ventilators, type RO-6) or using the so-called. active valve (in modern respirators). An active valve requires a constant flow, which is provided either by a respirator compressor or a compressed gas supply.

Now let's look at the basic principles of artificial inhalation. There are two of them (if we discard the outdated ones):
1) with volume control;
2) with pressure control.

Inhalation formation with volume control: The respirator delivers flow into the patient's lungs and switches to exhalation when the physician's preset inhalation volume (tidal volume) is reached.

Inhalation formation with pressure control: The respirator delivers flow into the patient's lungs and switches to exhalation when the doctor's preset pressure (inspiratory pressure) is reached.

Graphically it looks like this:

And now the main classification of ventilation modes, from which we will build:

1. forced
2. forced-auxiliary
3. auxiliary

Forced ventilation modes

The essence is the same - the MOD specified by the doctor is supplied to the patient’s respiratory tract (which is summed up from the specified tidal volume or inspiratory pressure and ventilation frequency), any activity of the patient is excluded and ignored by the respirator.

There are two main modes of forced ventilation:

1. volume controlled ventilation
2. pressure controlled ventilation

Modern respirators also provide additional modes (pressure ventilation with guaranteed tidal volume), but for the sake of simplicity we will omit them.

Volume Control Ventilation (CMV, VC-CMV, IPPV, VCV, etc.)
The doctor sets: tidal volume (in ml), ventilation rate per minute, inhalation and exhalation ratio. The respirator delivers a predetermined tidal volume to the patient's lungs and switches to exhalation when it is reached. Exhalation occurs passively.

Some ventilators (for example, Dräger Evitas) use volumetric forced ventilation using timed exhalation switching. In this case, the following occurs. As volume is delivered to the patient's lungs, the pressure in the airway increases until the respirator delivers the set volume. Peak pressure (Ppeak or PIP) appears. After this, the flow stops - a plateau pressure appears (the flat part of the pressure curve). After the end of the inhalation time (Tinsp), exhalation begins.

Pressure Control Ventilation (PCV, PC-CMV)
The doctor sets: inspiratory pressure (inhalation pressure) in cm of water. Art. or in mbar, ventilation rate per minute, inspiratory to expiratory ratio. The respirator delivers flow into the patient's lungs until inspiratory pressure is reached and switches to exhalation. Exhalation occurs passively.

A few words about the advantages and disadvantages of various principles of artificial respiration.

Volume controlled ventilation
Advantages:

1. guaranteed tidal volume and, accordingly, minute ventilation

Flaws:

1. danger of barotrauma
2. uneven ventilation of different parts of the lungs
3. impossibility of adequate ventilation with leaky DP

Pressure controlled ventilation
Advantages:

1. much lower risk of barotrauma (with correctly set parameters)
2. more uniform ventilation of the lungs
3. can be used in cases of air tightness in the airway (ventilation with cuffless tubes in children, for example)

Flaws:

1. no guaranteed tidal volume
2. Full monitoring of ventilation is required (SpO2, ETCO2, MOD, acid-base balance).

Let's move on to the next group of ventilation modes.

Forced-auxiliary modes

In fact, this group of ventilation modes is represented by one mode - SIMV (Synchronized Intermittent Mandatory Ventilation - synchronized intermittent forced ventilation) and its options. The principle of the mode is as follows: the doctor sets the required number of forced breaths and the parameters for them, but the patient is allowed to breathe on his own, and the number of spontaneous breaths will be included in the number set. Additionally, the word "synchronized" means that mandatory breaths will be initiated in response to the patient's breathing attempt. If the patient does not breathe at all, then the respirator will regularly give him the specified forced breaths. In cases where there is no synchronization with the patient’s breaths, the mode is called “IMV” (Intermittent Mandatory Ventilation).

As a rule, to support the patient’s spontaneous breaths, the mode of pressure support (more often) - PSV (Pressure support ventilation), or volume (less often) - VSV (Volume support ventilation) is used, but we will talk about them below.

If the patient is given the principle of volume ventilation to generate instrumental breaths, then the mode is simply called “SIMV” or “VC-SIMV”, and if the principle of pressure ventilation is used, then the mode is called “P-SIMV” or “PC-SIMV”.

Due to the fact that we started talking about modes that respond to the patient’s breathing attempts, we should say a few words about the trigger. A trigger in a ventilator is a trigger circuit that initiates a breath in response to a patient's attempt to breathe. The following types of triggers are used in modern ventilators:

1. Volume trigger - it is triggered when a given volume passes into the patient’s airway
2. Pressure trigger - triggered by a drop in pressure in the breathing circuit of the device
3. Flow trigger - reacts to changes in flow, most common in modern respirators.

Synchronized intermittent forced ventilation with volume control (SIMV, VC-SIMV)
The doctor sets the tidal volume, the frequency of forced breaths, the ratio of inhalation and exhalation, trigger parameters, and, if necessary, sets the pressure or volume of support (the mode in this case will be abbreviated “SIMV+PS” or “SIMV+VS”). The patient receives a predetermined number of volume-controlled breaths and can breathe independently with or without support. In this case, the patient’s attempt to inhale (change in flow) will trigger a trigger and the respirator will allow him to take his own breath.

Synchronized intermittent forced ventilation with pressure control (P-SIMV, PC-SIMV)
The doctor sets the inspiratory pressure, the frequency of forced breaths, the ratio of inhalation and exhalation, trigger parameters, and, if necessary, sets the pressure or volume of support (the mode in this case will be abbreviated “P-SIMV+PS” or “P-SIMV+VS”). The patient receives a predetermined number of pressure-controlled breaths and can breathe independently with or without support according to the same principle as described previously.

I think it has already become clear that in the absence of the patient’s spontaneous breaths, the SIMV and P-SIMV modes turn into forced ventilation with volume control and forced ventilation with pressure control, respectively, which makes this mode universal.

Let's move on to consider auxiliary ventilation modes.

Auxiliary modes

As the name implies, this is a group of modes whose task is to support the patient’s spontaneous breathing in one way or another. Strictly speaking, this is no longer mechanical ventilation, but VIVL. It should be remembered that all these regimens can only be used in stable patients, and not in critically ill patients with unstable hemodynamics, acid-base balance disorders, etc. I will not dwell on the complex, so-called. "intelligent" modes of auxiliary ventilation, because Every self-respecting manufacturer of breathing equipment has its own “trick” here, and we will analyze the most basic VIVL modes. If there is a desire to talk about any specific “intelligent” mode, we will discuss it all separately. The only thing is that I will write separately about the BIPAP mode, since it is essentially universal and requires a completely separate consideration.

So, the auxiliary modes include:

1. Pressure support
2. Volume support
3. Continuous positive airway pressure
4. Endotracheal/tracheostomy tube resistance compensation

When using auxiliary modes, the option is very useful "Apnea ventilation"(Apnea Ventilation) which consists in the fact that if there is no respiratory activity of the patient for a specified time, the respirator automatically switches to forced ventilation.

Pressure support - Pressure support ventilation (PSV)
The essence of the mode is clear from the name - the respirator supports the patient’s spontaneous breaths with positive inspiratory pressure. The doctor sets the support pressure value (in cm H2O or mbar) and trigger parameters. A trigger responds to the patient’s breathing attempt and the respirator delivers a preset pressure during inhalation and then switches to exhalation. This mode can be successfully used in conjunction with SIMV or P-SIMV, as I wrote about earlier, in this case the patient’s spontaneous breaths will be supported by pressure. The PSV mode is widely used for weaning from a respirator by gradually reducing support pressure.

Volume support - Volume Support (VS)
This mode implements the so-called. volume support, i.e. the respirator automatically sets the level of support pressure based on the tidal volume specified by the doctor. This mode is present in some fans (Servo, Siemens, Inspiration). The doctor sets the tidal support volume, trigger parameters, and inhalation limit parameters. During an inspiratory attempt, the respirator gives the patient a given tidal volume and switches to exhalation.

Continuous positive airway pressure - Continuous Positive Airway Pressure (CPAP)
This is a spontaneous ventilation mode in which the respirator maintains constant positive pressure in the airways. In fact, the option of maintaining continuous positive airway pressure is very common and can be used in any forced, forced-assisted or assisted mode. Its most common synonym is positive end-expiratory pressure (PEEP). If the patient breathes completely on his own, then with the help of CPAP the resistance of the respirator hoses is compensated, the patient is supplied with warmed and humidified air with a high oxygen content, and the alveoli are also maintained in a straightened state; thus, this regimen is widely used during respirator weaning. In the mode settings, the doctor sets the level of positive pressure (in cm H2O or mbar).

Endotracheal/tracheostomy tube resistance compensation - Automatic Tube Compensation (ATC) or Tube Resistance Compensation (TRC)
This mode is present in some respirators and is designed to compensate for the patient's discomfort from breathing through an ETT or TT. In a patient with an endotracheal (tracheostomy) tube, the lumen of the upper respiratory tract is limited by its internal diameter, which is significantly smaller than the diameter of the larynx and trachea. According to Poiseuille's law, as the radius of the tube lumen decreases, the resistance sharply increases. Therefore, during assisted ventilation in patients with persistent spontaneous breathing, the problem arises of overcoming this resistance, especially at the beginning of inspiration. If you don’t believe me, try breathing for a while through a “seven” taken into your mouth. When using this mode, the doctor sets the following parameters: the diameter of the tube, its characteristics and the percentage of resistance compensation (up to 100%). The mode can be used in combination with other VIVL modes.

Well, in conclusion, let's talk about the BIPAP (BiPAP) mode, which, it seems to me, is worth considering separately.

Two-phase positive airway pressure ventilation - Biphasic positive airway pressure (BIPAP, BiPAP)

The name of the mode and its abbreviation were at one time patented by Dreger. Therefore, when we mean BIPAP, we mean ventilation with two phases of positive airway pressure, implemented in respirators from Draeger, and when we talk about BiPAP, we mean the same thing, but in respirators from other manufacturers.

Here we will analyze two-phase ventilation as it is implemented in the classic version - in respirators from the Draeger company, so we will use the abbreviation "BIPAP".

So, the essence of ventilation with two phases of positive pressure in the airways is that two levels of positive pressure are set: upper - CPAP high and lower - CPAP low, as well as two time intervals time high and time low corresponding to these pressures.

During each phase, during spontaneous breathing, several respiratory cycles can take place, this can be seen on the graph. To help you understand the essence of BIPAP, remember what I wrote earlier about CPAP: the patient breathes on his own at a certain level of continuous positive airway pressure. Now imagine that the respirator automatically increases the pressure level, and then returns to the original level again and does this with a certain frequency. This is BIPAP.

Depending on the clinical situation, the duration, phase relationships and pressure levels may vary.

Now let's get to the fun part. Towards the universality of the BIPAP mode.

Situation one. Imagine that the patient has no respiratory activity at all. In this case, an increase in pressure in the airways in the second phase will lead to forced ventilation by pressure, which will be graphically indistinguishable from PCV (remember the abbreviation).

Situation two. If the patient is able to maintain spontaneous breathing at the lower pressure level (CPAP low), then when it increases to the upper one, forced pressure ventilation will occur, that is, the mode will be indistinguishable from P-SIMV + CPAP.

Situation three. The patient is able to maintain spontaneous breathing at both lower and upper pressure levels. BIPAP in these situations works like a true BIPAP, showing all its advantages.

Situation four. If we set the same value of upper and lower pressure during spontaneous breathing of the patient, then BIPAP will turn into what? That's right, CPAP.

Thus, the ventilation mode with two phases of positive airway pressure is universal in nature and, depending on the settings, can work as a forced, forced-assisted or purely auxiliary mode.

So we examined all the main modes of mechanical ventilation, thus creating the basis for further accumulation of knowledge on this issue. I would like to note right away that all this can only be understood by working directly with the patient and the respirator. In addition, manufacturers of breathing equipment produce many simulator programs that allow you to familiarize yourself and work with any mode without leaving the computer.

Shvets A.A. (Graph)

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One of the main tasks of the intensive care unit (ICU) is to provide adequate respiratory support. In this regard, for specialists working in this field of medicine, it is especially important to correctly navigate the indications and types of artificial pulmonary ventilation (ALV).

Indications for artificial ventilation of the lungs

The main indication for artificial pulmonary ventilation (ALV) is the presence of respiratory failure in the patient. Other indications include prolonged awakening of the patient after anesthesia, disturbances of consciousness, lack of protective reflexes, and fatigue of the respiratory muscles. The main goal of artificial pulmonary ventilation (ALV) is to improve gas exchange, reduce the work of breathing and avoid complications when the patient awakens. Regardless of the indication for artificial pulmonary ventilation (ALV), the underlying disease must be potentially reversible, otherwise weaning from artificial pulmonary ventilation (ALV) is impossible.

Respiratory failure

The most common indication for respiratory support is respiratory failure. This condition occurs in situations where gas exchange is disrupted, leading to hypoxemia. may occur alone or be combined with hypercapnia. The causes of respiratory failure can be different. So, the problem can arise at the level of the alveolar capillary membrane (pulmonary edema), respiratory tract (rib fracture), etc.

Causes of respiratory failure

Inadequate gas exchange

Causes of inadequate gas exchange:

• pneumonia,
• pulmonary edema,
• acute respiratory distress syndrome (ARDS).

Inadequate breathing

Causes of inadequate breathing:

• chest wall injury:
  • rib fracture,
  • floating segment;
• weakness of the respiratory muscles:
  • myasthenia gravis, poliomyelitis,
  • tetanus;
• depression of the central nervous system:
  • psychotropic drugs,
  • dislocation of the brain stem.

Airway obstruction

Causes of airway obstruction:

• upper airway obstruction:
  • croup,
  • edema,
  • tumor;
• obstruction of the lower respiratory tract (bronchospasm).

In some cases, indications for artificial pulmonary ventilation (ALV) are difficult to determine. In this situation, clinical circumstances should be guided.

Main indications for artificial ventilation of the lungs

The following main indications for artificial pulmonary ventilation (ALV) are distinguished:

• Respiratory rate (RR) >35 or< 5 в мин;
• Fatigue of the respiratory muscles;
• Hypoxia - general cyanosis, SaO2< 90% при дыхании кислородом или PaO 2 < 8 кПа (60 мм рт. ст.);
• Hypercapnia - PaCO 2 > 8 kPa (60 mm Hg);
• Decreased level of consciousness;
• Severe chest injury;
• Tidal volume (TO)< 5 мл/кг или жизненная емкость легких (ЖЕЛ) < 15 мл/кг.

Other indications for artificial pulmonary ventilation (ALV)

In a number of patients, artificial pulmonary ventilation (ALV) is performed as a component of intensive care for conditions not associated with respiratory pathology:

• Control of intracranial pressure in traumatic brain injury;
• Respiratory protection ();
• Condition after cardiopulmonary resuscitation;
• The period after long and extensive surgical interventions or severe trauma.

Types of artificial ventilation

The most common mode of artificial pulmonary ventilation (ALV) is intermittent positive pressure ventilation (IPPV). In this mode, the lungs are inflated by positive pressure generated by a ventilator, and gas flow is delivered through an endotracheal or tracheostomy tube. Tracheal intubation is usually performed through the mouth. With prolonged artificial pulmonary ventilation (ALV), patients in some cases tolerate nasotracheal intubation better. However, nasotracheal intubation is technically more difficult to perform; in addition, it is accompanied by a higher risk of bleeding and infectious complications (sinusitis).

Tracheal intubation not only allows for IPPV but also reduces the amount of dead space; In addition, it facilitates the toilet of the respiratory tract. However, if the patient is adequate and available for contact, mechanical ventilation (ALV) can be performed non-invasively through a tightly fitted nasal or face mask.

In principle, two types of ventilators are used in the intensive care unit (ICU) - those that are controlled by a predetermined tidal volume (VT) and those that are controlled by inspiratory pressure. Modern ventilators provide various types of mechanical ventilation (ALV); from a clinical point of view, it is important to select the type of artificial pulmonary ventilation (ALV) that is most suitable for this particular patient.

Types of artificial ventilation

Artificial pulmonary ventilation (ALV) by volume

Artificial pulmonary ventilation (AVV) by volume is carried out in cases where a ventilator delivers a predetermined tidal volume into the patient’s respiratory tract, regardless of the pressure set on the respirator. The pressure in the airways is determined by the compliance (stiffness) of the lungs. If the lungs are stiff, the pressure rises sharply, which can lead to the risk of barotrauma (rupture of the alveoli, which leads to pneumothorax and mediastinal emphysema).

Artificial pulmonary ventilation (ALV) by pressure

Artificial pulmonary ventilation (ALV) by pressure is when the artificial lung ventilation device (ALV) reaches a predetermined level of pressure in the respiratory tract. Thus, the tidal volume delivered is determined by lung compliance and airway resistance.

Modes of artificial ventilation

Controlled mechanical ventilation (CMV)

This mode of artificial pulmonary ventilation (ALV) is determined solely by the settings of the respirator (pressure in the respiratory tract, tidal volume (VT), respiratory rate (RR), inhalation to exhalation ratio - I:E). This mode is not very often used in intensive care units (ICU), as it does not provide synchronization with the patient’s spontaneous breathing. As a result, CMV is not always well tolerated by the patient, which requires sedation or the prescription of muscle relaxants to stop the “fight against the ventilator” and normalize gas exchange. Typically, CMV mode is widely used in the operating room during anesthesia.

Assisted mechanical ventilation (AMV)

There are several ventilation modes that allow you to support the patient's attempts at spontaneous respiratory movements. In this case, the ventilator detects the attempt to inhale and supports it.
These modes have two main advantages. Firstly, they are better tolerated by patients and reduce the need for sedation. Secondly, they allow you to preserve the functioning of the respiratory muscles, which prevents their atrophy. The patient's breathing is maintained by a predetermined inspiratory pressure or tidal volume (TIV).

There are several types of auxiliary ventilation:

Intermittent mechanical ventilation (IMV)

Intermittent mechanical ventilation (IMV) is a combination of spontaneous and forced breathing movements. Between forced breaths, the patient can breathe independently, without ventilator support. The IMV mode provides minimal minute ventilation, but can be accompanied by significant variations between mandatory and spontaneous breaths.

Synchronized intermittent mechanical ventilation (SIMV)

In this mode, forced breathing movements are synchronized with the patient’s own breathing attempts, which provides him with greater comfort.

Pressure-support ventilation - PSV or assisted spontaneous breaths - ASB

When you attempt your own breathing movement, a preset pressure inhalation is supplied to the airways. This type of assisted ventilation provides the patient with the greatest comfort. The degree of pressure support is determined by the level of airway pressure and can be gradually reduced during weaning from mechanical ventilation (MV). No forced breaths are given, and ventilation depends entirely on whether the patient can attempt spontaneous breathing. Thus, the PSV mode does not provide ventilation during apnea; in this situation, its combination with SIMV is indicated.

Positive end expiratory pressure (PEEP)

Positive end expiratory pressure (PEEP) is used for all types of IPPV. During exhalation, positive airway pressure is maintained, which inflates collapsed areas of the lungs and prevents atelectasis of the distal airways. As a result, they improve. However, PEEP increases intrathoracic pressure and may decrease venous return, resulting in decreased blood pressure, especially in the setting of hypovolemia. When using PEEP up to 5-10 cm water. Art. these negative effects, as a rule, can be corrected by infusion load. Continuous positive airway pressure (CPAP) is as effective as PEEP, but is used primarily during spontaneous breathing.

Start of mechanical ventilation

At the beginning of artificial pulmonary ventilation (ALV), its main task is to provide the patient with the physiologically necessary tidal volume (TV) and respiratory rate (RR); their values ​​are adapted to the initial condition of the patient.

Initial Ventilator Settings for Mechanical Ventilation

FiO 2	At the beginning of artificial pulmonary ventilation (ALV) 1.0, then a gradual decrease
PEEP	5 cm water. Art.
Tidal volume (TO)	7-10 ml/kg
Inspiratory pressure
Respiratory rate (RR)	10-15 per minute
Pressure support	20 cm water. Art. (15 cm water column above PEEP)
I:E	1:2
Thread trigger	2 l/min
Pressure trigger	From -1 to -3 cm water. Art.
"Sighs"	Previously intended for the prevention of atelectasis, their effectiveness is currently disputed
These settings are changed depending on the clinical condition and comfort of the patient.

Optimizing oxygenation during mechanical ventilation

When transferring a patient to artificial pulmonary ventilation (ALV), as a rule, it is recommended to initially set FiO 2 = 1.0 with a subsequent decrease in this indicator to a value that would allow maintaining SaO 2 > 93%. To prevent lung damage caused by hyperoxia, it is necessary to avoid maintaining FiO 2 > 0.6 for long periods of time.

One of the strategic directions to improve oxygenation without increasing FiO 2 may be to increase the average pressure in the respiratory tract. This can be achieved by increasing the PEEP to 10 cmH2O. Art. or, with pressure-controlled ventilation, by increasing the peak inspiratory pressure. However, it should be remembered that when this indicator increases > 35 cm of water. Art. the risk of pulmonary barotrauma increases sharply. Against the background of severe hypoxia (), it may be necessary to use additional methods of respiratory support aimed at improving oxygenation. One of these directions is a further increase in PEEP > 15 cm of water. Art. In addition, a low tidal volume strategy (6-8 ml/kg) can be used. It should be remembered that the use of these techniques may be accompanied by arterial hypotension, which is most common in patients receiving massive fluid resuscitation and inotropic/vasopressor support.

Another area of ​​respiratory support against the background of hypoxemia is increasing inspiratory time. Normally, the ratio of inhalation to exhalation is 1:2; if oxygenation is impaired, it can be changed to 1:1 or even 2:1. It should be remembered that increased inspiratory time may be poorly tolerated by those patients who require sedation. A decrease in minute ventilation may be accompanied by an increase in PaCO 2 . This situation is called "permissive hypercapnia." From a clinical point of view, it does not pose any particular problems, except when it is necessary to avoid increased intracranial pressure. In permissive hypercapnia, it is recommended to maintain arterial blood pH above 7.2. In severe ARDS, the prone position may be used to improve oxygenation by mobilizing collapsed alveoli and improving the ratio between ventilation and pulmonary perfusion. However, this position makes it difficult to monitor the patient, so it must be used with caution.

Improving carbon dioxide elimination during mechanical ventilation

Carbon dioxide removal can be improved by increasing minute ventilation. This can be achieved by increasing tidal volume (TV) or respiratory rate (RR).

Sedation for mechanical ventilation

Most patients on mechanical ventilation (ALV) require an endotracheal tube in the airway to adapt to it. Ideally, only light sedation should be prescribed, while the patient should remain contacted and, at the same time, adapted to ventilation. In addition, it is necessary that, against the background of sedation, the patient is able to attempt independent respiratory movements in order to eliminate the risk of atrophy of the respiratory muscles.

Problems during artificial ventilation

"Fighting the Fan"

When desynchronizing with a respirator during artificial pulmonary ventilation (ALV), a drop in tidal volume (TV) is observed due to an increase in inspiratory resistance. This leads to inadequate ventilation and hypoxia.

There are several reasons for desynchronization with a respirator:

• Factors determined by the patient's condition - breathing directed against inhalation from the artificial lung ventilation device (ventilator), holding one's breath, coughing.
• Decreased lung compliance - pulmonary pathology (pulmonary edema, pneumonia, pneumothorax).
• Increased resistance at the level of the respiratory tract - bronchospasm, aspiration, excessive secretion of the tracheobronchial tree.
• Disconnection of the ventilator or, leakage, equipment malfunction, blockage of the endotracheal tube, its torsion or dislocation.

Diagnosis of ventilation problems

High airway pressure due to endotracheal tube obstruction.

• The patient could squeeze the tube with his teeth - insert the airway, prescribe sedatives.
• Obstruction of the airways as a result of excessive secretion - suction the tracheal contents and, if necessary, lavage the tracheobronchial tree (5 ml of physiological NaCl solution). If necessary, reintubate the patient.
• The endotracheal tube has moved into the right main bronchus - pull the tube back.

High airway pressure due to intrapulmonary factors:

• Bronchospasm? (wheezing on inhalation and exhalation). Make sure that the endotracheal tube is not inserted too deeply and does not stimulate the carina. Prescribe bronchodilators.
• Pneumothorax, hemothorax, atelectasis, pleural effusion? (uneven chest excursions, auscultatory picture). Perform a chest x-ray and prescribe appropriate treatment.
• Pulmonary edema? (Foamy sputum, bloody, and crepitus). Prescribe diuretics, therapy for heart failure, arrhythmias, etc.

Factors of sedation/analgesia:

• Hyperventilation due to hypoxia or hypercapnia (cyanosis, tachycardia, arterial hypertension, sweating). Increase FiO2 and mean airway pressure using PEEP. Increase minute ventilation (if hypercapnia).
• Cough, discomfort or pain (increased heart rate and blood pressure, sweating, facial expression). Assess possible causes of discomfort (endotracheal tube location, full bladder, pain). Assess the adequacy of analgesia and sedation. Switch to the ventilation mode that is better tolerated by the patient (PS, SIMV). Muscle relaxants should be prescribed only in cases where all other causes of desynchronization with the respirator have been excluded.

Weaning from mechanical ventilation

Artificial pulmonary ventilation (ALV) can be complicated by barotrauma, pneumonia, decreased cardiac output and a number of other complications. In this regard, it is necessary to stop artificial pulmonary ventilation (ALV) as quickly as possible, as soon as the clinical situation allows.

Weaning from a respirator is indicated in cases where there is a positive trend in the patient’s condition. Many patients receive artificial ventilation (ALV) for a short period of time (for example, after long and traumatic surgical interventions). In some patients, on the contrary, artificial ventilation of the lungs (ALV) is carried out for many days (for example, ARDS). With prolonged artificial pulmonary ventilation (ALV), weakness and atrophy of the respiratory muscles develop; therefore, the rate of weaning from a respirator largely depends on the duration of artificial pulmonary ventilation (ALV) and the nature of its modes. To prevent atrophy of the respiratory muscles, auxiliary ventilation modes and adequate nutritional support are recommended.

Patients recovering from critical illness are at risk for developing “critical illness polyneuropathy.” This disease is accompanied by weakness of the respiratory and peripheral muscles, decreased tendon reflexes and sensory disturbances. Treatment is symptomatic. There is evidence that long-term administration of aminosteroid muscle relaxants (vecuronium) can cause persistent muscle paralysis. Therefore, vecuronium is not recommended for long-term neuromuscular blockade.

Indications for weaning from mechanical ventilation

The decision to initiate weaning from a respirator is often subjective and based on clinical experience.

However, the most common indications for weaning from artificial pulmonary ventilation (ALV) are the following conditions:

• Adequate therapy and positive dynamics of the underlying disease;
• Breathing function:
  • BH< 35 в мин;
  • FiO 2< 0,5, SaO2 >90%, PEEP< 10 см вод. ст.;
  • DO > 5 ml/kg;
  • VC > 10 ml/kg;
• Minute ventilation< 10 л/мин;
• No infection or hyperthermia;
• Hemodynamic stability and EBV.

Before weaning, there should be no evidence of residual neuromuscular blockade, and the dose of sedatives should be kept to a minimum to allow adequate contact with the patient. In the event that the patient’s consciousness is depressed, in the presence of agitation and the absence of a cough reflex, weaning from artificial pulmonary ventilation (ALV) is ineffective.

Modes of weaning from artificial ventilation

It is still unclear which method of weaning from artificial pulmonary ventilation (ALV) is the most optimal.

There are several main modes of weaning from a respirator:

1. Spontaneous breathing test without the support of an artificial lung ventilation device (ventilator). The artificial lung ventilation device (ventilator) is temporarily turned off and a T-shaped connector or breathing circuit is connected to the endotracheal tube to carry out CPAP. The periods of spontaneous breathing are gradually lengthened. Thus, the patient gets the opportunity for full breathing work with periods of rest when artificial pulmonary ventilation (ALV) is resumed.
2. Weaning using IMV mode. The respirator delivers a set minimum volume of ventilation into the patient's airways, which is gradually reduced as soon as the patient is able to increase the work of breathing. In this case, the hardware inhalation can be synchronized with one’s own inhalation attempt (SIMV).
3. Weaning using pressure support. In this mode, the device picks up all the patient’s inhalation attempts. This weaning method involves gradually reducing the level of pressure support. Thus, the patient becomes responsible for increasing the volume of spontaneous ventilation. When the level of pressure support decreases to 5-10 cm water. Art. above PEEP, you can start a spontaneous breathing test with a T-piece or CPAP.

Inability to wean from mechanical ventilation

During the process of weaning from artificial pulmonary ventilation (ALV), it is necessary to closely monitor the patient in order to promptly identify signs of fatigue of the respiratory muscles or inability to wean from the respirator. These signs include restlessness, shortness of breath, decreased tidal volume (VT), and hemodynamic instability, primarily tachycardia and hypertension. In this situation, it is necessary to increase the level of pressure support; it often takes many hours for the respiratory muscles to recover. It is optimal to begin weaning from a respirator in the morning to ensure reliable monitoring of the patient's condition throughout the day. In case of prolonged weaning from artificial pulmonary ventilation (ALV), it is recommended to increase the level of pressure support at night to ensure adequate rest for the patient.

Tracheostomy in the intensive care unit

The most common indication for tracheostomy in the ICU is to facilitate prolonged mechanical ventilation (ALV) and the process of weaning from the respirator. Tracheostomy reduces the level of sedation and thus improves the ability to communicate with the patient. In addition, it provides effective toilet of the tracheobronchial tree in those patients who are unable to independently drain sputum as a result of its excess production or weakness of muscle tone. A tracheostomy can be performed in the operating room like any other surgical procedure; in addition, it can be performed in the ICU at the patient's bedside. It is widely used to carry it out. The time to switch from an endotracheal tube to a tracheostomy is determined individually. As a rule, tracheostomy is performed if there is a high probability of prolonged artificial pulmonary ventilation (ALV) or there are problems with weaning from the respirator. Tracheostomy can be accompanied by a number of complications. These include tube blockage, tube disposition, infectious complications, and bleeding. Bleeding can directly complicate surgery; in the long-term postoperative period it can be erosive in nature due to damage to large blood vessels (for example, the innominate artery). Other indications for tracheostomy are obstruction of the upper respiratory tract and protection of the lungs from aspiration when laryngopharyngeal reflexes are suppressed. In addition, tracheostomy may be performed as part of anesthetic or surgical management for a number of procedures (eg, laryngectomy).

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Bogdanov A.A.
anesthesiologist, Wexham Park and Heatherwood Hospitals, Berkshire, UK,
e-mail

This work was written in an attempt to acquaint anesthesiologists and resuscitators with some new (and perhaps not so new) modes of ventilation for nostrils. Often these regimens are mentioned in various works in the form of abbreviations, and many doctors are simply not familiar with the very idea of ​​such techniques. In hopes of filling this gap, this article was written. It is in no way intended to be a guide to the use of any particular method of ventilation for the above-mentioned condition, since not only is discussion possible on each method, but a separate lecture is necessary for complete coverage. However, if there is interest in certain issues, the author will be happy to discuss them in detail, so to speak.

The repeatedly mentioned Consensus Conference of the European Society of Intensive Care Medicine and the American College of Chest Physicians, together with the American Society of Intensive Care Medicine, adopted a document that largely determines the attitude towards mechanical ventilation.

First of all, the fundamental settings for performing mechanical ventilation should be mentioned.

• The pathophysiology of the underlying disease varies over time, so the mode, intensity and parameters of mechanical ventilation must be reviewed regularly.
• Measures must be taken to reduce the risk of potential complications from the ventilation itself.
• In order to reduce such complications, physiological parameters may deviate from normal and one should not strive to achieve an absolute norm.
• Overdistension of the alveoli is the most likely factor in the occurrence of ventilator-dependent lung injuries; Plateau pressure currently serves as the most accurate factor reflecting overextension of the alveoli. Where possible, a pressure level of 35 mmH2O should not be exceeded.
• Dynamic overinflation often goes unnoticed. It needs to be measured, assessed and limited.

Physiological:

• Supporting or manipulating gas exchange.
• Increased lung capacity.
• Reducing or manipulating the work of breathing.

Clinical:

• Reversal of hypoxemia.
• Reversing life-threatening acid-base balance disorders.
• Respiratory distress.
• Prevention or relief of atelectasis.
• Fatigue of the respiratory muscles.
• If necessary, sedation and neuromuscular block.
• Reducing systemic or cardio oxygen consumption.
• Reduced ICP.
• Chest stabilization.

Barotrauma

Classically, barotrauma is defined as the presence of extra-alveolar air, which is clinically manifested by interstitial emphysema, pneumothorax, pneumoperitoneum, pneumopericardium, subcutaneous emphysema, and systemic gas embolism. All of these manifestations are believed to be caused by high pressure or volume during mechanical ventilation. In addition to this, the existence of so-called ventilator-induced lung injury (VILI) is now officially recognized (though based on experimental data), which clinically manifests itself in the form of lung damage, which is difficult to distinguish from nozzle as such. That is, mechanical ventilation may not only not improve the course of the disease, but also worsen it. Factors involved in the development of this condition include high tidal volume, high peak airway pressure, high residual volume at end expiration, gas flow, mean airway pressure, inspired oxygen concentration - all with the word "high". Initially, the focus was on high peak airway pressures (barotrauma), but recently it has become accepted that high pressure in itself is not so bad. Attention is focused more on high values ​​of DO (volutrauma). The experiment showed that only 60 minutes of mechanical ventilation with up to 20 ml/kg is necessary for the development of VILI. It should be noted that the development of VILI in humans is very difficult to trace, since the development of this condition overlaps with the main indication for mechanical ventilation. The presence of significant extra-alveolar air rarely goes unnoticed, but less dramatic manifestations (interstitial emphysema) may go undiagnosed.

Based on computed tomography data, it was possible to show that nosocomial fibrosis is characterized by the inhomogeneous nature of lung damage, when areas of infiltration alternate with atelectasis and normal lung tissue. It was noted that, as a rule, the affected areas of the lung are located more dorsally, while the healthier parts of the lung are more ventral. Thus, healthier areas of the lung will be subject to significantly greater aeration and will often receive higher amounts of oxygen compared to the affected areas. In such a situation, it is quite difficult to minimize the risk of developing VILI. Taking this into account, it is currently recommended when performing mechanical ventilation to maintain a balance between moderate DO values ​​and overinflation of the alveoli.

Permissive hypercapnia

This focus on VILI has led a number of authors to propose the concept that the need to maintain normal physiological parameters (especially PaCO2) may not be appropriate in some patients. Purely logically, such a statement makes sense if we take into account the fact that patients with chronic obstructive pulmonary diseases normally have high PaCO2 values. Thus, the concept of permissive hypercapnia states that it makes sense to reduce DV to protect the undamaged part of the lung by increasing PaCO2. It is difficult to predict standard indicators for this type of mechanical ventilation; it is recommended to monitor plateau pressure to diagnose the moment when a further increase in BP is accompanied by a significant increase in pressure (that is, the lung becomes overinflated).

It is well known that respiratory acidosis is associated with an unfavorable outcome, but it is believed (with good reason) that controlled and moderate acidosis caused by permissive hypercapnia should not cause any serious consequences. It should be borne in mind that hypercapnia causes stimulation of the sympathetic nervous system, which is accompanied by an increase in the release of catecholamines, pulmonary vasoconstriction, and an increase in cerebral blood flow. Accordingly, permissive hypercapnia is not indicated for TBI, coronary artery disease, or cardiomyation.

It should also be noted that to date, no controlled randomized studies have been published indicating an improvement in patient survival.

Similar reasoning led to the emergence of permissive hypoxia, when in cases of difficult ventilation the achievement of normal Pa02 values ​​is sacrificed, and a decrease in DO is accompanied by Pa02 values ​​of the order of 8 and higher kPa.

Pressure ventilation

Pressure ventilation has been widely used for treatment in neonatology, but only in the last 10 years has this technique begun to be used in adult intensive care. It is now believed that pressure ventilation is the next step when volume ventilation is not effective, when there is significant respiratory distress or there are problems with airway obstruction or patient synchronization with the ventilator, or when weaning from the ventilator is difficult.

Very often, volumetric ventilation is combined with WWTP, and many experts consider these two methods to be practically synonymous.

Pressure ventilation consists of the fact that during inhalation, the ventilator delivers a gas flow (whatever is required) to a predetermined pressure value in the respiratory tract within a predetermined time.

Volumetric ventilators require setting the tidal volume and respiratory rate (minute volume), as well as the inhalation-exhalation ratio. Changes in the impedance of the lung-ventilator system (such as increased airway resistance or decreased pulmonary compliance) result in changes in inspiratory pressure to achieve the preset tidal volume. In the case of pressure ventilation, it is necessary to set the desired airway pressure and inspiratory time.

Many models of modern ventilators have built-in pressure ventilation modules, including various modes of such ventilation: pressure support ventilation, pressure control ventilation, pressure ventilation with a reverse inhalation-exhalation ratio, pressure relief ventilation in the respiratory ventilators. ways (airway pressure release ventilation). All of these modes use a predetermined airway pressure value as a non-changeable parameter, while BP and gas flow are changeable values. In these modes of ventilation, the initial gas flow is quite high and then decreases quite quickly, the respiratory rate is determined by time, so that the respiratory cycle is independent of the patient's efforts (with the exception of pressure support, where the entire respiratory cycle is based on patient triggering).

Potential advantages of pressure ventilation over conventional volumetric ventilation methods include:

1. Faster gas flow during inspiration ensures better synchronization with the device, thereby reducing the work of breathing.
2. Early maximum alveolar congestion allows for better gas exchange because, at least theoretically, there is better diffusion of gas between the different types (fast and slow) of the alveoli, as well as between different parts of the lung.
3. Alveolar recruitment improves (involvement of previously atelectatic alveoli in ventilation).
4. Limiting pressure values ​​allows you to avoid barovolition injury during mechanical ventilation.

The negative aspects of this ventilation regime are the loss of guaranteed DO and the so far unexplored possibilities of potential VILI. One way or another, despite the widespread use of pressure ventilation and some positive reviews, there is no convincing evidence of the benefits of pressure ventilation, which only means that there are no convincing studies on this topic.

One of the varieties of pressure ventilation, or rather an attempt to combine the positive aspects of different ventilation techniques, is the ventilation mode, when a pressure-limited breath is used, but the cyclicity of breaths remains the same as with volume ventilation (pressure regulated volume control). In this mode, pressure and gas flow are constantly varied, which, at least theoretically, provides the best ventilation conditions from breath to breath.

Reverse expiratory ratio ventilation (RERV)

The lungs of patients with SNPF present a rather heterogeneous picture, where, along with healthy alveoli, damaged, atelectatic and fluid-filled alveoli coexist. The compliance of the healthy part of the lung is lower (that is, better) than that of the damaged part, so healthy alveoli receive the majority of the tidal volume during ventilation. When using normal tidal volumes (10 - 12 ml/kg), a significant part of the DO is blown into a relatively small undamaged part of the lung, which is accompanied by the development of significant tensile forces between the alveoli with damage to their epithelium, as well as alveolar capillaries, which in itself causes the appearance of an inflammatory cascade in the alveoli with all the ensuing consequences. This phenomenon is called volutrauma, correlating it with the significant tidal volumes used in the treatment of nostrils. Thus, the treatment method itself (ventilation) can cause lung damage, and many authors associate significant mortality in SOPF with volutrauma.

To improve treatment results, many researchers suggest using an inverse inhalation-exhalation ratio. Typically, during mechanical ventilation, we use a 1:2 ratio in order to create favorable conditions for normalizing venous return. However, with nostrils, when in modern intensive care units it is possible to monitor venous return (CVP, wedge pressure, esophageal Doppler), as well as when using inotropic support, this inhalation-exhalation ratio at least becomes secondary.

The proposed technique for reversing the ratio to 1:1 or up to 4:1 makes it possible to lengthen the inspiratory phase, which is accompanied by improved oxygenation in patients with nostrils and is widely used everywhere, since it becomes possible to maintain or improve oxygenation at lower pressure in the respiratory tract, and, accordingly, with a reduced risk of volutrauma.

The proposed mechanisms of action of OSVV include a decrease in arteriovenous shunting, an improvement in the ventilation-perfusion ratio, and a decrease in dead space.

Many studies indicate improved oxygenation and reduced shunting with this technique. However, with a decrease in expiratory time, there is a danger of increasing auto-PEEP, which has also been convincingly shown in a sufficient number of studies. Moreover, the decline in shunt is believed to parallel the development of auto-PEEP. A significant number of authors recommend not to use extreme values ​​of TSVV (such as 4:1), but to limit it to a moderate 1:1 or 1.5:1.

As for improving the ventilation-perfusion ratio, from a purely physiological point of view this is unlikely and there is currently no direct evidence of this.

A reduction in dead space has been demonstrated with the use of SVV, but the clinical significance of this finding is not entirely clear.

Research on the beneficial effects of this type of ventilation is conflicting. A number of researchers report positive results, while others disagree. There is no doubt that longer inspiration and possible auto-PEEP have an effect on cardiac function, reducing cardiac output. On the other hand, these same conditions (increased intrathoracic pressure) may be accompanied by improved cardiac performance as a result of decreased venous return and reduced left ventricular workload.

There are several other aspects of OSVV that are not sufficiently covered in the literature.

Slower gas flow during inspiration, as already mentioned, may reduce the incidence of volutrauma. This effect is independent of other positive aspects of OSVV.

In addition, some researchers believe that alveolar recruitment (that is, the return of flooded alveoli to a normal state under the influence of mechanical ventilation) with the use of PVV may occur slowly, taking more time than with PEEP, but the same level of oxygenation with lower values ​​of intrapulmonary pressure than when using conventional ventilation techniques with PEEP.

As with PEEP, the result varies and depends on the pulmonary compliance and degree of volume of each individual patient.

One of the negative aspects is the need to sedate and paralyze the patient to carry out such a ventilation regimen, since discomfort during prolonged inhalation is accompanied by poor synchronization of the patient with the ventilator. In addition, there is disagreement among experts on whether to use small values ​​of auto-PEEP, or use artificial (external) PEEP.

As already mentioned, ventilation by releasing pressure in the airways is close

resembles the previous ventilation method. In this technique, a predetermined pressure value is applied to achieve inspiration, and the release of pressure in the circuit is accompanied by passive exhalation. The difference lies in the fact that the patient can take voluntary breaths. The advantages and disadvantages of this technique remain to be assessed.

Liquid ventilation

This technique has existed in laboratories for at least 20 years, but has only recently been introduced into the clinic. This ventilation technique uses perfluorocarbons, which have high solubility for oxygen and carbon dioxide, allowing gas exchange. The advantage of this method is the elimination of the gas-liquid interface, which reduces surface tension, allowing inflation of the lungs with lower pressure, and also improves the ventilation-perfusion ratio. Disadvantages are the need for complex equipment and specially designed breathing systems. This factor, combined with the increased work of breathing (the liquid is viscous compared to air), led experts to the conclusion that the use of this technique is not yet practical.

To overcome the difficulties of liquid ventilation, a technique of partial liquid ventilation has been proposed, where small amounts of perfluorocarbons are used to partially or completely replace the functional residual volume in combination with conventional ventilation. The system is relatively simple and initial reports are quite encouraging.

Open lung concept

The open lung concept in the narrow sense of the word is not a ventilation technique as such, but rather a concept for the use of pressure ventilation in SLOP and related conditions. COL uses the characteristics of a healthy lung to preserve surfactant and prevent the lung from “flooding” and becoming infected. These goals are achieved by opening “flooded” alveoli (recruitment) and preventing them from closing during the entire ventilatory cycle. The immediate results of COL are improved pulmonary compliance, reduced alveolar edema and, ultimately, a reduced risk of developing multiple organ failure. The concept of this review does not include the task of evaluating or criticizing certain methods of conducting COL, so only the most basic method will be included here.

The idea of ​​COL arose as a result of the fact that during normal ventilation modes, intact alveoli are ventilated, and as for damaged ones, at best they inflate (recruitment) during inhalation and subsequently collapse during exhalation. This process of inflation - collapse is accompanied by the displacement of surfactant from the alveoli into the bronchioles, where it is destroyed. Accordingly, the idea arose that, along with the usual tasks of maintaining gas exchange, during mechanical ventilation it is desirable to maintain the end-tidal gas volume above the residual volume to prevent surfactant depletion and the negative effects of mechanical ventilation on fluid exchange in the lungs. This is precisely what is achieved by “opening” the lung and maintaining it in an “open” state.

The basic principle is illustrated in Fig. 1.

Rice. 1. Po pressure is necessary for the opening of the alveoli, but upon reaching this pressure (that is, upon opening the lung), ventilation continues with lower pressure values ​​(the area between D and C). However, if the pressure in the alveoli drops below Pc, their collapse will occur again.

Practice questions:

KOL does not require special equipment or monitoring. The required minimum consists of a ventilator capable of delivering pressure ventilation, an acid-base balance monitor, and a pulse oximeter. A number of authors recommend constant monitoring of acid-base balance in combination with constant monitoring of saturation. These are quite complex devices that are not accessible to everyone. Methods for using KOL with a more or less acceptable set of equipment are described.

So, how to do all this - the open lung method?

I’ll make a reservation right away - the description is quite basic, without any special details or details, but it seems to me that this is exactly what is necessary for a practical doctor.

Finding the opening point: First of all, the PEEP before performing the entire maneuver must be set at a level between 15 and 25 cmH2O until a peak pressure of about 45 - 60 cmH2O is reached as static airway pressure or a combination with auto- PEEP. This level of pressure is sufficient to open the alveoli, which at the moment will be subject to recruitment under the influence of high pressure (that is, open during inspiration). When the inhalation-exhalation ratio is sufficient to guarantee zero gas flow at the end of exhalation, the peak pressure is increased gradually by 3 - 5 cm H2O until the above level is reached. During the alveolar opening process, PaO2 (partial pressure of oxygen) is an indicator of successful alveolar opening (it is the only parameter that correlates with the physical amount of lung tissue involved in gas exchange). In the presence of a pronounced pulmonary process, frequent measurement of acid base level is necessary during the pressure titration process.

Fig. 2 Stages of the process when using the open lung technique.

A number of authors even recommend continuous measurement of PaO2 using special techniques, however, in my opinion, the lack of such specialized equipment should not serve as a deterrent to the use of this technique.

By finding the maximum value of PaO2, which does not increase further as the pressure in the respiratory tract increases - the first stage of the process is completed - the values ​​of the opening pressure of the alveoli are found.

Then the pressure begins to gradually decrease, continuing to monitor PaO2 until the pressure is found at which this value begins (but only begins) to decrease - which means finding the pressure at which part of the alveoli begins to collapse (close), which corresponds to the pressure Pc in Fig. 1. When PaO2 decreases, the pressure is again set to the opening pressure level for a short time (10 - 30 sec), and then carefully reduced to a level just above the closing pressure, trying to obtain the lowest possible pressure. In this way, a ventilation pressure value is obtained that allows the alveoli to open and keeps them open during the inhalation phase.

Maintaining the lung in an open state: it is necessary to ensure that the PEEP level is set slightly above Pc (Fig. 1), after which the above procedure is repeated, but for PEEP, finding the lowest PEEP value at which the maximum PaO2 value is achieved. This PEEP level is the “lower” pressure that allows the alveoli to remain open during exhalation. The process of opening the lungs is schematically depicted in Fig. 2.

It is believed that the process of opening the alveoli is almost always possible in the first 48 hours of mechanical ventilation. Even if it is not possible to open all lung fields, the use of such a ventilation strategy can minimize damage to lung tissue during mechanical ventilation, which ultimately improves treatment results.

In conclusion, we can summarize all of the above as follows:

• The lung is opened using high inhalation pressure.
• Maintaining the lung in an open state is achieved by maintaining the PEEP level above the level of alveolar closure.
• Optimization of gas exchange is achieved by minimizing the above pressures.

Face down or prone ventilation (FVV)

As already indicated, the lesion of the lung in SOPL is inhomogeneous and the most affected areas are usually localized dorsally, with a predominant location of unaffected areas ventrally. As a result, healthy areas of the lung receive a predominant amount of DO, which is accompanied by overinflation of the alveoli and leads to the above-mentioned lung damage as a result of mechanical ventilation itself. Approximately 10 years ago, the first reports appeared that turning the patient onto his stomach and continuing ventilation in this position was accompanied by a significant improvement in oxygenation. This was achieved without any changes in the ventilation mode except for a decrease in FiO2 as a result of improved oxygenation. This report led to significant interest in this technique, and initially only the speculative mechanisms of action of such ventilation were published. Recently, a number of works have appeared that more or less summarize the factors leading to improved oxygenation in the prone position.

1. Abdominal bloating (common in patients on mechanical ventilation) in the face-down position is accompanied by significantly lower intragastric pressure, and accordingly is accompanied by less restriction of diaphragm mobility.
2. It was shown that the distribution of pulmonary perfusion in the face-down position was much more uniform, especially when PEEP was used. And this, in turn, is accompanied by a much more uniform and close to normal ventilation-perfusion ratio.
3. These positive changes predominantly occur in the dorsal (that is, the most affected) parts of the lung.
4. Increase in functional residual volume.
5. Improvement of tracheo-bronchial drainage.

I have some personal experience of using VLV for nozzle. Typically, the use of such ventilation occurs in patients who are difficult to ventilate using conventional methods. As a rule, they are already pressure ventilated with high plateau pressure values, with TSVV and Fі02 approaching 100%. In this case, PaO2 is usually difficult to maintain at values ​​close to or below 10 kPa. Turning the patient onto his stomach is accompanied by an improvement in oxygenation within an hour (sometimes faster). As a rule, a ventilation session on the stomach lasts 6 - 12 hours, and is repeated if necessary. In the future, the duration of the sessions is reduced (the patient simply does not need as much time to improve oxygenation) and they are carried out much less frequently. This is certainly not a panacea, but in my own practice I was convinced that the technique works. Interestingly, an article by Gattinioni published in the last few days indicates that the patient's oxygenation actually improves under the influence of this ventilation technique. However, the clinical result of treatment does not differ from the control group, that is, mortality does not decrease.

Conclusion

In recent years, there has been a shift in the philosophy of mechanical ventilation for nostrils, moving away from the original concept of achieving normal physiological parameters at any cost and moving towards minimizing lung damage caused by ventilation itself.

Initially, it was proposed to limit DO in order not to exceed the plateau pressure (this is the pressure measured in the airways at the end of inspiration) more than 30-35 cm H2O. This limitation of DO is accompanied by a decrease in CO2 elimination and loss of lung volumes. Enough evidence has accumulated to suggest that patients tolerate such changes without problems. However, over time, it became clear that limiting DV or inspiratory pressure was associated with negative results. This is believed to be a consequence of a decrease (or complete cessation) of alveolar recruitment during each inspiration with a subsequent deterioration in gas exchange. Early research indicates that increased recruitment can overcome the negative effects of decreased pressure or volume.

There are at least two such techniques. One is to use moderately high inspiratory pressure for a relatively long time (on the order of 40 seconds) to increase recruitment. Ventilation then continues as before.

The second (and in my opinion more promising) strategy is the open lung strategy, which is described above.

The latest direction in the prevention of ventilator-dependent lung damage is the rational use of PEEP; a detailed description of the method is given in the open lung technique. However, it should be pointed out that recommended PEEP levels seriously exceed routinely used values.

Literature

1. 1 . Carl Shanholtz, Roy Brower "Should inverse ventilation ratio be used in Adult Respiratory Distress Syndrome?" Am J Respir Crit Care Med vol 149. pp 1354-1358, 1994
2. "Mechanical ventilation: a shifting philosophy" T.E. Stewart, A.S. Slutsky Current Opinion in Critical Sage 1995, 1:49-56
3. J. ViIIar, A. Slutskу “Is the outcome from acute respiratory distress syndrome improving?” Current Opinion in Critical Care 1996, 2:79-87
4. M.Mure, S. Lindahl “Prone position improves gas exchange - but how?” Acta Anaesthesiol Scand 2001, 45:50-159
5. W. Lamm, M. Graham, R. AIbert "Mechanism by which the Prone Position improves Oxygenation in Acute Lung injury" Am J Respir Crit Cre Med, 1994, voI 150, 184-193
6. H. Zang, V. Ranieri, A. Slutskу “CelluIar effects of ventilator induced lung inјuruу” Current Opinion in Critical Care, 2000, 6:71-74
7. M.O. Meade, G.H. Guyatt, T.E. Stewart "Lung protection during mechanical ventilation" ip Yearbook of Intensive Care Medicine, 1999, pp 269-279.
8. A.W. Kirpatrick, M.O. Meade, T.E. Stewart “Lung protective veterinary strategies in ARDS” in Yearbook of Intensive Care Medicine, 1996, pp 398 - 409
9. B. Lachmann "The concept of open lung management" The International Journal of Intensive Care, Winter 2000, 215 - 220
10. S. H. Bohm et al "The open lung concept" in Yearbook of Intensive Care Medicine, pp 430 - 440
11. J.Luce "Acute lung injury and acute respiratory distress syndrome" Crit Care Med 1998 vol 26, No 2369-76
12. L. Bigatello et al "Ventilatory management of severe acute respiratory failure for Y2K" Anesthesiology 1999, V 91, No 6, 1567-70

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Pathways

Nose - the first changes in the incoming air occur in the nose, where it is cleaned, warmed and moistened. This is facilitated by the hair filter, vestibule and turbinates. Intensive blood supply to the mucous membrane and cavernous plexuses of the shells ensures rapid warming or cooling of the air to body temperature. Water evaporating from the mucous membrane humidifies the air by 75-80%. Prolonged inhalation of air with low humidity leads to drying of the mucous membrane, entry of dry air into the lungs, development of atelectasis, pneumonia and increased resistance in the airways.

Pharynx separates food from air, regulates pressure in the middle ear.

Larynx provides vocal function by using the epiglottis to prevent aspiration, and the closure of the vocal cords is one of the main components of cough.

Trachea - the main air duct, in which the air is warmed and humidified. Mucosal cells capture foreign substances, and cilia move mucus up the trachea.

Bronchi (lobar and segmental) end in terminal bronchioles.

The larynx, trachea and bronchi are also involved in purifying, warming and humidifying the air.

The structure of the wall of the conducting airways (AP) differs from the structure of the airways of the gas exchange zone. The wall of the conducting airways consists of the mucous membrane, a layer of smooth muscle, submucosal connective and cartilaginous membranes. The epithelial cells of the airways are equipped with cilia, which, oscillating rhythmically, push the protective layer of mucus towards the nasopharynx. The mucous membrane of the EP and lung tissue contain macrophages that phagocytize and digest mineral and bacterial particles. Normally, mucus is constantly removed from the respiratory tract and alveoli. The mucous membrane of the EP is represented by ciliated pseudostratified epithelium, as well as secretory cells that secrete mucus, immunoglobulins, complement, lysozyme, inhibitors, interferon and other substances. The cilia contain many mitochondria, which provide energy for their high motor activity (about 1000 movements per minute), which allows them to transport sputum at a speed of up to 1 cm/min in the bronchi and up to 3 cm/min in the trachea. During the day, about 100 ml of sputum is normally evacuated from the trachea and bronchi, and in pathological conditions up to 100 ml/hour.

Cilia function in a double layer of mucus. The lower one contains biologically active substances, enzymes, immunoglobulins, the concentration of which is 10 times higher than in the blood. This determines the biological protective function of mucus. Its top layer mechanically protects the eyelashes from damage. Thickening or reduction of the upper layer of mucus due to inflammation or toxic effects inevitably disrupts the drainage function of the ciliated epithelium, irritates the respiratory tract and reflexively causes coughing. Sneezing and coughing protect the lungs from mineral and bacterial particles.

Alveoli

In the alveoli, gas exchange occurs between the blood of the pulmonary capillaries and the air. The total number of alveoli is approximately 300 million, and their total surface area is approximately 80 m2. The diameter of the alveoli is 0.2-0.3 mm. Gas exchange between alveolar air and blood occurs by diffusion. The blood of the pulmonary capillaries is separated from the alveolar space only by a thin layer of tissue - the so-called alveolar-capillary membrane, formed by the alveolar epithelium, a narrow interstitial space and the endothelium of the capillary. The total thickness of this membrane does not exceed 1 micron. The entire alveolar surface of the lungs is covered with a thin film called surfactant.

Surfactant reduces surface tension at the boundary between liquid and air at the end of exhalation, when the volume of the lung is minimal, increases elasticity lungs and plays the role of an anti-edematous factor(does not allow water vapor from the alveolar air to pass through), as a result of which the alveoli remain dry. It reduces surface tension when the volume of the alveoli decreases during exhalation and prevents its collapse; reduces shunting, which improves oxygenation of arterial blood at lower pressure and minimal O 2 content in the inhaled mixture.

The surfactant layer consists of:

1) the surfactant itself (microfilms of phospholipid or polyprotein molecular complexes at the border with the air);

2) hypophase (deeper hydrophilic layer of proteins, electrolytes, bound water, phospholipids and polysaccharides);

3) the cellular component, represented by alveolocytes and alveolar macrophages.

The main chemical components of surfactant are lipids, proteins and carbohydrates. Phospholipids (lecithin, palmitic acid, heparin) make up 80-90% of its mass. The surfactant also covers the bronchioles with a continuous layer, reduces breathing resistance, and maintains filling

At low tensile pressure, it reduces the forces that cause fluid accumulation in tissues. In addition, surfactant purifies inhaled gases, filters and traps inhaled particles, regulates the exchange of water between the blood and the alveolar air, accelerates the diffusion of CO 2, and has a pronounced antioxidant effect. Surfactant is very sensitive to various endo- and exogenous factors: circulatory disorders, ventilation and metabolism, changes in PO 2 in the inhaled air, and air pollution. With surfactant deficiency, atelectasis and RDS of newborns occur. Approximately 90-95% of alveolar surfactant is recycled, cleared, accumulated and resecreted. The half-life of surfactant components from the lumen of the alveoli of healthy lungs is about 20 hours.

Lung volumes

Ventilation of the lungs depends on the depth of breathing and the frequency of respiratory movements. Both of these parameters can vary depending on the needs of the body. There are a number of volume indicators that characterize the condition of the lungs. Normal average values ​​for an adult are as follows:

1. Tidal volume(DO-VT- Tidal Volume)- volume of inhaled and exhaled air during quiet breathing. Normal values ​​are 7-9ml/kg.

2. Inspiratory reserve volume (IRV) -IRV - Inspiratory Reserve Volume) - the volume that can additionally arrive after a quiet inhalation, i.e. difference between normal and maximum ventilation. Normal value: 2-2.5 l (about 2/3 vital capacity).

3. Expiratory reserve volume (ERV) - Expiratory Reserve Volume) - the volume that can be additionally exhaled after a quiet exhalation, i.e. difference between normal and maximum exhalation. Normal value: 1.0-1.5 l (about 1/3 vital capacity).

4.Residual volume (RO - RV - Residal Volume) - the volume remaining in the lungs after maximum exhalation. About 1.5-2.0 l.

5. Vital capacity of the lungs (VC - VT - Vital Capacity) - the amount of air that can be maximally exhaled after maximal inhalation. Vital capacity is an indicator of the mobility of the lungs and chest. Vital capacity depends on age, gender, body size and position, and degree of fitness. Normal vital capacity values ​​are 60-70 ml/kg - 3.5-5.5 l.

6. Inspiratory reserve (IR) -Inspiratory capacity (Evd - IC - Inspiration Capacity) - the maximum amount of air that can enter the lungs after a quiet exhalation. Equal to the sum of DO and ROVD.

7.Total lung capacity (TLC) - Total lung capacity) or maximum lung capacity - the amount of air contained in the lungs at the height of maximum inspiration. Consists of VC and OO and is calculated as the sum of VC and OO. The normal value is about 6.0 l.
Studying the structure of TLC is crucial in elucidating ways to increase or decrease vital capacity, which can have significant practical significance. An increase in vital capacity can be assessed positively only in cases where the vital capacity does not change or increases, but less than the vital capacity, which occurs when the vital capacity increases due to a decrease in the volume. If, simultaneously with an increase in VC, an even greater increase in TLC occurs, then this cannot be considered a positive factor. When VC is below 70% TLC, the function of external respiration is deeply impaired. Usually, in pathological conditions, TLC and vital capacity change in the same way, with the exception of obstructive pulmonary emphysema, when vital capacity, as a rule, decreases, VT increases, and TLC may remain normal or be higher than normal.

8.Functional residual capacity (FRC - FRC - Functional residual volume) - the amount of air that remains in the lungs after a quiet exhalation. Normal values ​​for adults are from 3 to 3.5 liters. FFU = OO + ROvyd. By definition, FRC is the volume of gas that remains in the lungs during a quiet exhalation and can be a measure of the area of ​​gas exchange. It is formed as a result of the balance between the oppositely directed elastic forces of the lungs and chest. The physiological significance of FRC is the partial renewal of the alveolar volume of air during inspiration (ventilated volume) and indicates the volume of alveolar air constantly present in the lungs. A decrease in FRC is associated with the development of atelectasis, closure of small airways, a decrease in lung compliance, an increase in the alveolar-arterial difference in O2 as a result of perfusion in atelectasis areas of the lungs, and a decrease in the ventilation-perfusion ratio. Obstructive ventilation disorders lead to an increase in FRC, restrictive disorders lead to a decrease in FRC.

Anatomical and functional dead space

Anatomical dead space called the volume of the airways in which gas exchange does not occur. This space includes the nasal and oral cavities, pharynx, larynx, trachea, bronchi and bronchioles. The amount of dead space depends on the height and position of the body. It can be approximately assumed that in a sitting person the volume of dead space (in milliliters) is equal to twice the body weight (in kilograms). Thus, in adults it is about 150-200 ml (2 ml/kg body weight).

Under functional (physiological) dead space understand all those areas of the respiratory system in which gas exchange does not occur due to reduced or absent blood flow. The functional dead space, in contrast to the anatomical one, includes not only the airways, but also those alveoli that are ventilated but not perfused with blood.

Alveolar and dead space ventilation

The part of the minute volume of respiration that reaches the alveoli is called alveolar ventilation, the rest of it is dead space ventilation. Alveolar ventilation serves as an indicator of the efficiency of breathing in general. The gas composition maintained in the alveolar space depends on this value. As for minute volume, it only to a small extent reflects the effectiveness of ventilation. So, if the minute volume of breathing is normal (7 l/min), but breathing is frequent and shallow (UP to 0.2 l, RR-35/min), then ventilate

There will be mainly dead space, into which air enters before the alveolar; in this case, the inhaled air will hardly reach the alveoli. Because the the volume of dead space is constant, alveolar ventilation is greater, the deeper the breathing and the lower the frequency.

Extensibility (compliance) of lung tissue
Lung compliance is a measure of elastic traction, as well as elastic resistance of the lung tissue, which is overcome during inhalation. In other words, extensibility is a measure of the elasticity of the lung tissue, i.e. its pliability. Mathematically, compliance is expressed as the quotient of the change in lung volume and the corresponding change in intrapulmonary pressure.

Compliance can be measured separately for the lungs and the chest. From a clinical point of view (especially during mechanical ventilation), the compliance of the lung tissue itself, which reflects the degree of restrictive pulmonary pathology, is of greatest interest. In modern literature, lung compliance is usually referred to as “compliance” (from the English word “compliance”, abbreviated as C).

Lung compliance decreases:

With age (in patients over 50 years old);

In a lying position (due to pressure from the abdominal organs on the diaphragm);

During laparoscopic surgery due to carboxyperitoneum;

For acute restrictive pathology (acute polysegmental pneumonia, RDS, pulmonary edema, atelectasis, aspiration, etc.);

For chronic restrictive pathology (chronic pneumonia, pulmonary fibrosis, collagenosis, silicosis, etc.);

With pathology of the organs that surround the lungs (pneumo- or hydrothorax, high standing of the dome of the diaphragm with intestinal paresis, etc.).

The worse the compliance of the lungs, the greater the elastic resistance of the lung tissue must be overcome in order to achieve the same tidal volume as with normal compliance. Consequently, in the case of deteriorating lung compliance, when the same tidal volume is achieved, the pressure in the airways increases significantly.

This point is very important to understand: with volumetric ventilation, when a forced tidal volume is supplied to a patient with poor lung compliance (without high airway resistance), a significant increase in peak airway pressure and intrapulmonary pressure significantly increases the risk of barotrauma.

Airway resistance

The flow of the respiratory mixture in the lungs must overcome not only the elastic resistance of the tissue itself, but also the resistive resistance of the airways Raw (an abbreviation for the English word “resistance”). Since the tracheobronchial tree is a system of tubes of varying lengths and widths, the resistance to gas flow in the lungs can be determined according to known physical laws. In general, flow resistance depends on the pressure gradient at the beginning and end of the tube, as well as on the magnitude of the flow itself.

Gas flow in the lungs can be laminar, turbulent, or transient. Laminar flow is characterized by layer-by-layer translational movement of gas with

Varying speed: the flow speed is highest in the center and gradually decreases towards the walls. Laminar gas flow predominates at relatively low speeds and is described by Poiseuille's law, according to which the resistance to gas flow depends most on the radius of the tube (bronchi). Reducing the radius by 2 times leads to an increase in resistance by 16 times. In this regard, the importance of choosing the widest possible endotracheal (tracheostomy) tube and maintaining the patency of the tracheobronchial tree during mechanical ventilation is clear.
The resistance of the respiratory tract to gas flow increases significantly with bronchiolospasm, swelling of the bronchial mucosa, accumulation of mucus and inflammatory secretions due to narrowing of the lumen of the bronchial tree. Resistance is also affected by flow rate and length of the tube(s). WITH

By increasing the flow rate (forcing inhalation or exhalation), airway resistance increases.

The main reasons for increased airway resistance are:

Bronchiolospasm;

Swelling of the bronchial mucosa (exacerbation of bronchial asthma, bronchitis, subglottic laryngitis);

Foreign body, aspiration, neoplasms;

Accumulation of sputum and inflammatory secretions;

Emphysema (dynamic compression of the airways).

Turbulent flow is characterized by the chaotic movement of gas molecules along the tube (bronchi). It predominates at high volumetric flow rates. In the case of turbulent flow, airway resistance increases, since it depends to an even greater extent on the flow speed and the radius of the bronchi. Turbulent movement occurs at high flows, sudden changes in flow speed, in places of bends and branches of the bronchi, and with a sharp change in the diameter of the bronchi. This is why turbulent flow is characteristic of patients with COPD, when even in remission there is increased airway resistance. The same applies to patients with bronchial asthma.

Airway resistance is unevenly distributed in the lungs. The greatest resistance is created by bronchi of medium caliber (up to the 5th-7th generation), since the resistance of large bronchi is small due to their large diameter, and small bronchi - due to the large total cross-sectional area.

Airway resistance also depends on lung volume. With a large volume, the parenchyma has a greater “stretching” effect on the airways, and their resistance decreases. The use of PEEP helps to increase lung volume and, consequently, reduce airway resistance.

Normal airway resistance is:

In adults - 3-10 mm water column/l/s;

In children - 15-20 mm water column/l/s;

In infants under 1 year - 20-30 mm water column/l/s;

In newborns - 30-50 mm water column/l/s.

On exhalation, the airway resistance is 2-4 mm water column/l/s greater than on inspiration. This is due to the passive nature of exhalation, when the condition of the wall of the airways affects gas flow to a greater extent than during active inhalation. Therefore, it takes 2-3 times longer to fully exhale than to inhale. Normally, the inhalation/exhalation time ratio (I:E) for adults is about 1: 1.5-2. The completeness of exhalation in a patient during mechanical ventilation can be assessed by monitoring the expiratory time constant.

Work of breathing

The work of breathing is performed primarily by the inspiratory muscles during inhalation; exhalation is almost always passive. At the same time, in the case of, for example, acute bronchospasm or swelling of the mucous membrane of the respiratory tract, exhalation also becomes active, which significantly increases the overall work of external ventilation.

During inhalation, the work of breathing is mainly spent on overcoming the elastic resistance of the lung tissue and the resistive resistance of the respiratory tract, while about 50% of the expended energy accumulates in the elastic structures of the lungs. During exhalation, this stored potential energy is released, allowing the expiratory resistance of the airways to be overcome.

The increase in resistance to inhalation or exhalation is compensated by the additional work of the respiratory muscles. The work of breathing increases with a decrease in lung compliance (restrictive pathology), an increase in airway resistance (obstructive pathology), and tachypnea (due to dead space ventilation).

Normally, only 2-3% of the total oxygen consumed by the body is spent on the work of the respiratory muscles. This is the so-called “cost of breathing”. During physical work, the cost of breathing can reach 10-15%. And with pathology (especially restrictive), more than 30-40% of the total oxygen absorbed by the body can be spent on the work of the respiratory muscles. In severe diffuse respiratory failure, the cost of breathing increases to 90%. At some point, all the additional oxygen obtained by increasing ventilation goes to cover the corresponding increase in the work of the respiratory muscles. That is why, at a certain stage, a significant increase in the work of breathing is a direct indication for starting mechanical ventilation, at which the cost of breathing is reduced to almost 0.

The work of breathing required to overcome elastic resistance (lung compliance) increases as tidal volume increases. The work required to overcome airway resistance increases with increasing respiratory rate. The patient seeks to reduce the work of breathing by changing the respiratory rate and tidal volume depending on the prevailing pathology. For each situation, there are optimal respiratory rates and tidal volumes at which the work of breathing is minimal. Thus, for patients with reduced compliance, from the point of view of minimizing the work of breathing, more frequent and shallow breathing is suitable (hard lungs are difficult to straighten). On the other hand, when airway resistance is increased, deep and slow breathing is optimal. This is understandable: an increase in tidal volume allows you to “stretch”, expand the bronchi, and reduce their resistance to gas flow; for the same purpose, patients with obstructive pathology compress their lips during exhalation, creating their own “PEEP”. Slow and infrequent breathing helps lengthen exhalation, which is important for more complete removal of the exhaled gas mixture in conditions of increased expiratory resistance of the respiratory tract.

Breathing regulation

The breathing process is regulated by the central and peripheral nervous system. In the reticular formation of the brain there is a respiratory center, consisting of the centers of inhalation, exhalation and pneumotaxis.

Central chemoreceptors are located in the medulla oblongata and are excited when the concentration of H+ and PCO 2 in the cerebrospinal fluid increases. Normally, the pH of the latter is 7.32, PCO 2 is 50 mmHg, and the HCO 3 content is 24.5 mmol/l. Even a slight decrease in pH and an increase in PCO 2 increase ventilation. These receptors respond to hypercapnia and acidosis more slowly than peripheral ones, since additional time is required to measure the values ​​of CO 2, H + and HCO 3 due to overcoming the blood-brain barrier. Contractions of the respiratory muscles are controlled by the central respiratory mechanism, consisting of a group of cells in the medulla oblongata, pons, and pneumotaxic centers. They tone the respiratory center and, based on impulses from mechanoreceptors, determine the threshold of excitation at which inhalation stops. Pneumotaxic cells also switch inspiration to expiration.

Peripheral chemoreceptors, located on the inner membranes of the carotid sinus, aortic arch, and left atrium, control humoral parameters (PO 2, PCO 2 in arterial blood and cerebrospinal fluid) and immediately respond to changes in the internal environment of the body, changing the mode of spontaneous breathing and, thus, correcting pH, PO 2 and PCO 2 in arterial blood and cerebrospinal fluid. Impulses from chemoreceptors regulate the amount of ventilation required to maintain a certain metabolic level. In optimizing the ventilation mode, i.e. Mechanoreceptors are also involved in establishing the frequency and depth of breathing, the duration of inhalation and exhalation, and the force of contraction of the respiratory muscles at a given level of ventilation. Ventilation of the lungs is determined by the level of metabolism, the effect of metabolic products and O2 on chemoreceptors, which transform them into afferent impulses of the nervous structures of the central respiratory mechanism. The main function of arterial chemoreceptors is the immediate correction of breathing in response to changes in blood gas composition.

Peripheral mechanoreceptors, localized in the walls of the alveoli, intercostal muscles and the diaphragm, respond to the stretching of the structures in which they are located, to information about mechanical phenomena. The main role is played by the mechanoreceptors of the lungs. The inhaled air flows through the VP to the alveoli and participates in gas exchange at the level of the alveolar-capillary membrane. As the walls of the alveoli stretch during inspiration, the mechanoreceptors are excited and send an afferent signal to the respiratory center, which inhibits inspiration (Hering-Breuer reflex).

During normal breathing, intercostal-diaphragmatic mechanoreceptors are not excited and have an auxiliary value.

The regulatory system ends with neurons that integrate impulses that come to them from chemoreceptors and send excitation impulses to respiratory motor neurons. The cells of the bulbar respiratory center send both excitatory and inhibitory impulses to the respiratory muscles. Coordinated excitation of respiratory motor neurons leads to synchronous contraction of the respiratory muscles.

The breathing movements that create air flow occur due to the coordinated work of all respiratory muscles. Motor nerve cells

The neurons of the respiratory muscles are located in the anterior horns of the gray matter of the spinal cord (cervical and thoracic segments).

In humans, the cerebral cortex also takes part in the regulation of breathing within the limits allowed by the chemoreceptor regulation of breathing. For example, volitional breath holding is limited by the time during which PaO 2 in the cerebrospinal fluid rises to levels that excite arterial and medullary receptors.

Biomechanics of breathing

Ventilation of the lungs occurs due to periodic changes in the work of the respiratory muscles, the volume of the chest cavity and lungs. The main muscles of inspiration are the diaphragm and the external intercostal muscles. During their contraction, the dome of the diaphragm is flattened and the ribs are raised upward, as a result of which the volume of the chest increases and the negative intrapleural pressure (Ppl) increases. Before the start of inhalation (at the end of exhalation) Ppl is approximately minus 3-5 cm water column. Alveolar pressure (Palv) is taken as 0 (i.e. equal to atmospheric pressure), it also reflects the pressure in the airways and correlates with intrathoracic pressure.

The gradient between alveolar and intrapleural pressure is called transpulmonary pressure (Ptp). At the end of exhalation it is 3-5 cm of water column. During spontaneous inspiration, an increase in negative Ppl (up to minus 6-10 cm water column) causes a decrease in pressure in the alveoli and respiratory tract below atmospheric pressure. In the alveoli, the pressure drops to minus 3-5 cm of water column. Due to the pressure difference, air enters (sucks in) from the external environment into the lungs. The chest and diaphragm act as a piston pump, drawing air into the lungs. This “suction” action of the chest is important not only for ventilation, but also for blood circulation. During spontaneous inspiration, additional “suction” of blood to the heart occurs (maintaining preload) and activation of pulmonary blood flow from the right ventricle through the pulmonary artery system. At the end of inspiration, when gas movement stops, alveolar pressure returns to zero, but intrapleural pressure remains reduced to minus 6-10 cm water column.

Exhalation is normally a passive process. After relaxation of the respiratory muscles, the forces of elastic traction of the chest and lungs cause the removal (squeezing out) of gas from the lungs and restoration of the original volume of the lungs. If the patency of the tracheobronchial tree is impaired (inflammatory secretion, swelling of the mucous membrane, bronchospasm), the exhalation process is difficult, and the exhalation muscles (internal intercostal muscles, pectoral muscles, abdominal muscles, etc.) also begin to take part in the act of breathing. When the expiratory muscles are exhausted, the exhalation process becomes even more difficult, the exhaled mixture is retained and the lungs become dynamically overinflated.

Non-respiratory lung functions

The functions of the lungs are not limited to the diffusion of gases. They contain 50% of all endothelial cells in the body, which line the capillary surface of the membrane and participate in the metabolism and inactivation of biologically active substances passing through the lungs.

1. The lungs control general hemodynamics by varying the filling of their own vascular bed and influencing biologically active substances that regulate vascular tone (serotonin, histamine, bradykinin, catecholamines), converting angiotensin I to angiotensin II, and participating in the metabolism of prostaglandins.

2. The lungs regulate blood clotting by secreting prostacyclin, an inhibitor of platelet aggregation, and removing thromboplastin, fibrin and its degradation products from the bloodstream. As a result, the blood flowing from the lungs has higher fibrinolytic activity.

3. The lungs participate in protein, carbohydrate and fat metabolism, synthesizing phospholipids (phosphatidylcholine and phosphatidylglycerol - the main components of surfactant).

4. The lungs produce and eliminate heat, maintaining the body's energy balance.

5. The lungs cleanse the blood of mechanical impurities. Cell aggregates, microthrombi, bacteria, air bubbles, and fat droplets are retained by the lungs and are subject to destruction and metabolism.

Types of ventilation and types of ventilation disorders

A physiologically clear classification of ventilation types has been developed, based on the partial pressures of gases in the alveoli. In accordance with this classification, the following types of ventilation are distinguished:

1.Normoventilation - normal ventilation, in which the partial pressure of CO2 in the alveoli is maintained at about 40 mmHg.

2. Hyperventilation - increased ventilation that exceeds the metabolic needs of the body (PaCO2<40 мм.рт.ст.).

3. Hypoventilation - reduced ventilation compared to the metabolic needs of the body (PaCO2>40 mmHg).

4. Increased ventilation - any increase in alveolar ventilation compared to the resting level, regardless of the partial pressure of gases in the alveoli (for example, during muscular work).

5.Eupnea - normal ventilation at rest, accompanied by a subjective feeling of comfort.

6. Hyperpnea - an increase in the depth of breathing, regardless of whether the frequency of respiratory movements is increased or not.

7.Tachypnea - increase in respiratory rate.

8.Bradypnea - decreased respiratory rate.

9. Apnea - cessation of breathing, caused mainly by the lack of physiological stimulation of the respiratory center (decrease in CO2 tension in arterial blood).

10.Dyspnea (shortness of breath) is an unpleasant subjective feeling of insufficient breathing or difficulty breathing.

11. Orthopnea - severe shortness of breath associated with stagnation of blood in the pulmonary capillaries as a result of left heart failure. In a horizontal position, this condition is aggravated, and therefore it is difficult for such patients to lie.

12. Asphyxia - cessation or depression of breathing, associated mainly with paralysis of the respiratory centers or closure of the airways. Gas exchange is sharply impaired (hypoxia and hypercapnia are observed).

For diagnostic purposes, it is advisable to distinguish between two types of ventilation disorders - restrictive and obstructive.

The restrictive type of ventilation disorders includes all pathological conditions in which the respiratory excursion and the ability of the lungs to expand are reduced, i.e. their extensibility decreases. Such disorders are observed, for example, with lesions of the pulmonary parenchyma (pneumonia, pulmonary edema, pulmonary fibrosis) or with pleural adhesions.

The obstructive type of ventilation disorders is caused by a narrowing of the airways, i.e. increasing their aerodynamic resistance. Similar conditions occur, for example, when mucus accumulates in the respiratory tract, swelling of their mucous membrane or spasm of the bronchial muscles (allergic bronchiolospasm, bronchial asthma, asthmatic bronchitis, etc.). In such patients, the resistance to inhalation and exhalation is increased, and therefore, over time, the airiness of the lungs and their FRC increase. A pathological condition characterized by an excessive decrease in the number of elastic fibers (disappearance of alveolar septa, unification of the capillary network) is called pulmonary emphysema.

(Continuous positive pressure ventilation - CPPV - Positive end-expiratory pressure - PEEP). In this mode, the pressure in the airways during the final phase of exhalation does not decrease to 0, but is maintained at a given level (Fig. 4.6). PEEP is achieved using a special unit built into modern respirators. A large amount of clinical material has been accumulated indicating the effectiveness of this method. PEEP is used in the treatment of ARF associated with severe pulmonary diseases (ARDS, common pneumonia, chronic obstructive pulmonary diseases in the acute stage) and pulmonary edema. However, it has been proven that PEEP does not reduce and may even increase the amount of extravascular water in the lungs. At the same time, the PEEP mode promotes a more physiological distribution of the gas mixture in the lungs, reducing venous shunt, improving the mechanical properties of the lungs and oxygen transport. There is evidence that PEEP restores surfactant activity and reduces its bronchoalveolar clearance.

Rice. 4.6. Ventilation mode with PEEP.
Airway pressure curve.

When choosing the PEEP mode, you should keep in mind that it can significantly reduce CO. The higher the final pressure, the more significant the effect of this regime on hemodynamics. A decrease in CO can occur at a PEEP of 7 cm water column. and more, which depends on the compensatory capabilities of the cardiovascular system. Increasing pressure to 12 cm water column. contributes to a significant increase in the load on the right ventricle and an increase in pulmonary hypertension. The negative effects of PEEP may largely depend on errors in its use. You should not immediately create a high level of PEEP. The recommended initial PEEP level is 2-6 cm of water column. Increasing end-expiratory pressure should be carried out gradually, “step by step” and in the absence of the desired effect from the set value. Increase PEEP by 2-3 cm of water column. no more than every 15-20 minutes. PEEP is especially carefully increased after 12 cm of water column. The safest level of the indicator is 6-8 cm of water column, but this does not mean that this mode is optimal in every situation. With a large venous shunt and severe arterial hypoxemia, a higher level of PEEP with a VFC of 0.5 or higher may be required. In each specific case, the PEEP value is selected individually! A prerequisite is a dynamic study of arterial blood gases, pH and central hemodynamic parameters: cardiac index, filling pressure of the right and left ventricles and total peripheral resistance. In this case, the compliance of the lungs should also be taken into account.
PEEP promotes the “opening” of non-functioning alveoli and atelectatic areas, resulting in improved ventilation of alveoli that were insufficiently ventilated or not ventilated at all and in which blood shunting occurred. The positive effect of PEEP is due to an increase in the functional residual capacity and compliance of the lungs, an improvement in ventilation-perfusion relationships in the lungs and a decrease in the alveolar-arterial oxygen difference.
The correctness of the PEEP level can be determined by the following main indicators:
no negative effect on blood circulation;
increased lung compliance;
reduction of pulmonary shunt.
The main indication for PEEP is arterial hypoxemia, which is not eliminated by other modes of mechanical ventilation.

Characteristics of ventilation modes with volume regulation:
the most important parameters of ventilation (DO and MOB), as well as the ratio of the duration of inhalation and exhalation, are established by the doctor;
precise control of the adequacy of ventilation with the selected FiO2 is carried out by analyzing the gas composition of arterial blood;
established volumes of ventilation, regardless of the physical characteristics of the lungs, do not guarantee optimal distribution of the gas mixture and uniform ventilation of the lungs;
To improve ventilation-perfusion relationships, periodic inflation of the lungs or mechanical ventilation in the PEEP mode is recommended.