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Respiratory insufficiency

Table of contents
Respiratory insufficiency
Diagnosis
Principles of treatment of respiratory insufficiency

Respiratory insufficiency — morbid condition of an organism at which maintenance of normal gas composition of blood is not provided, or it is reached at the expense of tension of compensatory mechanisms of external respiration.

Decrease in partial pressure of oxygen is considered diagnostic criterion of the expressed respiratory insufficiency <60 mm of mercury. and/or increase of partial pressure of carbon dioxide in an arterial blood> 45 mm of mercury.

Epidemiology

The generalized data on epidemiology of respiratory insufficiency are practically absent. By approximate estimates, in industrialized countries, the number of the patients with chronic respiratory insufficiency demanding carrying out an oxygen therapy or DDVL (generally patients with HOBL, are more rare with pulmonary fibroses, diseases of a thorax, respiratory muscles, etc.), makes about 8 — 10 people on 10 000 population.
During life to 3 — 5% of patients with bronchial asthma transfer at least one heavy aggravation (weight is caused by expressiveness of acute respiratory insufficiency), which in the absence of the adequate help can end with death.
The share of the community-acquired pneumonia demanding hospitalization of patients in intensive care units owing to respiratory insufficiency fluctuates from 3 to 10% of total number of pneumonia.
Incidence of RDSV (acute respiratory a distress syndrome of adults or "an acute respiratory distress syndrome at adults") depending on the region fluctuates from 1,5 to 13,5 cases on 100 000 people a year. Among all patients of intensive care units at which IVL is carried out 16 — 18% answer criteria of RDSV.

Classification

There are several classifications of respiratory insufficiency.

1. Pathogenetic classification.
Distinguish two big categories of respiratory insufficiency:
• parenchymatous (hypoxemic, pulmonary or respiratory insufficiency of the I type);
• ventilating (giperkapnichesky, "pumping" or respiratory insufficiency of the II type)
Parenchymatous respiratory insufficiency is characterized by an anoxemia, difficult a korrigiruyemy oxygen therapy.

The most frequent reasons of parenchymatous respiratory insufficiency:
• pneumonia;
• RDSV;
• cardiogenic fluid lungs.
The main manifestation of ventilating respiratory insufficiency is the hypercapnia; the anoxemia is also present, but it usually well gives in to therapy by oxygen.
Ventilating respiratory insufficiency can develop owing to:
• exhaustions/weaknesses   of respiratory muscles;
• mechanical defect of a musculoskeletal framework of a thorax;
•  dysfunctions of a respiratory center.
The most frequent reasons of ventilating respiratory insufficiency:
• HOBL;
• damage of respiratory muscles;
• obesity;
• kyphoscoliosis.

2. On the speed of development allocate:
• acute respiratory insufficiency;
• chronic respiratory insufficiency.

The following features are characteristic of acute respiratory insufficiency:
• develops within several days, hours or even minutes;
• practically is always followed by disturbances of a hemodynamics;
• can pose direct threat for the patient's life (demands carrying out an intensive care).
acute respiratory insufficiency can develop also at patients with already existing chronic respiratory insufficiency (a sharpening of chronic respiratory insufficiency, a decompensation of chronic respiratory insufficiency).
chronic respiratory insufficiency:
• develops within several months — years;
• the beginning can be imperceptible, gradual, development at incomplete recovery after acute respiratory insufficiency is possible. 3. Classification of respiratory insufficiency by severity:

Degree

Rao2, mm of mercury.

SaO2, %

Norm

> 80

> 95

I

60 — 79

90 — 94

II

40 — 59

75 — 89

III

<40

<75

Etiology and pathogeny of a disease

Respiratory insufficiency can develop at defeat of any department or a link of system of external respiration:
• central nervous system and respiratory center:
— overdose     of drugs;
— hypothyroidism,
— central apnoea;
— disturbance of cerebral circulation;
• neuromuscular system:
— Giyen's syndrome — Barret;
— botulism;
— myasthenia;
— Dyushen's illness;
— weakness and exhaustion of respiratory muscles;
• thorax:
— kyphoscoliosis;
— obesity;
— a state after a thoracoplasty;
— pheumothorax;
— pleural exudate;
• respiratory tracts:
— laryngospasm;
— throat hypostasis;
— foreign body;
bronchial asthma;
— HOBL;
mucoviscidosis;
— obliterating bronchiolitis;
• alveoluses:
pneumonia;
— RDSV;
— atelectasis;
— fluid lungs;
— alveolites;
— pulmonary fibroses;
— sarcoidosis.

Main pathophysiological mechanisms of development of an anoxemia:
• decrease in partial pressure of oxygen in the inhaled air;
• general hypoventilation of lungs;
• disturbances of diffusion of gases through an alveolocapillary membrane;
• disturbance of the ventilating and perfused relation;
• shunt (direct dumping of a venous blood into the arterial blood circulatory system).
• decrease in partial pressure of oxygen in the mixed venous blood.

Decrease in partial pressure of oxygen in the inhaled air

Low partial pressure of oxygen in the inhaled air can be noted:
• at big heights as a result of reduction of atmospheric pressure;
• at inhalation of poison gas;
• near fire because of oxygen absorption when burning.

General hypoventilation of lungs

At hypoventilation of lungs increase in partial pressure of CO2 in alveoluses is noted. Between pressure of O2 and CO2 in alveoluses there is feedforward, increase of the last leads to pressure decrease of O2 in alveoluses and an arterial blood.
Disturbances of diffusion of gases through an alveolocapillary membrane
At disturbance of diffusion of gases through an alveolocapillary membrane during passing of blood through pulmonary capillaries it is not reached optimum balance in the content of gases in blood and alveoluses. This phenomenon received naming of a syndrome of "the alveolar and capillary block".
This mechanism of development of an anoxemia is characteristic of intersticial diseases of lungs, such as:
• alveolites;
• intersticial fibrosis;
• sardoidoz;
• asbestosis;
• carcinomatosis.

Disturbances of the ventilating and perfused relation the Ventilating and perfused imbalance is the most frequent mechanism leading to development of an anoxemia. Average VA/Q value normal makes 0,8 — 1,0.
At various conditions of VA/Q value can vary from 0 (the perfusing, but not ventilated alveoluses — the shunt) indefinitely (ventilated, but not perfusing alveoluses — dead space).

Irregularity of the ventilating and perfused relations can increase:
• with age;
• at change of position of a body and lung volume;
• at respiratory diseases, alveoluses or intersticial tissue of lungs.
At various diseases compliance of processes of ventilation and perfusion is broken, in this case in lungs emergence of two pathological zones is possible: with dominance of sites with high or low VA/Q.
The main contribution to development of an anoxemia is made by sites of lungs with low VA/Q. In these departments the venous blood is not exposed to full oxygenation and, mixing up with the blood flowing from the ventilated sites creates a so-called "venous adulteration" to an arterial blood.
Sites of lungs with high VA/Q enter the volume of physiological dead space. The anoxemia at the same time, as a rule, does not develop, however a metabolic cost on breath as ensuring the normal RASO2 level requires increase in minute ventilation of the lungs considerably increases.

Blood shunting

When shunting the venous blood poor in oxygen or completely passes a pulmonary circulator bed — the anatomic shunt (at endocardiac and intra pulmonary vascular defects), or passes through vessels in sites of lungs where there is no gas exchange — the alveolar shunt (for example, through the vessels located in zones of a full atelectasis). In this case the relation of VA/Q comes nearer to 0 (the true or absolute shunt). The size of the pulmonary shunt normal does not exceed 5% of cordial emission and is caused by existence of bronchial pulmonary circulation. The anoxemia which reason the intra pulmonary shunt is badly gives in to an oxygen therapy even from high FiO2.
Decrease in partial tension of oxygen in the mixed venous blood
SvO2 depends on balance between delivery and consumption of oxygen. Any factor breaking this balance can lead to decrease in SvO2.
This mechanism plays an important role in development of respiratory insufficiency at:
• shock of various etiology;
• thromboembolisms of a pulmonary artery;
• to an exercise stress at patients with chronic pulmonary diseases.

Mechanisms of development of a hypercapnia:

• general hypoventilation of lungs;
• increase in volume of physiological dead space;
• increase of products of CO2.
General hypoventilation of lungs
Is a consequence of disturbance of difficult relationship between the central regulation of breath and mechanical work made by a thorax on inflating of lungs which depends on function of respiratory muscles and a pliability (distensibility) of a thorax.
Increase in volume of physiological dead space
Important pathophysiological disturbance at diseases of lungs is increase in physiological dead space which is defined as the sum of anatomic and alveolar dead space (regions of lungs with high VA/Q). Maintenance of the normal RASO2 level in this case requires substantial increase minute and alveolar a ventilyatsiiya. If the device of breath is not able to increase ventilation to required level, the hypercapnia develops.
At healthy faces almost all physiological dead space is provided by anatomic dead space.
Increase in products of O2
The raised products of OO2 are characteristic of the following situations:
• fever (fervescence on 1 °C leads to increase of products of CO2 for 9 — 14%);
• spasms, convulsions, agitation (the main mechanism in these situations strengthening of muscular activity is);
• excessive parenteral food (especially with the high content of carbohydrates). This mechanism practically is never the leading reason of a hypercapnia, and only makes the contribution at existence of one of two above-stated mechanisms.

Clinical signs and symptoms of an illness

Clinical manifestations of respiratory insufficiency depend on an etiology and type of respiratory insufficiency, its weight.

The most universal symptoms of respiratory insufficiency are:
• asthma;
• anoxemia symptoms;
• hypercapnia signs,
• signs of exhaustion and weakness of respiratory muscles.
The most characteristic symptom of respiratory insufficiency is an asthma which decides by patients on respiratory insufficiency as "feeling of respiratory effort" and is very closely connected with activity of respiratory muscles and a respiratory center.
There is practically no feedforward between expressiveness of an asthma and degree of an anoxemia and a hypercapnia therefore this criterion is not an objective sign of weight of respiratory insufficiency and is not used in classifications.

Clinical manifestations of an anoxemia it is difficult to delimit from other manifestations of respiratory insufficiency (for example hypercapnias).
• An important clinical sign of an anoxemia is cyanosis which reflects its weight irrespective of the reason and develops usually at Rao2 <60 mm of mercury. and SjiO2 <90% (at the normal Hb level).
• Characteristic hemodynamic effects of an anoxemia are tachycardia and moderate arterial hypotonia.
• At decrease in Rao2 to 55 mm of mercury. it is noted disturbances of memory on the current events, and at reduction of Rao2 to 30 mm of mercury. there is a loss of consciousness.
• Signs of a chronic anoxemia are the secondary polycythemia and pulmonary arterial hypertension.

Clinical effects of a hypercapnia can be result of both increase of activity of a sympathetic nervous system, and direct action of surplus of CO2 on fabric.
Main manifestations of a hypercapnia:
• hemodynamic effects:
— tachycardia;
— increase of cordial emission,
— system vazodilatation;
• effects from the central nervous system:
— the clapping tremor;
— sleeplessness;
— frequent awakenings at night and drowsiness in the afternoon;
— morning headaches;
— nausea.
At fast increase of RASO2 development of a giperkapnichesky coma is possible that it is connected with increase of a brain blood-groove, increase of intracranial pressure and edematization of a brain.
Symptoms of exhaustion and weakness of respiratory muscles
• Change of a respiration rate. ChD> 25/mines can be a sign of the beginning of exhaustion of respiratory muscles. ChD <12/mines — more serious predictive sign, can be an apnoea harbinger.
• Involvement in breath of auxiliary groups of muscles (a muscle of upper respiratory tracts in the form of active razduvaniye of wings of a nose, a muscle tension of a neck, synchronous with breath, and active reduction of belly muscles during an exhalation). In extreme cases of exhaustion and weakness of respiratory muscles can come to light explicit paradoxical dykhaniye*.

* Normal during a breath the thorax extends and rises, and the abdominal wall moves because of lowering of a dome of a diaphragm forward. At paradoxical breath the direction of movements opposite.



 
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