Respiratory failure
Respiratory failure kinds (not to confuse to hypoxia kinds) according to their pathophysiological causes it is possible to secure only such two kinds:
A ventilating respiratory failure
Characteristic signs of a ventilating respiratory failure are:
- A total hypoventilation, respiratory minute volume depression (RMV), an insufficient exchange of gases in convection region
- A hypoventilation consequence - a hypercapnia, and then and an anoxemia
- Almost all causes of a ventilating respiratory failure lay out of a lung
What concrete causes of a total hypoventilation? All of them can be parted on some bunches:
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Disturbances of the central regulation of breath.
At the wet brain grasping its stem parts and region of a respiratory centre, oppression of its activity is possible, the hypoventilation will be a consequence of that. Such situation can educe in connection with a brain trauma, toxic or its hypoxic damage.
Enough as the frequent cause of oppression of work of a respiratory centre introduction of various medical products, more often narcotic analgetics and barbiturates serves. Such descends and at an independent drug intake the patient and in a medical institution, for example at a satisfying of pains after operation. Last cause can be rightfully carried in the discharge of the iatrogenic. The overdosage of analgetics is the frequent cause of development of a hypoventilation and the subsequent pneumonia at patients after various surgical interventions. Thereupon often urge to refuse application of narcotic analgetics for anaesthesia in the postoperative season. However, the real alternative to such anaesthesia is not present and consequently more expediently to think not of abandoning of application of these preparations, and about perfection of the procedure of introduction of narcotic analgetics.
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The Second bunch of the causes of a ventilating respiratory failure is bound to disturbances of function of the apparatus of ventilation of the lungs.
Here it is necessary to include various mechanical damages of a thorax and a diaphragm: fractures of ribs, a thoracotomy, a pheumothorax and a hydrothorax, high standing of a diaphragm at paresises of a gastrointestinal tract.
Cases of a chronic hypoventilation and respiratory failure owing to the poliomyelitis tolerated in the childhood with a particulate atrophy of the muscular apparatus of breath are probable. In the same bunch it is possible to carry patients with an alimentary atrophy of respiratory muscles, for example at an esophagus and cardia cancer
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The Separate bunch is compounded by patients with restrictive lesions of lungs which lead to depression of elasticity of a pulmonary tissue, to resistance augmentation to a gas stream at breath and to a hypoventilation. This bunch of the causes is an exception of a rule according to which the causes of a ventilating respiratory failure have out of pulmonary character.
A parenchymatous respiratory failure
This kind of a respiratory failure as already it became perceptible, is completely connected to disturbances VA/Q. As such disturbances happen two types also the parenchymatous respiratory failure differs depending on a type of disturbance VA/Q. In other words, it is necessary to distinguish the parenchymatous respiratory failure bound:
- With augmentation of alveolar dead space when the blood stream concerning volume of alveolar ventilation is reduced and
- With augmentation of volume of shunting or venous shunt in an arterial blood! As the augmentation of volume of shunting is (from right to left accompanied by reduction of volume of ventilation concerning blood flow volume, this kind of a respiratory failure is always connected to a particulate and full obturation of this or that bronchus or bunch of bronchuses. On this cause the described kind of a respiratory failure name an obstructive respiratory failure.
Basic signs of a parenchymatous respiratory failure (PRF):
- Disturbance VA/Q
- An anoxemia
- A hyperventilation and a hypocapnia
- All disturbances PRF are bound to disturbances in lungs
Augmentation of alveolar dead space
Classical example of the termination of a blood flow in the presence of ventilation in a certain field of a pulmonary parenchyma is the thrombembolia of branches of a pulmonary artery. In this case there is a full termination of inflow of blood to the given field of a lung that leads to augmentation of alveolar dead space and disturbance of a trophicity of tissues with the subsequent infarction in region the blood flow terminations. We will not be intercepted on details of development of a thrombembolia of branches of a pulmonary artery as this kind of a pulmonary pathology understands the literature devoted to disturbances of coagulating system of blood. But other damage of lungs accompanied by augmentation of dead space, deserves more detailed description here, at analysis of the causes of a respiratory failure.
We have in view of a pathology which wore until recently the name "shock lung", and now is called as "a respiratory distress-syndrome of adults". The syndrome has received the first name because for the first time has been noticed and described, how one of consequences of a hypovolemic shock. However, subsequently it has appeared, that many kinds of a pathology can lead to development of this syndrome.
In difference from the majority of diseases of lungs where the basic localisation of pathological process are respiratory tracts, development of a respiratory distress-syndrome begins with a vascular network of lungs. Better others development of the pulmonary distress-syndrome complicating flow of a hemorrhagic, hypovolemic shock is studied. "Shock lung" can be in many respects regarded, as an iatrogenic pathology as treatment substantially causes development of vascular disturbances in lungs.
On the other hand, the diagnosis "shock lung" has appeared only when certain successes in treatment of a massive blood loss have been reached. Till this time patients, as a rule, died earlier, than the pulmonary distress-syndrome had time to educe.
At development of a hypovolemia and a hypovolemic shock some factors promote "shock lung" appearance. First it is a hypotension and blood flow retardation, both in big, and in a small circle of a circulation. Secondly, as reaction to a hypovolemia, educes centralisation of a circulation and, hence, disturbance of perfusion of peripheric tissues. Result of centralisation is the hypoxia and accumulation of the increasing quantity sub the oxidised products and metabolites of many biologically active materials (catecholamins, kinins, a serotonin, etc.).
The third important factor promoting development of a distress-syndrome, it is necessary to consider a decompensation of one of not respiratory functions of the lungs, bound to excision of many biologically active materials and their metabolites. This decompensation descends, as consequence of action of first two factors: hypotensions and augmentations of production of the materials which are subject to excision.
Simultaneous action of all three factors leads to sharp disturbance of a trophicity of a vascular side and first of all an endothelium, to a progressing thrombogenesis, augmentation of a porosity of pots and thereof to filling of alveoluses and fine bronchuses to contents of pots with the subsequent micro-and makro - atelectases and formation of the fine, gradually merging pneumonic locuses.
On this background the major factor breaking a local blood stream in a small circle of a circulation is microembolization by clots and other microparticles which are washed away from tissues owing to a reperfusion (restoration of a blood flow after resuscitation, the centralisation terminations at a blood loss restore etc.).
Considerably aggravates blood flow disturbances in lungs and educing at treatment of a massive blood loss a so-called syndrome massive transfusions. The main reacting factor of this syndrome in this case is microembolization of a capillary bed of a small circle by units of erythrocytes of stored blood.
Exact and timely diagnostics of a pulmonary distrees-syndrome as the diagnosis assumes probably earlier appointment ALV and direct anticoagulants, along with correction of rheologic disturbances, cardial therapy and other actions is very important. Careful finding-out of evolution of development of the respiratory failure as which main difference (evolution) from development of other kinds of a pulmonary pathology early appearance of an anoxemia and a dyspnea accompanying it without physical and radiological semiology from lungs serves can help with syndrome diagnostics. In other words, if at the patient educes the expressed dyspnea and an anoxemia without reduction of respiratory volume and without appearance of a local hypoventilation (according to auscultation) if the dyspnea is not accompanied by rhonchuses in lungs and disturbance of a transparency of pulmonary fields on the roentgenogram is speaks about development of a pulmonary distress-syndrome. The diagnosis can be put even more confidently if the anamnesis speaks about possibility of development of a syndrome: the tolerated massive blood loss, a long hypotension, an intoxication at extensive inflammatory processes, etc. Even at in due time begun treatment, this complication leads to mors appreciable number of patients. "Shock lung" deserves special attention and consequently, that this syndrome very brightly shows the pathophysiological nature of an anoxemia in connection with disturbance VA/Q and at the same time shows, that at baking by the effective there can be only those actions which resolve the disturbances descending in alveolar (diffusion) region of lungs.
An obstructive respiratory failure
The second kind of a parenchymatous respiratory failure is bound to obstructive disturbances in respiratory tracts, a local hypoventilation and changes VA/Q to some shunting and shunt of a venous blood without oxygenation or with insufficient oxygenation, in an arterial bed. Dynamics of volume of venous shunting (measured by an oxygen method) and its size give the chance to judge degree of disturbance of bronchial passableness, about volume of region of a hypoventilation and about process development. This dynamics allows to estimate and results of our medical actions.
As the cause of a primary obstructive respiratory failure it is necessary to survey very wide spectrum of a pulmonary pathology, beginning from occlusive a bronchus of the central cancer of lungs, to a pneumonia and a tuberculosis where the obturation of bronchuses of a various order and number takes place. Here it is possible to include a various productive bronchitis with disturbance of a bronchial drainage and an obturation of the conforming bronchuses. But not only purely obstructive pathology leads to disturbances VA/Q with shunting of a part of warm outlier. Variety of diseases in which basis restrictive disturbances lay, also finally come to the end with obstruction of bronchuses and patients suffer not only from ventilating, but also from a parenchymatous respiratory failure. Differently, the admixed respiratory failure not accident, and is faster pattern.
It is necessary to notice, that the term "shunting" in this case (at obstruction of bronchuses) is applied conditional as there are no special anatomical formations, called to shunt a blood stream as it happens at insufficiency of microcirculation (direct arteriovenous shunts). In this case the blood stream in lungs does not vary neither on volume, nor on vascular pathes. The effect of shunting is bound to a hypoventilation (or absence of ventilation). As a result the gradient (difference) of partial pressure of gases in capillars and out of them gradually decreases and can disappear completely, as leads to the gas exchange termination between blood and alveolar gas and to shunt (shunting) of not oxyogenised blood in an arterial bed. Such is an anoxemia parentage at PRF. It is natural, that shunting results not only in an anoxemia, but also to rising of level СО2 in an arterial blood. However, respiratory centre reaction (on rising РаСО2) and chemoceptors of a carotid sine (on an anoxemia) leads to a hyperventilation of normally functioning parts of lungs, that not only resolve an initial hypercapnia, but also reduces level PaCO2 in comparison with norm. Differently, disturbances VA/Q lead to a hypocapnia. It is important to notice, that the hyperventilation and a hypocapnia at PRF (during independent breath or ALV) aggravates a hypoxia bound to an anoxemia. The matter is that the hypocapnia (depression РаС02, a gas alkalosis) is accompanied by a spastic stricture peripheric (including cerebral) arteries and depression of a volume blood flow in tissues. Besides, at low РаСО2 the dissociation curve окcигемоглобина is displaced to the left, that means rising of affinity О2 to Hb, and, hence, reduction of return to tissues of the oxygen brought by blood. In this connection sometimes it is necessary that or other is by artificial to enlarge concentration CO2 in a rebreathing system and that to eliminate a hypocapnia.
This or that degree of shunting accompanies practically all diseases of lungs as each disease finally comes to the end with development of obstructive process. Really, if the ventilating respiratory failure causes in the beginning a hypercapnia, and then an anoxemia further the in itself hypoventilation becomes complicated depression of drainage function of bronchuses, that finally comes to the end with an obturation of bronchuses, disturbance VA/Q and an anoxemia already bound with the shunted. Similar process descends and at development of a pulmonary distress-syndrome. Disturbances in a vascular side and augmentation of a porosity of pots lead to fluid "transuding" in a lumen of alveoluses. Gradually obstructive bronchioles and fine bronchuses. There are micro, and then and macroatelectases, and on their basis the fine pneumonic locuses which are enlarged and merge in larger pneumonic locuses. Thus, in region pathological disturbances gas exchange does not descend not only in connection with blood flow disturbances. The blood proceeding and on the intact capillars has no possibility to receive enough of oxygen and to give excessive Carbonei dioxydum.
Principles of treatment of a respiratory failure
Treatment of a ventilating respiratory failure should be referred on elimination of the cause which have caused a hypoventilation. If such elimination not probably or demands many time, the patient should be translated on ALV or an assisted breast against which actions for therapy of the basic pathological process should be carried out.
As more or less long hypoventilation which even not is not leading to disturbance of gas exchange, as a rule is accompanied by an obturation of bronchuses in connection with weakening of a bronchial drainage, it is necessary to struggle with an anoxemia caused by this obturation. Differently, the ventilating respiratory failure is accompanied by insufficiency parenchymatous and, hence, medical actions should be referred and on elimination of an obturation of bronchuses.
As we more than once underlined, the respiratory failure of any nature finally is accompanied by disturbance of bronchial passableness. For this reason treatment of a respiratory failure of any parentage needs to be begun or accompanied the actions referred on preventive maintenance and treatment of disturbances of drainage function of bronchuses.
It is necessary to tell, that in any unit of resuscitation and an intensive care where patients after the big cavitary operations are treated, appreciable, and it is frequent also the most part of an operating time of the medical personnel it is spent for the decision of this problem.
The big arsenal of the agents promoting enriching of bronchial passableness, it is possible to present in ascending order traumatic medical action. At first there are agents of the general influence. First of all building of necessary "inhabitancy" of the patient concerns them with optimum humidity, temperature, ionic structure of air.
Some authors, it can lower probability of development and facilitate the permission of an obturation of bronchuses approximately twice.
The general for all patients is the demand of adequate anaesthesia. Without performance of this condition it is difficult to count on success of other medical actions.
When we speak about adequacy of anaesthesia we have in view of anaesthesia sufficient for active behaviour of patients including effective tussis. At the same time, adequacy of anaesthesia assumes prevention of overdosages of the analgetics, which (overdosages) in itself can lead to oppression of the central regulation of breath and, hence, only to accelerate stagnation development in lungs and their obturation. From numerous means of anaesthesia including after operation, sufficient on analgetic effect and at the same time not oppressing activity of patients, apparently, it is possible to recognise only two methods:
- An epidural anaesthesia
- An analgesia on demand
As the epidural anaesthesia is applied not in all medical institutions, bound to certain risk and is rather complex on the technician of performance, a predominant agent of anaesthesia after the big cavitary operations and traumas there are narcotic analgetics and their synthetic analogues. A recommended method of their application - "the analgesia on demand" (autoanalgesia) allows to provide sufficient analgesia without overdosages and oppression of activity of patients. The method short "analgesias on demand" consists that after introduction of a certain loading dose of an analgetic for building of therapeutic concentration of a preparation in the blood, sick receives constant introduction of solution of a medicine, but also, has possibility to "cause" additional introduction of a preparation by simple pressing of the contact button of a batcher. Sizes of a loading dose, rate of constant introduction and grant dose on demand, no less than "an interdiction interval" between grants - are defined by the doctor and establishes parametres of these sizes on the panel of the block of control of a batcher. Thus, the patient can define anaesthesia level according to intensity is sick. The overdosage is quenched by "an interdiction interval".
If against adequate anaesthesia of the patient by means of tussis cannot provide a qualitative bronchial drainage, it is necessary to resort to agents of activization of tussis and inhalation therapy, including Mucolyticums. Inhalation therapy pursues the aim and humidifications and bronchial tree sanations. As sanifying preparations decoctions and infusions of leaves of a messmate, a sage, a camomile, solutions of phytoncids can be applied. For carrying out of sessions of inhalation therapy it is necessary to prefer ultrasonic inhalers as only they provide a sufficient disperse of an aerosol at temperature below a body temperature. Otherwise, (at steam inhalation) there is a fluid condensation on mucous the top respiratory tracts and a trachea. The inhalated agent does not reach fineer branches of a bronchial tree.
Powerful stimulus of tussis are purely mechanical influences on mucous larynxes, a trachea and bronchuses. More often than others for this purpose the so-called microtracheostomy, i.e. paracentetic carrying out of a thin plastic tube in a trachea through membrane Crycothyreoidea was used. The boring of respiratory tracts is effected both the tube, and the fluid periodically introduced through it in a trachea. In most cases such mechanical boring causes a strong fit of coughing and remission of bronchuses of a sputum. Unfortunately, effective this action happens not longly. In some hours or in day, mucous tracheas becomes a little sensitive to a boring and necessary medical effect already to reach it is not possible. Moreover, persevering attempts of medical staff by means of injections in a trachea to cause tussis, can lead to a clump of fluid and in bronchuses that aggravates a respiratory failure.
More reliable results can be received from so-called sounding of a trachea which is effected thin (0,5-0,6см.) a plastic probe through a nasal course after processing by Dicainum mucous a nose and a larynx. The probe is spent through vocal chords blindfold under the control of respiratory hums. The probe is a stimulus causing strong tussis, but also, connection to a suction device probe gives the chance to evacuate a sputum within reach of a probe. Thus, joint efforts of tussic jerks and a suction device the sputum leaves from a bronchial tree that recovers passableness of bronchuses.
The described procedure, despite the efficacyy, does not maintain a competition to a fiber-optic bronchoscopy as last allows to delete a sputum not only from a trachea and the right primary bronchus as at sounding, but also from other parts of a bronchial tree, up to segmental bronchuses from both parties. Besides, procedure less traumatic also gives the chance not only to establish a condition of bronchuses and their mucous, but also to sanify mucous various medicinal solutions. It is desirable, to consider, that the bronchoscope a foreign body and its stay in a lumen of respiratory tracts puts them a trauma. Besides, it is impossible to name procedure aseptic as bronchoscope disinfection, as a rule, does not reach a full decontamination of its surface. From here danger of a transmission of infection from one patient to another.
If by means of a bronchoscopy and bronchial tree sanation it is not possible to release a lumen of bronchuses from an obturation causing sufficient degree of shunting and a respiratory failure, there are indications to artificial lung ventilation. These indications can arise and earlier if degree of disturbance of gas exchange does not allow to test consistently all listed methods of the permission of an obstructive respiratory failure.
ALV certainly solves a problem of a ventilating respiratory failure. However, if it is a question of the parenchymatous respiratory failure caused not by depression of volume of ventilation, and disturbances of ventiljatsionno-perfused attitudes application ALV reduces an anoxemia only so, the power consumption for work of breath both how much enlarged volume of ventilation and pressure on an inspiration how much decreases enrich an exchange of gases between alveolar (diffusion) and convection regions lungs at the expense of enrichment of convection region by oxygen. In other words, ALV cannot considerably eliminate an anoxemia bound to disturbances in alveolar region of lungs as influence ALV extends mainly on an exchange of gases in convection region. Probably only indirect influence on enrichment of alveolar region by oxygen at the expense of augmentation of a gradient of concentration of oxygen between convection and alveolar regions at augmentation of the maintenance of oxygen in an inhaled admixture and RMV.
Some augmentation Ра02 is possible and at the expense of pressure augmentation at an expiration, buildings of a plateau of pressure in the end of an inspiration. However possibilities of these maneuvers, as a rule, are exaggerated for a long time also the special hopes of anoxemia correction at a parenchymatous respiratory failure by means of these regimens ALV, to assign it is not necessary. Medical possibilities ALV at a parenchymatous respiratory failure are circumscribed. At serious disturbances of ventiljatsionno-perfused attitudes, especially at a shock lung to count on appreciable effect from application ALV it is not necessary. Practice shows, that at expressed disturbances VA/Q, in particular at a distress-syndrome, despite early beginning ALV, to stop an anoxemia it is possible far not always. In those cases where the anoxemia "does not give in" to treatment by means of volume ALV and continues to accrue, when life of the patient depends on, whether we will manage to offer for treatment any additional, more effective, than volume ALV agents.
The real augmentation of oxygenation of blood at disturbances VA/Q and anoxemias managed to be received by means of so-called high-pitched ventilation of the lungs (HF ALV), both jet, and oscillometric (last against routine volume ventilation).
Some words about these kinds of ventilation of the lungs. HF ALV such ventilation at which change of inspiratory phases and an expiration descends 60-200 times in minute for jet HF ALV and 1-2тыс is called. Once a minute at oscillometric HF ALV. At these kinds of ventilation the concept "inspiration" and "expiration" are conditional enough, especially it concerns oscillometric HF ALV.
Observations have shown, as jet (a stream of oxygen from thin - 1 mm. In diameter - moves in an endotracheal tube or in a trachea under pressure about 2 atmospheres with frequency 50-200 in minute) and oscillometric (membrane fluctuations in a contour of an inspiration usual ALV with frequency of 1-2 thousand fluctuations in minute) allow to raise РаО2 on 20-50 mm Hg and more at those patients where usual ALV did not give effect at attempts to liquidate an anoxemia.
The standard explanation of an intensification of gas exchange under the influence of HF ALV while is not present. Despite it, already now it is possible to assert, that effect HF ALV is bound to influence on gas exchange in diffusion region for the anoxemia at a parenchymatous respiratory failure grows out of disturbance VA/Q in this region. From here follows, that enriching of oxygenation of blood can descend only as a result of gas exchange enriching in diffusion region.
Meaningly to choose mean HF ALV and its optimum regimen, the hypothesis explaining the mechanism of influence of this kind of ventilation of the lungs on gas exchange is necessary at least.
The numerous facts received at application HF ALV well "keep within" the theory where reverberatory fluctuations are a stimulus or the cause of an intensification of gas exchange at HF ALV.
Shortly short of this theory consists in the following: at carrying out jet or oscillometric HF ALV in respiratory tracts and a pulmonary tissue fluctuations provoke. The voltage of these fluctuations as show calculations, is insufficient to make appreciable impact on alveoluses and fine bronchuses. However, at building of reverberatory conditions in system: respiratory tracts - a pulmonary tissue - a thoracal side - (these conditions are framed when frequency of submitted fluctuations coincides or it is close to frequency of own fluctuations of system) are framed reverberatory fluctuations which have voltage, in 20 times exceeding voltage of initial fluctuations. The voltage of these reverberatory fluctuations becomes comparable to the dimensions of alveoluses (0,3мм) and compounds 0,8 mm. There are establishments to assume, that with such voltage purely mechanical influence has on anatomical formations of alveolar region fluctuations. There is as though an additional hashing (a convection out of convection region) gas in diffusion region, that necessarily leads to a gas exchange acceleration, to its enriching. This enriching descends first because the gas blanket on border of alveolar and convection regions that enlarges РО2 this layer is more often regenerates. Secondly, the same descends to change of gas at a side of an alveolus and it promotes augmentation of gradient РАО2 - РаО2, as a result of РаО2 raises. The specified mechanical influence of reverberatory fluctuations effects one more favorable effect on structures of alveolar region. It is a question of reduction of adhesion of contents of the smallest bronchuses to their mucous, that leads to enriching of a drainage of these bronchuses and, finally, to augmentation of volume of alveolar ventilation, i.e. reduction of disturbances of ventiljatsnonno-perfused attitudes. This last effect of reverberatory fluctuations at HF ALV often is solving. It leads to normalisation of gas exchange and anoxemia cupping. Value of this mechanism of remission of fine bronchuses from a secret increases also because in alveolar (diffusion) region there is no mechanical moving of gas and progression of a secret at the expense of tussic jerks is impossible.
Thus, blockage of fine bronchuses can be resolved natural by only at the expense of endogenous Mucolyticums and "fusion" of mucopurulent stoppers. Process this long enough and a little controlled. Hence, vibratory process and reverberatory fluctuations are in essence is unique the real mean of influence accelerating remission of a lumen of fine bronchuses and augmentation of volume of alveolar ventilation.
Clinical application oscillometric HF ALV (with frequency of fluctuations of 60-80 Hz) against usual volume ventilation of the lungs has allowed to raise РаО2 on 20-30 mm Hg practically at all patients with a respiratory failure where routine ALV stable congenial result did not give, despite appreciable minute volume of ventilation and high FiO2. At two of such 30 patients HF ALV has not variated РаО2. Inspection of these patients has taped a pheumothorax (air small amount in a pleural cavity did not reduce a respiratory surface of a lung). After excision of air from a pleural cavity at both patients the usual effect from application HF ALV has been received. These observations are argument in favour of the stated theory. The matter is that "reverberatory conditions" or "a reverberatory contour" include: respiratory tracts, a parenchyma of lungs and a thoracal side. At dissociation of these elements of a contour, reverberatory conditions and reverberatory fluctuations are broken not formed. It also has descended at patients to a pheumothorax. Air has abjointed a thoracal side from a lung parenchyma, reverberatory fluctuations were not formed, from here and absence of effect from HF ALV. The Same result observed both at an open pleural cavity and in experiment on a pulmonary preparation: here again HF ALV does not variate gas exchange.
The offered explanation of the mechanism of an intensification of oxygen exchange at HF ALV has not only theoretical, but also purely practical value. The hypothesis explains, for example, why at jet ALV frequency of change of the cycles, exceeding 150-200 in minute becomes noneffective. The interval between cycles that the effect of fading fluctuations has had time to be realised is too small. Besides, the hypothesis variates a scale of values of various means HF ALV. Till now it is considered, that the priority belongs injection (jet) HF ALV, agrees to new representations, oscillometric HF ALV against volume ventilation of the lungs, in most cases has advantage before string HF ALV. This advantage in simplicity of an oscillator, in possibility widely to vary frequency of fluctuations and by that to choose influence localisation. Besides, oscillometric HF ALV can be applied with already functioning equipment for ALV. And, at last, oscillometric therapy can be used and at independent breath.
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