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Respiratory insufficiency, acute

Table of contents
Respiratory insufficiency, acute
Anamnesis of respiratory insufficiency
Diagnostic testings

Close concepts: hypoxia, hypercapnia, carbon dioxide delay, cyanosis, respiratory acidosis, asphyxia, asthma

Strictly speaking, respiratory insufficiency is a disturbance of all process of breath, including intake of oxygen in an organism, its distributions in fabrics and utilization together with nutrients at the cellular level, and also educations and releases of carbon dioxide. In spite of the fact that in the present article the main attention is paid to intra pulmonary aspects of this problem, some clinical disturbances affecting extra pulmonary areas, for example disturbance of breath at the level of mitochondrions at a poisoning with cyanides ("gray cyanosis"), reduction of oxygen capacity of blood at poisoning with carbon monoxide ("cerise cyanosis"), circulator shock ("peripheral cyanosis") actually represent respiratory insufficiency. Besides, as it will be shown below, an essential role in physiological process of gas exchange in lungs is played by the general metabolic rate and a condition of blood circulation.

Clinically acute respiratory insufficiency means rather sudden disturbance of one or both main functions of lungs — oxygenation of an arterial blood and removal of carbon dioxide, leading respectively to a hypoxia and (or) a giperkapkiya. If the amount of the inhaled oxygen does not increase, accumulation of carbon dioxide in alveoluses leads to reduction of content in alveolar gas of oxygen and developing of a hypoxia.

Traditionally medical students are taught that are the physiological reasons of a hypoxia:
1. The general hypoventilation at which increase in partial pressure of CO2 in alveoluses is followed by decrease in content of oxygen. At reduction of content of oxygen in alveoluses its content in blood is reduced even if complete equilibrium between the partial pressure of gases in blood and alveoluses takes place.
2. Shunting at which the venous blood poor in oxygen completely passes a pulmonary circulator bed (for example, at endocardiac anatomic defects) or passes through vessels in sites of lungs where there is no gas exchange (for example, at malformations of arteries and veins or in the vessels located in areas of a full atelectasis).
3. Disturbance of balance between ventilation and perfusion, for example the strengthened blood stream in the small, badly ventilated sites of lungs and as a result — relative deficit of oxygen. One of extreme options of discrepancy of ventilation and perfusion is the shunting mentioned above (perfusion for lack of ventilation). Ventilation of dead space (ventilation without perfusion) which directly does not influence blood oxygenation can be other example and therefore does not promote a hypoxia, but can increase breath work. Possibly, disturbance of balance between ventilation and perfusion is the main mechanism of development of a hypoxia at the majority of diseases.
4. Diffusion disturbances at which the obstacle of diffusion of alveolar gases and blood gases is increased so that during passing of blood through pulmonary capillaries of optimum balance in the content of gases in blood and in alveoluses it is not reached. At histologic research it is confirmed by a thickening and fibrosis of walls of alveoluses which is observed at a pneumosclerosis.

As in these cases time of passing of blood through lungs has special value, reduction of this indicator owing to increase in cordial emission at an exercise stress aggravates a hypoxia. This phenomenon received the name of a syndrome of "the alveolar and capillary block". More modern data based on morphometric pathoanatomical researches of drugs of pulmonary fabric and mathematical models of a pulmonary blood-groove and diffusion of gases demonstrate that disturbances of diffusion do not play so essential role in development of respiratory insufficiency. However still there is no uniform explanation of the mechanism of development of a hypoxia during an exercise stress at many chronic diseases of lungs.

Though the listed pathophysiological mechanisms are a basis of our understanding of essence of a hypoxia, clinical data and new researches can change the existing idea of these phenomena. Let's give a clinical example: in the presence of shunting degree of the arising hypoxia, obviously, depends on amount of the blood dumped from venous system in arterial, but it is possible, the hypoxia depends also on the content of oxygen in a venous blood. At the patient of peripheric circulation, shocked owing to delay, from blood the bigger amount of oxygen therefore shunting of a venous blood with the low content of oxygen will lead to proportional increase of a hypoxia will be extracted. The same can occur at increase of intensity of metabolic processes in combination with relative circulator insufficiency when there is a need for increase in consumption of oxygen, and the blood stream is inadequate for its satisfaction without oxygen extraction increase with peripheral fabrics. As an example of new concepts, believing that the theory of disturbance of diffusion as a result of a thickening of an alveolar membrane is not rather convincing, it is possible to give another according to which at some diseases there can be a disturbance of "radial" diffusion, i.e. the movements of gases from a capillary wall to its center. Expansion of pulmonary capillaries is found in patients with similar disturbances. Diffusion of oxygen from an internal surface of an endothelium to the erythrocyte which is in the center of such capillary requires a considerable interval of time. If the speed of the movement of an erythrocyte on an axis of an expanded capillary is big, the content of oxygen in a capillary low. It is easy to explain with this mechanism developing of a hypoxia during an exercise stress, but further researches are necessary for establishment of its clinical value.

When alveolar ventilation is insufficient for removal coming to easy CO2, there is an increase of partial pressure of carbon dioxide in alveoluses. As it was already stated above, efficiency of alveolar ventilation in turn depends on pumping function of a thorax and compliance between ventilation and perfusion. In the majority of clinical situations disturbance of ventilating and perfused compliance does not make an essential contribution to process of a delay of CO2 as:
1) diffusion capacity of carbon dioxide is much higher, than oxygen, and the problems connected with a hypoxia arise at less expressed dysfunctions of lungs;
2) in some limits CO2 delay — the self-limited process because at CO2 delay its concentration in expired air is higher, therefore, increases also allocation of CO2;
3) even at the expressed changes in lungs when the volume of dead space or area of not perfusing alveoluses makes from 70 to 80% of the general ventilation if pumping function of a thorax is not broken, for the purpose of maintenance of a normal homeostasis of CO2 there can be a significant increase in the general ventilation. In other words, pathophysiological mechanisms of ventilating insufficiency with a delay of CO2 gain value if the patient is not able to increase work of breath to necessary level ("cannot breathe") or the respiratory center of a myelencephalon cannot carry out the correct regulation of the act of breath ("will not breathe").

Receipt of CO2 in lungs increases at increase in a metabolism (an exercise stress, fever, a stress and other states), a metabolic acidosis (as a result of influence of the bicarbonate buffer), administration of drugs with the increased content of carbohydrates (for example, at parenteral excess food — all these states can be distinguished clinically).
Work of breath is the mechanical phenomenon including "resistive" work * which increases at the diseases proceeding with obstruction of respiratory tracts, and "elastic work ** which increases at diseases of restrictive type. Diseases of restrictive type can be caused by pathology actually easy (for example, increase in rigidity of lungs at fibrosis or other parenchymatous diseases of lungs) or extra pulmonary pathology (for example, weight of a chest wall at pathological obesity or damage of a pleura, for example, at a mesothelioma and an exudate in a pleural cavity).
Ability of the respiratory device of the patient to resist to stressful situations depends on interaction and coordination of a number of factors, including a condition of a nervous system, neuromuscular connections, respiratory muscles and a thorax. Integrity of this chain can be broken at such clinical states as degenerative neurologic diseases, muscular dystrophy, a myasthenia and fractures of edges. According to modern data, it is supposed that dystrophy and an incoordination of reductions of respiratory muscles can play a significant role in development of acute respiratory insufficiency, aggravating chronic diseases of lungs.

* Work on overcoming of resistance of respiratory tracts.
** Work on overcoming of an elastic energy of lungs.

The respiratory center as the central regulator possesses the main role in equalizing of ventilating requirements and operation of the respiratory device. Function of the most respiratory center can be broken as a result of direct influences, for example an injury or effect of sedative drugs, as a result of the inborn weakness (which is the possible reason of a syndrome of sudden death of newborns) or owing to the hyper adaptation allowing excess increase of partial pressure of CO2 in the absence of simultaneous increase in work of breath. Depends on existence of hyper adaptation, giperkapnichesky respiratory insufficiency will develop at this patient with the increased breath work or not. For example, among patients the content of gases in blood will decide on identical degree of pathological obesity at some close to normal, at others the Pickwickian syndrome develops, and among persons with chronic obstructive diseases of lungs and the seeming identical extent of increase of resistance of respiratory tracts at one the normocapnia ("pink puffiness"), and at others — a hypercapnia ("blue puffiness") is noted.

HISTORICAL INFORMATION

Experience of modern medicine in treatment of the big contingents of patients with acute respiratory insufficiency began to form during poliomyelitis epidemics about five decades ago. Poliomyelitis causes the disturbance in system of the neuromuscular device representing true giperkapnichesky ventilating insufficiency at which the hypoxia developed for the second time or as a result of emergence of complications, for example an atelectasis or pneumonia. Now this type of respiratory insufficiency meets in the form of acute paralysis of respiratory muscles at such diseases as Giyen's syndrome — Barret and a myasthenia.

After in the developed countries as a result of mass immunization poliomyelitis was liquidated, there was a new form of epidemic respiratory insufficiency which is result of smoking. In 1950 — 1960 the acute respiratory insufficiency caused by chronic obstructive diseases of lungs became the most widespread. It represents respiratory insufficiency owing to damage of airways at which the thorax and lungs remain intact. At early stages quite often giperkapnichesky respiratory insufficiency prevails hypoxemic, and in process of progressing of a disease. Chronic obstructive diseases of lungs remain the main reason of acute respiratory insufficiency to this day. Within the last 15 — 20 years considerable interest of clinical physicians was caused by other form of respiratory insufficiency. Usually it is accepted to call it "a respiratory distress syndrome of adults". Though this term appeared in connection with use of modern methods of reanimation and life support systems, it is applicable at any acute diffusion diseases of the lungs which are characterized by diffusion defeat of a pulmonary parenchyma at which lungs become edematous (owing to damage of vessels of lungs, but not increase of pulmonary pressure at left ventricular heart failure) and in a clinical picture microatelectases and disturbance of a ventilating and perfused ratio prevail. At such frustration the thorax and airways of an intaktna, and is surprised directly a parenchyma of lungs. At early stages the hypoxia, and only at the last stages prevails if methods on breath function maintenance are not applied, the hypercapnia appears.

In spite of the fact that respiratory insufficiency is usually considered from gas exchange positions in lungs, by definition it is not always a synonym of pulmonary insufficiency. Lungs carry out important not respiratory functions, the most essential of which — biochemical, consisting in an inactivation of certain vasoactive amines and other substances, and also activation of some enzymes circulating in blood which probably play an important role in development of pathological process.



 
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