Light shock treatment. How does shock lung develop and what are the methods of treating it? Causes and mechanism of development of shock lung
"Shock" lung is a progressive damage to lung tissue in response to a number of extreme conditions accompanied by acute pulmonary failure and hemodynamic impairment. This syndrome is a nonspecific reaction of lung tissue to a primary violation of general and then pulmonary circulation after massive trauma, blood loss, severe surgery, etc.
Symptoms of shock lung:
Progressive shortness of breath.
Rapid breathing.
Lack of oxygen.
Decreased urine output.
Causes of shock lung:
Shock lung is usually a consequence of shock. Blood flow in the capillaries of the lungs, the smallest blood vessels that weave through the alveoli, decreases. Blood vessels contract, capillary walls are damaged, greatly increasing their permeability. In this case, blood plasma can penetrate into the lung tissue. When blood flow is weakened, the cells of the walls of the pulmonary alveoli are affected, producing a certain substance that does not allow the alveoli of a healthy person to collapse. As a result, foci of atelectasis appear in the lungs: the walls of the pulmonary alveoli are pressed against each other, and when inhaling, the alveoli are not filled with air. In addition, during shock, blood clotting begins in the smallest blood vessels. Small blood clots (microthrombi) appear in the capillaries of the lungs, increasing circulatory problems. As a result, lung function is impaired.
Etiology
Often the primary etiological factors of acute respiratory distress syndrome in adults are trauma and traumatic shock. Acute respiratory distress syndrome in adults complicates burns and mechanical injuries, including bone fractures, head injuries, lung contusion, and internal organ damage. This complication often develops after surgical interventions, in patients with cancer after operations such as Gerlock and Lewis. Massive transfusion of preserved blood without microfilters can also be a source of significant pulmonary microembolism and the primary etiological factor of the disease. The possibility of developing respiratory distress syndrome in adults after the use of extracorporeal circulation (“post-perfusion lung”) has been proven.
Dissemination of intravascular blood coagulation is one of the causes of multiple organ failure and pulmonary dysfunction. Previous critical conditions (prolonged hypotension, hypovolemia, hypoxia, blood loss), transfusion of large volumes of blood and solutions are considered as possible etiological factors of acute respiratory distress syndrome in adults. Fat embolism is one of the causes of pulmonary damage. Medicines (narcotic analgesics, dextrans, salicylates, thiazides and others) can also cause this complication.
The prevalence of adult acute respiratory distress syndrome in intensive care units depends on the patient population and the diseases in which the syndrome is likely to develop.
Pathogenesis
The main pathology is damage (destruction) of the pulmonary alveolar-capillary barrier. Pathophysiological changes: swelling and edema of the alveolar-capillary membrane, the formation of intercellular gaps in it, the development of interstitial edema. Adult acute respiratory distress syndrome is not just a form of pulmonary edema caused by increased capillary permeability, but also a manifestation of a general systemic pathological reaction leading to dysfunction not only of the lungs, but also of other organs.
The pathophysiological consequences of pulmonary edema in adult respiratory distress syndrome include decreased lung volumes, significantly decreased lung compliance, and the development of large intrapulmonary shunts. The predominance of blood flow in the ventilation/blood flow ratio is due to the perfusion of non-ventilated lung segments. A decrease in residual lung volume is also reflected in the unevenness of this ratio.
The destruction of pulmonary surfactant and a decrease in its synthesis can also be the reasons for a decrease in functional lung volumes and contribute to the increase in pulmonary edema. An increase in alveolar surface tension reduces hydrostatic pressure in the interstitium and increases water content in the lungs. A decrease in the compliance of an edematous lung leads to an intensification of the respiratory system and is accompanied by fatigue of the respiratory muscles. Quantitatively, the degree of pulmonary edema corresponds to the volume of intravascular water in the lungs, the value of which gradually increases, which largely determines the clinical and radiological picture of the disorder. A nonspecific disseminated reaction contributes to the formation of intravascular thrombi in the pulmonary artery system and an increase in pressure in it. The symptom of increased pressure in the pulmonary artery system is usually reversible, is not associated with left ventricular failure and, as a rule, does not exceed 18 mm Hg. The reversibility of pulmonary hypertension in adult acute respiratory distress syndrome within 72 hours of its development is confirmed by the administration of nitroprusside. In other words, pulmonary hypertension in acute respiratory distress syndrome in adults is not as manifest as in hydrostatic (cardiogenic) pulmonary edema. Typically, pulmonary artery wedge pressure is within normal limits. Only in the terminal stage of adult acute respiratory distress syndrome is it possible to increase pulmonary artery wedge pressure, which is associated with heart failure. Patients dying from progression of pulmonary failure and the inability of the lungs to perform gas exchange function in adult acute respiratory distress syndrome typically experience a marked decrease in lung compliance (extensibility), profound hypoxemia, and increased dead space with hypercapnia. Pathomorphological studies reveal extensive interstitial and alveolar fibrosis.
In the presence of shock lung, a large amount of fluid accumulates in the alveoli of the lungs and in the interstitial tissue in a short time, and pulmonary edema begins. Meanwhile, the alveoli of other parts of the lungs collapse and their filling with air stops (so-called atelectasis occurs).
Symptoms
- Rapid breathing.
- Lack of oxygen.
- Decreased urine output.
- Coma.
Shock lung occurs several hours (sometimes three days) after the onset of hypovolemic shock; its first symptoms are minor. The first pronounced symptom is mild shortness of breath. At this stage, by analyzing the patient’s blood, it is possible to determine how much the blood pH has decreased. At the second stage of the disease, shortness of breath increases greatly, breathing becomes more frequent to compensate for the lack of oxygen, and breathing becomes difficult. Now there is an obvious lack of oxygen in the patient’s blood, and the number of leukocytes and platelets is reduced. At this stage, symptoms of pulmonary edema can already be seen on an x-ray. With the onset of the third stage, the patient suffocates, loses consciousness, and falls into a coma. Shock can be fatal.
Shock lung (traumatic lung, wet lung, respiratory lung, progressive pulmonary consolidation, hemorrhagic atelectasis, post-perfusion or post-transfusion lung, hyaline membranes in adults, etc.) - adult respiratory distress syndrome (ARDS) - a syndrome of severe respiratory failure with specific changes in lungs, characteristic of shock, edema, loss of elasticity, alveolar collapse.
ARDS develops gradually, reaching a peak on average 24-48 hours after the onset of damage, and ends with massive, usually bilateral damage to the lung tissue. Regardless of the cause, RDV has a clearly defined clinical picture.
There are four stages of ARDS:
Stage I - damage (up to 8 hours after stress exposure). Clinical and radiological examination usually does not reveal changes in the lungs.
Stage II - apparent stability (6-12 hours after stress exposure). Tachypnea, tachycardia, normal or moderately reduced oxygen pressure in arterial blood (PaO 2). A dynamic study reveals the progression of arterial hypoxemia, the appearance of dry wheezing in the lungs, and hard breathing. The X-ray shows the first manifestations of changes in the lungs: an increase in the vascular component of the pulmonary pattern, turning into interstitial pulmonary edema.
Stage III - respiratory failure (12-24 hours after stress exposure). Clinical picture of severe acute respiratory failure: shortness of breath, hyperpnea, participation of auxiliary muscles in breathing, tachycardia, significant drop in PaO 2 (less than 50 mm Hg), harsh breathing, dry rales from the lungs. The appearance of moist rales indicates the accumulation of fluid in the alveolar space. The radiograph shows pronounced interstitial edema of the lobes; against the background of an enhanced vascular pattern, focal-like shadows appear, sometimes horizontal. The shadows of the vessels are blurred, especially in the lower sections. Obvious infiltrative shadows representing perivascular fluid are visible.
Stage IV - terminal. Progression of symptoms. Deep arterial hypoxemia, cyanosis. Respiratory and metabolic acidosis. Cardiovascular failure. Alveolar pulmonary edema.
Occurs when:
Accidents (aspiration of water or acidic gastric contents);
Effects of medications;
Injuries;
Inhalation of toxic gases, inhalation of high concentrations of oxygen;
Diseases (pneumonia, sepsis, pancreatitis, tuberculosis, diabetic ketoacidosis, carcinomatosis, eclampsia, shock of any etiology);
Artificial circulation;
Microembolism of the pulmonary circulation,
Extensive surgical interventions;
Suffered critical conditions (prolonged hypotension, hypovolemia, hypoxia, bleeding).
Transfusion of large volumes of blood and solutions.
DIFFERENTIAL DIAGNOSIS with:
Left ventricular failure;
Severe pneumonia (bacterial, viral, fungal, aspiration, atelectatic);
PREHOSPITAL STAGE
1. Elimination of the cause that caused ARDS.
2. Oxygen therapy.
3. Pain relief: analgin 50% 2-4 ml, possible combination with diphenhydramine 1% 1 ml IM or pipolfen 2.5% 1 ml IM.
4. If blood pressure drops: mezaton 1% 2 ml s.c. or i.v.
5. For heart failure: strophanthin 0.05% 0.5 ml i.v. per physical. solution.
6. For bronchospastic syndrome - Euphyllip 2.4% K) ml
7. Hospitalization in the intensive care unit.
HOSPITAL STAGE
1. Treatment of the underlying disease.
2. Overcoming the pulmonary barrier to O2 transport:
a) oxygen therapy;
b) application of positive pressure at the end of the outlet (PEEP);
c) gentle modes of artificial pulmonary ventilation (ALV);
d) physical therapy.
3. For the bronchospastic component - aminophylline 2.4% 10 ml IV, prednisolone 60 mg IV bolus and 60 mg n/m and further depending on the stage of the status (see "treatment of status asthmaticus").
a) analgin 50% 2-4 ml in combination with diphenhydramine 1% 1 ml IM or pipolphen 2.5% 1 ml IM;
b) sodium hydroxybutyrate (GHB) 20% 5 ml IV slowly on glucose 5%" 10 ml;
c) inhalation of a mixture of nitrous oxide and oxygen in a ratio of 1:1 or 2:1 for 10-15 minutes.
5. For hypotension:
a) mezaton 1% 0.5-1 ml IV;
b) norepinephrine 0.2% 0.5-1 ml intravenously in a 5% glucose solution or saline solution;
c) dopamine 0.5% - 20 ml (100 mg) diluted in 125-400 ml of isotonic sodium chloride solution or 5% glucose solution intravenously;
d) steroid hormones - prednisolone 90-150 mg or hydrocortisone 150-300 mg in isotonic sodium chloride solution intravenously.
6. Normalization of rheology and microcirculation, CBS:
a) reopolyglucin or reomacrodex;
b) heparin, streptodecase;
c) sodium bicarbonate 4% - 200 ml intravenously;
d) infusion electrolyte solutions.
The total volume of fluid for a patient weighing 70 kg (in the absence of pathological losses) should be 2.3-2.5 l/day.
The term “shock lung” was first introduced into the scientific medical literature, apparently, by Ashbaugh (1967) to designate the syndrome of progressive acute respiratory failure (APF), characteristic of the terminal period of various diseases.
Along with the above name, other terms are used to denote this condition: “wet (moist) lung”, “water lung”, acute lung compaction syndrome, pulmonary disorder syndrome in adults, perfusion lung syndrome, etc.
Shock lung occurs in traumatic brain, thoracic, abdominal injuries, with blood loss, prolonged hypotension, aspiration of acidic gastric contents, massive transfusion therapy, acute renal failure, increasing cardiac decompensation, pulmonary embolism, with complications of intensive anti-shock therapy (prolonged artificial ventilation , excessive infusion of blood and fluid, use of pure oxygen), etc.
The essence of the process is the “hepatization” of the lung with a sharp increase in the extravascular volume of water, accumulation of blood clots in the capillaries, thickening of the alveolar-capillary membrane, and the formation of hyaline membranes. Thus, we can assume that the occurrence of “shock lung” syndrome is a direct consequence of overload of the non-gas exchange functions of the lungs - cleansing and participation in the blood coagulation system, etc.
The following mechanisms can be distinguished in the pathogenesis of shock lung:
1. Increasing the permeability of pulmonary capillaries:
a) direct trauma,
b) aspiration,
c) pulmonary hypoxia (hypoperfusion, neurovascular reflexes, hypocapnia, vascular occlusion [fat and tissue embolism, platelet embolism, diffuse intravascular coagulation, etc.]),
The main links in the pathogenesis of “shock lung”
(V.K. Kulagin, 1978).
d) uxins (fatty acids, histamine, serotonin, kinins, wound endotoxins, inhaled gases, lysosomal enzymes, catecholamines, acidosis, oxygen),
e) homologous blood (post-transfusion reactions, host reaction to the transplant),
e) pulmonary infections.
2. Increased pressure in the pulmonary capillaries:
a) neurovascular reactions (damage to the central nervous system, constriction of postcapillary vessels, postcapillary pulmonary veins and vessels of the systemic circulation with the movement of fluid into the pulmonary circulation, loss of elasticity of the left ventricle),
b) excessive transfusion,
c) myocardial failure.
3. Reduced intravascular oncotic pressure (hypochroteinemia, excessive infusion of crishaploid solutions).
4. Decrease in intra-alveolar pressure.
5. Increased oncotic pressure in tissues.
6. Deterioration of surface activity. An important role in this process and the development of atelectasis is played by pulmonary surfactant, the function of which is sharply impaired (its inactivation occurs).
All this ultimately leads to increased resistance of the upper respiratory tract to the passage of gases, an increase in the peripheral resistance of the vessels of the pulmonary circulation, thickening of the interalveolar septa and a decrease in arterial blood oxygen saturation.
The main links in the pathogenesis of “shock lung” are presented in the diagram (see page 465).
The clinical picture of “shock lung” is shortness of breath, in severe cases, loss of consciousness, agitation (due to hypoxia), blood pressure, despite severe injury, within normal or even elevated levels, facial cyanosis, scleral hyperemia. The acid-base state may be within normal limits, or metabolic acidosis or respiratory alkalosis may develop. In the lungs there are areas of hemorrhage, atelectasis, hepatization, and the alveolar space is reduced due to thickening of the interstitial tissue, the lungs are edematous and rigid.
In the case of a shock lung, a significant amount of fluid accumulates in the interstitial tissue and alveoli for a short time, and pulmonary edema begins to form. In addition, the alveoli in other parts of the lungs collapse and stop filling with air - atelectasis is formed.
Symptoms:
increasing shortness of breath;
rapid breathing;
decreased amount of urine;
lack of oxygen;
Shock lung develops several hours and sometimes days after the onset of hypovolemic shock; its first symptoms are minor. Among the pronounced symptoms, the first is mild shortness of breath. At this stage, a blood test can detect a slight decrease in blood pH levels. The second stage of the pathology is characterized by greatly increased shortness of breath, increased frequency of respiratory contractions to compensate for hypoxia, and difficulty in inhaling. Now, with an obvious lack of oxygen in the blood, the number of platelets and leukocytes decreases. At this stage, fluorography allows you to visualize the presence of symptoms of pulmonary edema. Before the onset of the third stage, the patient begins to choke, may lose consciousness and fall into a coma. Shock can be fatal.
The first signs of hypovolemic shock are internal restlessness, pallor, cold sweat, and chills. In most cases, the pressure drops sharply and a rapid pulse appears. To confirm the diagnosis, you need to press on the nail plate of the thumb. If the nail takes on a normal color for more than one and a half seconds, the patient may be in shock.
Causes
In most cases, shock lung is the result of shock. Blood flow in the capillaries of the lungs, the smallest blood vessels that encircle the alveoli, decreases. Blood vessels begin to contract, as a result, the walls of the capillaries are damaged, which significantly increases their permeability. This allows blood plasma to enter the lung tissue. When blood flow weakens, the walls of the alveoli (more precisely, the cells of the walls) begin to be affected. These structures are responsible for the secretion of a substance that prevents the alveoli of a healthy person from collapsing. As a result of such changes, foci of atelectasis appear: the walls of the alveoli are pressed against each other and collapse; therefore, when inhaling, such alveoli are not filled with air. In addition, in the presence of shock, blood begins to clot in small blood vessels. Small blood clots appear in the capillaries, which only worsen circulatory problems. This leads to impaired pulmonary function.
Treatment
In such cases, the person needs to receive emergency medical care. The main remedy is artificial ventilation. This device eliminates pulmonary edema and prevents the alveoli from collapsing. In addition, the patient is administered glucocorticoids in large doses, for example, Prednisolone. Glucocorticoids should reduce the permeability of cell walls and prevent fluid from entering the alveoli from blood vessels.
In case of shock, medications are required to maintain and stimulate the blood circulation process; for this purpose, intravenous fluid is used to increase the volume of circulating blood. In order to empty the lungs, diuretics are introduced into the body. But it is worth understanding that elimination of pulmonary edema is possible only in the early stages of shock lung. The patient is also given antibiotics to prevent infection and intravenous Heparin to slow down the natural process of blood clotting.
Treatment is carried out in a hospital setting. First of all, the doctor provides symptomatic therapy for an acute disorder, and only then tries to establish its cause. This disease can be easily diagnosed using x-rays. Having made a diagnosis, adequate therapy is prescribed.
Shock lung is a life-threatening condition that requires emergency medical attention. Otherwise, hypoxemia begins, which leads to death.
