PCV (pressure control ventilation) - pressure controlled ventilation is similar to CMV mode, and when the trigger is set, to ACMV. The only difference is the need for the doctor to set not BEFORE, but inspiratory pressure.
BiPAP (biphasic positive airway pressure) - ventilation with two phases of positive airway pressure. In terms of its technical implementation, this ventilation mode is similar to PCV.
A distinctive feature is the possibility of independent respiratory attempts at the height of inhalation (segment 2-3 in Fig. 3.5). Thus, the mode provides the patient with greater freedom of breathing. BiPAP is used when transitioning from PCV to more assisted ventilation modes.
With an increase in the level of wakefulness in patients with intracranial hemorrhages, the aggressiveness of respiratory support is gradually reduced and switched to auxiliary ventilation modes.
The main modes of auxiliary ventilation, Used when transferring the patient to spontaneous breathing
Rice. 3.6. Airway pressure (Paw) curve as the patient breathes in SIMV mode. Alternation of breaths with a given tidal volume (1) (the frequency of these breaths is set by the doctor) and spontaneous breathing of the patient (2).
Rice. 3.7. Airway pressure (Paw) curve when the patient breathes in Pressure Support mode. Independent breathing of the patient with little pressure support of each breath (Psup); СРАР - see in the text.
Rice. 3.8. Airway pressure (Paw) curve as the patient breathes in CPAP mode. Breathing is independent, without any support (1).
The patient will breathe spontaneously with a lower DO (eg, 350 ml). Thus, MO ventilation of the patient will be 700 ml x 5 + 350 ml x 10 = 7 liters. The mode is used to train patients' spontaneous breathing. The alternation of the patient's own respiratory attempts with a small number of triggered breaths makes it possible to inflate the lungs with a large DO and prevent atelectasis.
PS (pressure support) - pressure support for breathing. The principle of inhalation in this mode is similar to PCV, but fundamentally differs from it in the complete absence of set hardware breaths. When switching to PS mode, the doctor gives the patient the opportunity to breathe on his own and sets only a slight pressure support for the patient's own respiratory attempts (Fig. 3.7). For example, the doctor sets the pressure support to 10 cm of water. Art. above the PEEP level. If the patient breathes at a rate of 15 breaths per minute, then all his attempts will be triggered and supported by an inspiratory pressure of 10 cmH2O. Art.
CPAP (continuous positive airway pressure) - independent breathing with constantly positive airway pressure. This is the most supportive mode of IVL. The doctor does not establish any forced breaths or pressure support (Fig. 3.8). Positive pressure is generated using the PEEP knob. The usual CPAP level is 8-10 cm of water. Art. The presence of constant positive pressure in the airways facilitates the patient's independent breathing and helps prevent atelectasis.
Due to the fact that in the auxiliary modes of ventilation, the frequency of forced breaths is minimized or absent, in the event that a patient develops severe bradypnea or apnea, the so-called apneic mode of ventilation is set on the ventilator. If the patient does not make independent respiratory attempts within a certain period of time (set by the doctor), the device starts ventilation in the CMV mode with the set RR and DO.
08.05.2011 44341
Once, at one of the professional medical forums, the question of ventilation modes was raised. There was an idea to write about this "simple and accessible", 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 equipment of ambulances led to the appearance of modern respirators in them (for example, the Dreger “Karina” device), which allow ventilation at a high level, using a wide variety of modes. However, the orientation of SME workers in these regimes 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 basis on which further knowledge in this area will already be superimposed.
So what is ventilator mode? In simple terms, the ventilation mode is a flow control algorithm in the breathing circuit. The flow can be controlled with the help of mechanics - fur (old ventilators, type RO-6) or with the help of 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 consider the basic principles of the formation of artificial inspiration. There are two of them (if we discard the obsolete ones):
1) with volume control;
2) with pressure control.
Volume controlled inspiration: The respirator delivers flow to the patient's lungs and switches to exhalation when the physician-specified inspiratory volume (tidal volume) is reached.
Inspiratory shaping with pressure control: The respirator delivers flow to the patient's lungs and switches to exhalation when the pressure (inspiratory pressure) set by the physician is reached.
Graphically it looks like this:
And now the main classification of ventilation modes, from which we will build:
- forced
- forced-auxiliary
- auxiliary
Forced ventilation modes
The essence is the same - the MOD specified by the doctor (which is summed from the specified tidal volume or inspiratory pressure and ventilation frequency) is supplied to the patient's respiratory tract, any activity of the patient is excluded and ignored by the respirator.
There are two main modes of forced ventilation:
- volume controlled ventilation
- pressure controlled ventilation
Modern respirators also provide additional modes (ventilation by pressure with a guaranteed tidal volume), but we will omit them for the sake of simplicity.
Volume Control Ventilation (CMV, VC-CMV, IPPV, VCV, etc.)
The doctor sets: tidal volume (in ml), ventilation rate per minute, the ratio of inhalation and exhalation. The respirator delivers a predetermined tidal volume to the patient's lungs and switches to exhalation when it is reached. Exhalation is passive.
In some ventilators (for example, Dräger Evitas), during mandatory ventilation by volume, switching to exhalation by time is used. In this case, the following takes place. When volume is delivered to the patient's lungs, the pressure in the DP increases until the respirator delivers the set volume. The peak pressure appears (Ppeak or PIP). After that, the flow stops - a plateau pressure occurs (sloping part of the pressure curve). After the end of the inspiratory time (Tinsp), exhalation begins.
Pressure Control Ventilation - Pressure Control Ventilation (PCV, PC-CMV)
The doctor sets: inspiratory pressure (inspiratory pressure) in cm of water. Art. or in mbar, ventilation rate per minute, inspiratory to expiratory ratio. The respirator delivers flow to the patient's lungs until the inspiratory pressure is reached and switches to exhalation. Exhalation is passive.
A few words about the advantages and disadvantages of various principles for the formation of artificial inspiration.
Volume Controlled Ventilation
Advantages:
- guaranteed tidal volume and, accordingly, minute ventilation
Flaws:
- danger of barotrauma
- uneven ventilation of various parts of the lungs
- impossibility of adequate ventilation with leaky DP
Pressure controlled ventilation
Advantages:
- much less risk of barotrauma (with properly set parameters)
- more even ventilation
- can be used when the airway is leaking (ventilation with cuffless tubes in children, for example)
Flaws:
- no guaranteed tidal volume
- complete monitoring of ventilation is required (SpO2, ETCO2, MOD, KShchS).
Let's move on to the next group of ventilation modes.
Forced-assisted modes
In fact, this group of ventilation modes is represented by one mode - SIMV (Synchronized Intermittent Mandatory Ventilation - synchronized intermittent mandatory ventilation) and its options. The principle of the mode is as follows - the doctor sets the required number of forced breaths and 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 of given ones. In addition, the word "synchronized" means that mandatory breaths will be triggered in response to the patient's breath attempt. If the patient does not breathe at all, then the respirator will regularly give him the given 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 independent breaths, the pressure support mode (more often) - PSV (Pressure support ventilation), or volume (less often) - VSV (Volume support ventilation) is used, but we will talk about them below.
If for the formation of hardware breaths the patient is given the principle of ventilation by volume, then the mode is simply called "SIMV" or "VC-SIMV", and if the principle of ventilation by pressure is used, then the mode is called "P-SIMV" or "PC-SIMV".
In connection with the fact that we started talking about modes that respond to the patient's respiratory attempts, a few words should be said about the trigger. A trigger in a ventilator is a trigger circuit that triggers inspiration in response to a patient's attempt to breathe. The following types of triggers are used in modern ventilators:
- Volume trigger - it is triggered by the passage of a given volume into the patient's airways
- Pressure trigger - triggered by a pressure drop in the breathing circuit of the device
- Flow trigger - reacts to a change in flow, most common in modern respirators.
Synchronized intermittent mandatory 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, if necessary, sets the pressure or volume of support (in this case, the mode will be abbreviated "SIMV + PS" or "SIMV + VS"). The patient receives a predetermined number of volume-controlled breaths and can breathe spontaneously with or without assistance. At the same time, a trigger will work on the patient’s attempt to inhale (flow change) and the respirator will allow him to carry out his own breath.
Synchronized intermittent mandatory ventilation with pressure control (P-SIMV, PC-SIMV)
The doctor sets the inspiratory pressure, the frequency of mandatory breaths, the ratio of inhalation and exhalation, trigger parameters, if necessary, sets the pressure or volume of support (in this case, the mode will be abbreviated "P-SIMV + PS" or "P-SIMV + VS"). The patient receives a predetermined number of pressure-controlled breaths and can breathe spontaneously with or without support in the same manner as described previously.
I think it has already become clear that in the absence of spontaneous patient breaths, the SIMV and P-SIMV modes turn into volume-controlled mandatory ventilation and pressure-controlled mandatory ventilation, respectively, which makes this mode universal.
We turn to the consideration of auxiliary modes of ventilation.
Auxiliary Modes
As the name implies, this is a group of modes, the task of which is to support the patient's spontaneous breathing in one way or another. Strictly speaking, this is no longer IVL, but IVL. 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 complex, so-called. "intelligent" modes of auxiliary ventilation, tk. every self-respecting manufacturer of breathing equipment has its own “chip” here, and we will analyze the most basic ventilator modes. If there is a desire to talk about any particular "intelligent" mode, we will discuss it all separately. The only thing I will write separately about the BIPAP mode, since it is essentially universal and requires a completely separate consideration.
So, the auxiliary modes include:
- Pressure support
- Volume support
- Continuous positive airway pressure
- Endotracheal/tracheostomy tube resistance compensation
When using auxiliary modes, the option is very useful. "Apnea ventilation"(Apnoe Ventilation) which lies in the fact that in the absence of the patient's respiratory activity 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 amount of support pressure (in cm H2O or mbar), trigger parameters. The trigger reacts to the patient's respiratory attempt and the respirator gives the set pressure on 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. PSV mode is widely used when weaning from a respirator by gradually reducing the 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 set by the doctor. This mode is present in some fans (Servo, Siemens, Inspiration). The doctor sets the tidal volume of support, trigger parameters, limiting inspiratory parameters. On an inspiratory attempt, the respirator gives the patient a predetermined 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 a constant positive airway pressure. In fact, the option to maintain a constant positive airway pressure is very common and can be used in any mandatory, 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 warm and humidified air with a high oxygen content, and the alveoli are maintained in a straightened state; thus, this mode is widely used when weaning from a respirator. 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 patient 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 inner diameter, which is much smaller than the diameter of the larynx and trachea. According to Poiseuille's law, with a decrease in the radius of the lumen of the tube, the resistance increases sharply. Therefore, during assisted ventilation in patients with persistent spontaneous breathing, there is a problem of overcoming this resistance, especially at the beginning of inspiration. Who does not believe, try to breathe for a while through the "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 IVL modes.
Well, in conclusion, let's talk about the BIPAP (BiPAP) mode, which, in my opinion, should be considered separately.
Ventilation with two phases of positive airway pressure - Biphasic positive airway pressure (BIPAP, BiPAP)
The name of the mode and its abbreviation were once patented by Draeger. Therefore, when referring to BIPAP, we mean ventilation with two phases of positive airway pressure, implemented in Dräger respirators, and when talking 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 Dräger respirators, so we will use the abbreviation "BIPAP".
So, the essence of ventilation with two phases of positive airway pressure 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, with spontaneous breathing, several respiratory cycles can take place, this can be seen in the graph. To help you understand the essence of BIPAP, remember what I wrote earlier about CPAP: the patient breathes spontaneously 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 one again and does this with a certain frequency. This is what BIPAP is.
Depending on the clinical situation, the duration, phase ratios and pressure levels may vary.
Now we pass to the most interesting. Toward the universality of the BIPAP regime.
Situation one. Imagine that the patient has no respiratory activity at all. In this case, the increase in airway pressure in the second phase will lead to mandatory pressure ventilation, which will be graphically indistinguishable from PCV (remember the acronym).
Situation two. If the patient is able to maintain spontaneous breathing at the lower pressure level (CPAP low), then when it is increased to the upper one, mandatory 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 low and high pressure levels. BIPAP in these situations works like a true BIPAP, showing all its advantages.
Situation four. If we set the same value of the upper and lower pressures during spontaneous breathing of the patient, then BIPAP will turn into what? That's right, in 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 have considered all the main modes of mechanical ventilation, thus creating the basis for further accumulation of knowledge on this issue. I want to note right away that all this can be comprehended only through direct work with the patient and the respirator. In addition, manufacturers of respiratory equipment produce many simulation programs that allow you to get acquainted and work with any mode without leaving your computer.
Shvets A.A. (Graph)
Pressure Control Ventilation(PCV)
In Pressure Controlled Ventilation (PCV) mode, set the following parameters:
airway pressure (P),
time to maintain this pressure (t INSP),
number of machine breaths per minute (f)
PEEP.
In many modern respirators, the rate of increase in airway pressure can also be controlled by changing the slope of the pressure curve.
The usual values are P = 18-20 cm of water column, t INSP = 0.7-0.8 sec, f = 10-12 in 1 min, PEEP = 5 cm of water. Art., the slope of the pressure curve from (-2) to (+2).
mode algorithm. When inhaling, an oxygen-air mixture is supplied to the respiratory tract until the set pressure is established there. Then this pressure is maintained for a predetermined time, after which the flow of the respiratory mixture stops, the exhalation valve opens, and exhalation occurs.
The value of the tidal volume depends on the compliance of the lungs: the more compliant they are, the greater the volume of the respiratory mixture will enter them at the pressure created by the respirator (Fig. 6.11). Depending on the needs of the patient, the slope of the pressure curve is changed. A smaller angle of inclination of the curve allows for a slower flow of oxygen-air mixture into the respiratory tract, a larger angle - faster. Although the choice of this indicator is individual each time, more often faster flows are required for patients with chronic pulmonary problems and increased airway resistance.
Given the importance of the tidal volume for ventilation and oxygenation, the main alarms are set to control it: the value of the minimum MOD, the maximum respiratory rate. Classic PCV mode is similar to CMV in that all breaths are untrigged. However, a modified PCV is most often used, in which sensitivity is set, and it becomes analogous to the usual Assist Control mode, in contrast to which machine breaths are focused not on supplying volume, but on creating pressure in the airways.
Additional parameter of the modified PCV:
trigger sensitivity (usually (-3) - (-4) cmH2O or (-2) - (-3) L/min).
In some models of respirators, machine breaths by pressure can be set in SIMV mode.
It is generally accepted that all pressure ventilation modes lead to a more rational distribution of the respiratory mixture in the lungs than volume modes. It is believed that this may be more beneficial for damaged lungs. It seems to us that this assumption has no such serious grounds. There is no significant difference what the respirator focuses on - the pressure under which a certain volume of the respiratory mixture enters the lungs, or the volume that creates a certain pressure in the lungs. It is important how this volume is supplied (at what speed, what form of flow), what pressure is created, and what amount of oxygen-air mixture ultimately enters the lungs.
Pressure Support (PS)
Pressure Support (called Assisted Spontanious Breathing, ASB in some models) can be used as a separate mode (Fig. 6.12), or to support spontaneous breaths along with the SIMV mode (Fig. 6.13). In this mode, the following parameters are set:
Airway pressure (P),
trigger sensitivity
PEEP.
Usual values: Р = 18-20 cm of water column, PEEP = 5 cm of water. Art.
mode algorithm. When a patient makes a respiratory attempt, the respirator creates a predetermined pressure in the airways, "supporting" the patient's inhalation. The difference between Pressure Support and Pressure Control Ventilation should be immediately noted. The first occurs only in response to respiratory attempts, the second - and without them. But the main thing is not in this, but in the principle of interrupting inhalation and switching the ventilator from inhalation to exhalation. In PCV, this is a predetermined time during which the patient's airway pressure is maintained, in Pressure Support, it is a decrease in the peak inspiratory flow to 25-30% of the initial flow. This feature of Pressure Support is one of its shortcomings. If the patient does not have a complete airway seal, such as an incompletely inflated tracheostomy tube cuff, the airway pressure will never reach the target level due to air leakage. As a result, the desired reduction in peak flow will not occur and exhalation will not begin. To prevent such a situation, a limiting inspiratory time is usually set, for example, no more than 3 seconds. If the inhalation exceeds 3 seconds, then the exhalation necessarily occurs. In modern models of respirators, the amount of reduction in peak flow, which switches inspiration to exhalation, can be set to not only 25-30%, but several different levels, which helps to prevent leakage problems of the oxygen-air mixture.
Another problem is the mandatory respiratory efforts of the patient. If the patient breathes in Pressure Support mode, then there is a theoretical possibility of apnea due to the termination of his respiratory attempts. In this case, an emergency ventilation mode is provided, which is usually represented by CMV. When breathing attempts are restored, this mode is turned off. It must be remembered that not all respirators provide inspiratory limitation and emergency ventilation.
Biphasic Positive Airway Pressure (BiPAP)
This mode is called Spontaneous Positive Airway Pressure (SPAP) in some respirators and is a biphasic alternating airway pressure. Despite the similarity in name, SPAP should not be confused with CPAP.
In BiPAP mode, set the following parameters:
Upper airway pressure (P max),
lower airway pressure (P min),
inspiratory time (t INSP),
number of machine breaths per minute (f).
Usual values: P max = 18-20 cm of water column, P min = 5 cm of water. Art., t INSP = 0.8 sec, f = 10 in 1 min.
mode algorithm. Two different levels of constant positive pressure are alternately created in the airways. The upper level is maintained for a certain time, regulated by the doctor. The duration of maintaining the lower pressure level is determined by the set frequency of breaths. The upper pressure level actually creates a pressure control type breath, the lower one is similar to CPAP. At each of the levels, the patient's spontaneous breathing is allowed (Fig. 6.14). Due to spontaneous breaths, the ventilation-perfusion relationship and arterial oxygenation are improved.
BiPAP is one of the most interesting ventilation modes. It does not require synchrony of the patient and the operation of the respirator at all. At the same time, the patient does not struggle with the ventilator and intrathoracic pressure does not increase. However, there are no universal regimens for all patients. There is a category of patients who, when using the BiPAP regimen, develop severe tachypnea, accompanied by hypocapnia.
Usually, in such cases, switching the respirator to Assist Control helps. It is possible in this case to use the BiPAP Assist modification. Unlike conventional BiPAP, this mode does not always maintain a constant exhalation time. If the patient makes a respiratory attempt during expiration, then the respirator immediately creates upper airway pressure (P max), i.e. breath comes.
Airway Pressure Release Ventilation (APRV)
Airway Pressure Relief Ventilation (ARPV) mode is similar to BiPAP in that it also creates two levels of airway pressure. At the upper level of pressure, the patient can breathe on his own. Unlike BiPAP, the lower pressure level is created only for a short period of time, the duration of which is not adjustable. The patient exhales, there is a "release of airway pressure" and the upper level of pressure is again created (Fig. 6.15).
Automatic Tube Compensation (ATC)
The automatic tube resistance compensation (ATC) mode is also called "electronic extubation". It is based on the following principles. The endotracheal tube has resistance that restricts airflow and increases the work of breathing. These problems are compensated to some extent by the use of Pressure Support. But PS creates a constant pressure in the airways during inspiration, while the flow of air blown varies during inspiration from 1.5-2 L/min to zero. Accordingly, at the beginning of inspiration, pressure support will not be enough to compensate for the resistance of the endotracheal tube, and at the end of inspiration, support will be excessive. Unnecessary overinflation of the lungs appears, and there is no full compensation for the increased work of breathing. ATC mode focuses on the amount of gas flow, taking into account the size of the tube and creates a greater pressure of the air mixture at the beginning of inspiration, and less at the end.
Rapid progress in electronics and computer technology has made it possible to implement more complex algorithms for controlling the flow of a gas mixture and ventilation modes based on them. Two main directions can be distinguished:
- The use of two levels of positive pressure, which is denoted by the term "BiPAP".
- Dynamic change of ventilation parameters based on feedback.
There are at least five situations where the term is used:
a) as a synonym for the combination of CPAP and PS ("Respironics"). This sets the level of expiratory "E-PAP" and inspiratory "I-PAP" pressure in the breathing circuit. In addition, it becomes possible to periodically, with a frequency of several times per minute, reduce expiratory pressure (IMPRV - Intermittent Mandatory Pressure Release Ventilation, "Cesar");
b) as a synonym for pressure-controlled ventilation, when the CPAP level acts as the expiratory pressure - "E-PAP", and the setpoint for the inspiratory pressure - "I-PAP".
c) during spontaneous breathing at two different levels of positive pressure in the ventilation circuit, which are replaced every 5-10 s (Drager Evita).
d) as a variant of the case described above (c), when the duration of high pressure is relatively short, and the patient breathes at a lower pressure most of the time, similar to the SIMV regimen with pressure control.
e) another variant of this case (c) - ventilation with a decrease in airway pressure, or APRV - Airway re Release Ventilation, when the patient most of the time breathes at high pressure in the circuit. Attitudes towards the APRV regimen are ambiguous. A number of experimental studies on the ARDS model showed worse results compared to CPAP. At the same time, there is evidence of an improvement in the ratio of ventilation and perfusion with unimpeded spontaneous breathing in the APRV mode compared with pressure support ventilation. There are isolated reports of a positive effect of the APRV regimen in various lung pathologies.
Feedback-based ventilation modes are becoming more and more widespread. The obsolete term "servo", which, in fact, means feedback, is often used in those devices where the ventilation parameters change automatically depending on the state of the lungs. In each case, it is necessary to single out the controlled parameter and those changes in the characteristics of the respiratory cycle that are the result of the feedback action.
PRVC (Pressure-regulated volume control) - a mode that provides for changing the tidal volume depending on the value of the inspiratory pressure. Similar to pressure-controlled ventilation: the limiting parameter is inspiratory pressure; switching takes place over time. It differs in that the operator sets the tidal volume, and the device selects the inspiratory pressure necessary to achieve this volume based on the results of several previous respiratory cycles (Siemens Servo 300).
Auto flow - similar to PRVC but combined with BiPAP - BiPAP type 3, see above (Drager Evita Dura). Volume Support is another modification of PRVC, which differs in that the switching is carried out on a stream.
Minimum Minute Ventilation - a mode that guarantees the specified minimum minute ventilation. It uses feedback mechanisms like Volume Support (Hamilton Weolar).
Mandatory Rate Ventilation - Conversely, Mandatory Rate Ventilation controls the respiratory rate by increasing the level of inspiratory pressure if the patient breathes faster.
Mandatory Minute Ventilation - ventilation mode with a given minute ventilation (not to be confused with Minimum Minute Ventilation), regulates the respiratory rate. When the patient's spontaneous breathing provides an adequate minute ventilation, the device does not add mandatory breaths - unlike ot SIMV, where the set number of mandatory breaths remains constant Erica Engstrom).
Proportion Assist Ventilation - proportional auxiliary ventilation - a rather complex mode in which the device, at each attempt to inhale, based on the determination of the flow and tidal volume, evaluates the patient's effort and sets the appropriate inspiratory pressure. This regimen has been shown to be more comfortable than PCV in healthy volunteers with artificially reduced respiratory compliance.
The wide choice of different ventilation modes already in itself reflects the fact that, to date, there is no convincing evidence of significant advantages of any particular technique. Differences in the results of treatment can be associated to a greater extent with the design features of the devices used, rather than with the control algorithm.
An important recent achievement, which has greatly facilitated the selection of parameters and made ventilation more convenient, is the monitoring and graphical display of ventilation indicators (flow, pressure and tidal volume). This can be clearly demonstrated by the following examples:
Rice. 2. Graphic display of ventilation parameters in a patient with ARDS
Due to a sharp decrease in lung compliance, a high value of inspiratory pressure is noted with a small tidal volume. A kink in the inspiratory portion of the flow curve (marked with an arrow) indicates that inhalation is terminated before the maximum tidal volume is reached. Increasing the duration of inspiration (next cycle) allows you to use this reserve and increase the efficiency of ventilation without reaching the critical inspiratory pressure.
On fig. 2 shows curves reflecting the dynamics of ventilation parameters in a patient with ARDS. In this case, a serious problem is a sharp decrease in lung tissue compliance, high inspiratory pressure with a small tidal volume. However, the kink (indicated by the arrow) in the flow curve, which is most informative for pressure-limited ventilation, indicates that lung expansion is still ongoing by the start of the next breath and there are some tidal volume reserves. Their use requires an increase in the duration of inspiration, which is accompanied by an increase in tidal volume and ventilation efficiency.
Rice. 3. Graphic display of ventilation parameters in a patient with bronchospastic syndrome
Due to the high resistance of the airways, a “gas trap phenomenon” develops, which is reflected in the expiratory part of the flow curve in the form of a break (marked with an arrow). Increasing expiratory duration by reducing the respiratory rate avoids this, reduces residual airway pressure, and increases effective tidal volume.
During mechanical ventilation in a patient with exacerbation of bronchial asthma and severe bronchospasm (Fig. 3), high airway resistance leads to the so-called gas trap phenomenon, when a significant part of the respiratory volume remains in the lungs by the beginning of the next breath. This is evidenced by a break in the expiratory part of the flow curve (marked with an arrow). In such a situation, the residual pressure in the airways (auto-PEEP) can reach critical values, causing a decrease in ventilation efficiency and decompensation of blood circulation.
The only way out is to increase the duration of the exhalation. This is achieved by reducing the respiratory rate and the inspiratory to expiratory ratio (I/E).
Rice. 4. Indicators of ventilation during mechanical ventilation in a patient with a normal state of the lungs
A tidal volume of 12-15 ml/kg is achieved with an inspiratory pressure not exceeding 15 cm of water. Art.
For comparison, in Fig. 4 shows the corresponding indicators during mechanical ventilation in a patient with a normal state of the lungs. A tidal volume of 12–15 ml/kg is achieved with an inspiratory pressure of 15 cm of water. Art. without significant changes in respiratory rate and I/E ratio.
Significant progress in the pathophysiology of artificial ventilation allows us to determine the main ways to reduce the incidence of complications. The ARDSNET (the Acute Respiratory Distress Syndrome Network) study is probably the most important work on ventilation in the last decade. It is well organized and clearly demonstrates that a decrease in tidal volume to 6 ml per 1 kg ideal weight compared with the "usual" 12 ml / kg is associated with a decrease in mortality and improved treatment outcomes. Even more interesting is the observation that this occurred against a background of moderate hypoxemia. Another significant aspect concerns the respiratory rate. Contrary to the opinion of some researchers that it should be low in ARDS, the ARDSNET group showed an improvement in treatment outcomes at an average respiratory rate of 29 per minute (compared to 1/2 of this value in the control). Attention should be paid to the introduction of the specific term "volume injury". This is redundant, since pressure and volume are closely related. This neologism seems to be the result of a misunderstanding that the relationship between transalveolar and transthoracic pressure is non-linear. However, measurement of intrapleural pressure (or intraesophageal pressure as its equivalent) is generally not available in intensive care settings. Therefore, the value of the tidal volume reflects the degree of lung damage to a greater extent than the pressure in the ventilation circuit. Regardless of the terminology, it is obvious that the overstretching of the alveoli leads to the destruction of the alveolar-capillary membranes and the rapid development of inflammation in the lung tissue.
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You are reading the topic:
Choice of artificial lung ventilation mode in intensive care of acute respiratory failure
- Modern modes of IVL.
Conducting paths
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, the vestibule and conchas of the nose. 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 of low humidity leads to the drying of the mucous membrane, the ingress of dry air into the lungs, the development of atelectasis, pneumonia and increased resistance in the airways.
Pharynx
separates food from air, regulates pressure in the middle ear.
Larynx
provides a voice function, with the help of the epiglottis preventing aspiration, and the closure of the vocal cords is one of the main components of a cough.
Trachea - the main air duct, it warms and humidifies the air. The cells of the mucous membrane capture foreign substances, and the cilia move the mucus up the trachea.
Bronchi (lobar and segmental) end with terminal bronchioles.
The larynx, trachea and bronchi are also involved in cleansing, warming and moistening the air.
The structure of the wall of the conductive airways (EP) differs from the structure of the airways of the gas exchange zone. The wall of the conducting airways consists of a mucous membrane, a layer of smooth muscles, a submucosal connective and cartilaginous membranes. The epithelial cells of the airways are equipped with cilia, which, oscillating rhythmically, advance the protective layer of mucus towards the nasopharynx. The EP mucosa and lung tissue contain macrophages that phagocytize and digest mineral and bacterial particles. Normally, mucus is continuously removed from the airways 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. Cilia contain many mitochondria that provide energy for their high motor activity(about 1000 movements per 1 min.), which allows you 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 up to 100 ml/hour in pathological conditions.
The cilia function in a double layer of mucus. In the lower one there are 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 cilia from damage. Thickening or reduction of the upper layer of mucus during inflammation or toxic exposure inevitably disrupts the drainage function of the ciliated epithelium, irritates the respiratory tract and reflexively causes cough. Sneezing and coughing protect the lungs from entry of mineral and bacterial particles.
Alveoli
In the alveoli, gas exchange occurs between the blood of the pulmonary capillaries and air. The total number of alveoli is approximately 300 million, and their total surface area is approximately 80 m 2. The diameter of the alveoli is 0.2-0.3 mm. Gas exchange between alveolar air and blood is carried out 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 µm. The entire alveolar surface of the lungs is covered with a thin film called surfactant.
Surfactant reduces surface tension at the border between liquid and air at the end of exhalation, when lung volume is minimal, increases elasticity lungs and plays the role of a decongestant factor(does not let water vapor from the alveolar air), as a result of which the alveoli remain dry. It reduces surface tension with a decrease in the volume of the alveoli during exhalation and prevents its collapse; reduces shunting, which improves oxygenation of arterial blood at lower pressure and a minimum content of O 2 in the inhaled mixture.
The surfactant layer consists of:
1) the surfactant itself (microfilms of phospholipid or polyprotein molecular complexes at the boundary with the air);
2) hypophase (a deep-lying hydrophilic layer of proteins, electrolytes, bound water, phospholipids and polysaccharides);
3) the cellular component represented by alveolocytes and alveolar macrophages.
The main chemical constituents of surfactant are lipids, proteins and carbohydrates. Phospholipids (lecithin, palmitic acid, heparin) make up 80-90% of its mass. The surfactant coats the bronchioles in a continuous layer, reduces breathing resistance, maintains filling
At low tensile pressure, it reduces the action of forces that cause fluid accumulation in tissues. In addition, the surfactant purifies inhaled gases, filters and traps inhaled particles, regulates the exchange of water between the blood and the air of the alveoli, accelerates the diffusion of CO 2 , and has a pronounced antioxidant effect. The surfactant is very sensitive to various endo- and exogenous factors: circulatory, ventilation and metabolic disorders, changes in PO 2 in the inhaled air, and its pollution. With a deficiency of surfactant, atelectasis and RDS of newborns occur. Approximately 90-95% of alveolar surfactant is recycled, cleared, stored and resecreted. The half-life of the 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 characterizing the state of the lungs. Normal averages for an adult are as follows:
1. Tidal volume(DO-VT- Tidal volume)- the 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 be additionally received after a quiet breath, i.e. difference between normal and maximum ventilation. Normal value: 2-2.5 liters (about 2/3 VC).
3. Expiratory reserve volume (ERV - ERV - Expiratory Reserve Volume) - the volume that can be additionally exhaled after a quiet exhalation, i.e. the difference between normal and maximum expiration. Normal value: 1.0-1.5 liters (about 1/3 VC).
4.Residual volume (OO - RV
- Residal Volume) - the volume remaining in the lungs after maximum exhalation. About 1.5-2.0 liters.
5. Vital capacity of the lungs (VC - VT
- Vital Capacity) - the amount of air that can be maximally exhaled after a maximum inspiration. VC is an indicator of lung mobility and chest. VC depends on age, gender, size and position of the body, degree of fitness. Normal values of VC - 60-70 ml / kg - 3.5-5.5 liters.
6. Inspiratory reserve (IR)
-Inspiratory capacity (Evd - IC
- Inspiritory 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 - 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 GR and is calculated as the sum of VC and GR. The normal value is about 6.0 liters.
The study of the structure of the HL is decisive in finding ways to increase or decrease the VC, which can be of significant practical importance. An increase in VC can be regarded positively only if the CL does not change or increases, but is less than the VC, which occurs with an increase in VC due to a decrease in RO. If, simultaneously with an increase in VC, there is an even greater increase in RL, then this cannot be considered a positive factor. When VC is below 70% of the CL, the function of external respiration is deeply impaired. Usually, in pathological conditions, TL and VC change in the same way, with the exception of obstructive pulmonary emphysema, when VC, as a rule, decreases, VR increases, and TL may remain normal or be above 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 in adults are from 3 to 3.5 liters. FOE \u003d 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 a balance between the oppositely directed elastic forces of the lungs and chest. The physiological significance of the FRC is the partial renewal of the alveolar air volume during inhalation (ventilated volume) and indicates the volume of alveolar air that is constantly in the lungs. With a decrease in FRC, the development of atelectasis, closure of small airways, a decrease in lung compliance, an increase in the alveolar-arterial difference in O 2 as a result of perfusion in atelectatic areas of the lungs, and a decrease in the ventilation-perfusion ratio are associated. Obstructive ventilation disorders lead to an increase in FRC, restrictive disorders - 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. Approximately, we can assume 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 of body weight).
Under functional (physiological) dead space understand all those parts 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 by blood.
Alveolar ventilation and dead space ventilation
The part of the minute volume of respiration that reaches the alveoli is called alveolar ventilation, the rest is dead space ventilation. Alveolar ventilation serves as an indicator of the effectiveness of breathing in general. It is on this value that the gas composition maintained in the alveolar space depends. As for the minute volume, it only slightly reflects the efficiency of lung ventilation. So, if the minute volume of breathing is normal (7 l / min), but breathing is frequent and shallow (DO-0.2 l, respiratory rate-35 / min), then ventilate
There will be mainly dead space, into which air enters earlier than into 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 breath and the lower the frequency.
Extensibility (compliance) of lung tissue
Lung compliance is a measure of the elastic recoil, as well as the 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, that is, its compliance. Mathematically, compliance is expressed as a quotient of the change in lung volume and the corresponding change in intrapulmonary pressure.
Compliance can be measured separately for the lungs and chest. From a clinical point of view (especially during mechanical ventilation), the compliance of the lung tissue itself, which reflects the degree of restrictive lung pathology, is of greatest interest. In modern literature, lung compliance is usually denoted by the term "compliance" (from the English word "compliance", abbreviated as C).
Lung compliance decreases:
With age (in patients older than 50 years);
In the supine position (due to the pressure of the abdominal organs on the diaphragm);
During laparoscopic surgery due to carboxyperitoneum;
In acute restrictive pathology (acute polysegmental pneumonia, RDS, pulmonary edema, atelectasis, aspiration, etc.);
In chronic restrictive pathology (chronic pneumonia, pulmonary fibrosis, collagenosis, silicosis, etc.);
With the 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 respiratory volume as with normal compliance. Consequently, in the case of deteriorating lung compliance, when the same tidal volume is reached, the airway pressure increases significantly.
This provision is very important to understand: with volumetric ventilation, when a forced tidal volume is delivered 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 various lengths and widths, the resistance to gas flow in the lungs can be determined according to known physical laws. In general, the resistance to flow 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 motion of gas with
Varying velocity: the flow velocity is highest in the center and gradually decreases towards the walls. Laminar gas flow prevails at relatively low velocities and is described by Poiseuille's law, according to which the resistance to gas flow depends to the greatest extent on the radius of the tube (bronchus). 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 understandable.
Airway resistance to gas flow increases significantly with bronchiolospasm, swelling of the bronchial mucosa, accumulation of mucus and inflammatory secretion due to narrowing of the lumen of the bronchial tree. Resistance is also affected by the flow rate and the length of the tube (bronchi). FROM
By increasing the flow rate (forcing inhalation or exhalation), airway resistance increases.
The main causes of increased airway resistance are:
Bronchiospasm;
Edema of the mucous membrane of the bronchi, (exacerbation of bronchial asthma, bronchitis, subglottic laryngitis);
Foreign body, aspiration, neoplasms;
Accumulation of sputum and inflammatory secretion;
Emphysema (dynamic compression of the airways).
Turbulent flow is characterized by the chaotic movement of gas molecules along the tube (bronchi). It dominates at high volumetric flow rates. In the case of turbulent flow, the resistance of the airways increases, since it is even more dependent on the flow rate and the radius of the bronchi. Turbulent movement occurs at high flows, abrupt changes in flow velocity, in places of bends and branches of the bronchi, with a sharp change in the diameter of the bronchi. That 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. Medium-sized bronchi create the greatest resistance (up to the 5-7th generation), since the resistance of large bronchi is small due to their large diameter, and small bronchi - due to a 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 (PEEP) contributes to an increase in lung volume and, consequently, a decrease in 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 old - 20-30 mm of water column / l / s;
In newborns - 30-50 mm water column / l / s.
On exhalation, the airway resistance is 2-4 mm w.c./l/s greater than on inspiration. This is due to the passive nature of exhalation, when the state of the wall of the airways affects the gas flow to a greater extent than with active inspiration. Therefore, for a full exhalation, it takes 2-3 times more time than for inhalation. Normally, the ratio of inhalation / exhalation time (I: E) for adults is about 1: 1.5-2. The fullness of exhalation in a patient during mechanical ventilation can be assessed by monitoring the expiratory time constant.
The work of breathing
The work of breathing is performed predominantly by the inspiratory muscles during inhalation; expiration 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.
An increase in resistance to inhalation or exhalation is compensated by 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), tachypnea (due to ventilation of the dead space).
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 in case of 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 the beginning of mechanical ventilation, in which the cost of breathing decreases to almost 0.
The work of breathing required to overcome elastic resistance (lung compliance) increases as the tidal volume increases. The work required to overcome the resistive airway resistance increases as the respiratory rate increases. 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 is an optimal respiratory rate and tidal volume at which the work of breathing is minimal. So, for patients with reduced compliance, from the point of view of minimizing the work of breathing, more frequent and shallow breathing is suitable (slowly compliant lungs are difficult to straighten). On the other hand, with increased airway resistance, deep and slow breathing is optimal. This is understandable: an increase in tidal volume allows you to "stretch", expand the bronchi, reduce their resistance to gas flow; for the same purpose, patients with obstructive pathology compress their lips during exhalation, creating their own "PEEP" (PEEP). Slow and rare breathing contributes to the lengthening of the exhalation, which is important for a more complete removal of the exhaled gas mixture in conditions of increased expiratory airway resistance.
Breathing regulation
The process of breathing is regulated by the central and peripheral nervous system. In the reticular formation of the brain there is a respiratory center, consisting of centers of inhalation, exhalation and pneumotaxis.
Central chemoreceptors are located in the medulla oblongata and are excited by an increase in the concentration of H + and PCO 2 in the cerebrospinal fluid. Normally, the pH of the latter is 7.32, RCO 2 is 50 mm Hg, and the content of HCO 3 is 24.5 mmol / l. Even a slight decrease in pH and an increase in PCO 2 increase ventilation of the lungs. These receptors respond to hypercapnia and acidosis more slowly than peripheral ones, since additional time is required to measure the value of CO 2 , H + and HCO 3 due to overcoming the blood-brain barrier. Respiratory muscle contractions control the central respiratory mechanism, which consists of a group of cells in the medulla oblongata, the pons, and pneumotaxic centers. They tone the respiratory center and determine the threshold of excitation at which the inhalation stops by the impulses from the mechanoreceptors. Pneumotaxic cells also switch inhalation to exhalation.
Peripheral chemoreceptors, located on the inner membranes of the carotid sinus, aortic arch, left atrium, control humoral parameters (PO 2 , RCO 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, RO 2 and RCO 2 in arterial blood and cerebrospinal fluid. Impulses from chemoreceptors regulate the amount of ventilation required to maintain a certain level of metabolism. In optimizing the ventilation mode, i.e. determining the frequency and depth of breathing, the duration of inhalation and exhalation, the force of contraction of the respiratory muscles at a given level of ventilation, mechanoreceptors are also involved. Lung ventilation is determined by the level of metabolism, the impact 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 respiration in response to changes in the gas composition of the blood.
Peripheral mechanoreceptors, localized in the walls of the alveoli, intercostal muscles and 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 enters the alveoli through the VP 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 (the Hering-Breuer reflex).
During normal breathing, the intercostal-diaphragmatic mechanoreceptors are not excited and have an auxiliary value.
The regulatory system is completed by neurons that integrate impulses that come to them from chemoreceptors and send excitatory 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.
Breathing movements that create airflow 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 respiration within the limits allowed by the chemoreceptor regulation of respiration. 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 respiration
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 flattens and the ribs rise upward, as a result, the volume of the chest increases, and negative intrapleural pressure (Ppl) increases. Before inhalation (at the end of exhalation) Ppl is approximately minus 3-5 cm of water. Alveolar pressure (Palv) is taken as 0 (i.e., equal to atmospheric), it also reflects airway pressure 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. During spontaneous inspiration, the growth of negative Ppl (up to minus 6-10 cm of water column) causes a decrease in pressure in the alveoli and airways below atmospheric pressure. In the alveoli, the pressure drops to minus 3-5 cm of water. Due to the difference in pressure, air enters (is sucked in) from the external environment into the lungs. The thorax and diaphragm act as a piston pump, drawing air into the lungs. This "sucking" action of the chest is important not only for ventilation, but also for blood circulation. During spontaneous inspiration, there is an additional “suction” of blood to the heart (preload maintenance) and activation of pulmonary blood flow from the right ventricle through the pulmonary artery system. At the end of inhalation, when the movement of gas stops, the alveolar pressure returns to zero, but the intrapleural pressure remains reduced to minus 6-10 cm of water.
Expiration is normally a passive process. After relaxation of the respiratory muscles, the elastic recoil forces of the chest and lungs cause the removal (squeezing) of gas from the lungs and the restoration of the original volume of the lungs. In case of impaired patency of the tracheobronchial tree (inflammatory secretion, swelling of the mucous membrane, bronchospasm), the exhalation process is difficult, and the exhalation muscles also begin to take part in the act of breathing (internal intercostal muscles, pectoral muscles, abdominal muscles, etc.). When the expiratory muscles are depleted, the process of exhalation is even more difficult, the exhaled mixture is delayed and the lungs are dynamically overinflated.
Non-respiratory functions of the lungs
The functions of the lungs are not limited to the diffusion of gases. They contain 50% of all endothelial cells of the body that line the capillary surface of the membrane and are involved in the metabolism and inactivation of biologically active substances passing through the lungs.
1. The lungs control general hemodynamics by filling their own vascular bed in various ways and by 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 coagulation 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 a higher fibrinolytic activity.
3. The lungs are involved in protein, carbohydrate and fat metabolism, synthesizing phospholipids (phosphatidylcholine and phosphatidylglycerol are the main components of the surfactant).
4. The lungs produce and eliminate heat, maintaining the energy balance of the body.
5. The lungs purify the blood from mechanical impurities. Cell aggregates, microthrombi, bacteria, air bubbles, fat drops are retained by the lungs and undergo 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.Normal ventilation - normal ventilation, in which the partial pressure of CO2 in the alveoli is maintained at a level of about 40 mm Hg.
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 mm Hg).
4. Increased ventilation - any increase in alveolar ventilation compared to the level of rest, 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 - an increase in the frequency of breathing.
8. Bradypnea - decrease in respiratory rate.
9. Apnea - respiratory arrest, mainly due to the lack of physiological stimulation of the respiratory center (decrease in CO2 tension in arterial blood).
10. Dyspnea (shortness of breath) - an unpleasant subjective feeling of shortness of breath or shortness of breath.
11. Orthopnea - severe shortness of breath associated with stagnation of blood in the pulmonary capillaries as a result of insufficiency of the left heart. In a horizontal position, this condition is aggravated, and therefore it is difficult for such patients to lie.
12. Asphyxia - respiratory arrest or depression, mainly associated with paralysis of the respiratory centers or closure of the airways. At the same time, gas exchange is sharply disturbed (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 elasticity decreases. Such disorders are observed, for example, in lesions of the lung parenchyma (pneumonia, pulmonary edema, pulmonary fibrosis) or pleural adhesions.
The obstructive type of ventilation disorders is due to the narrowing of the airways, i.e. increasing their aerodynamic resistance. Similar conditions occur, for example, with the accumulation of mucus 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 FRC increase in them. A pathological condition characterized by an excessive decrease in the number of elastic fibers (disappearance of the alveolar septa, unification of the capillary network) is called pulmonary emphysema.
