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 radiography. 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.

"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 contusions, and internal organ injuries. 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.

Grade 1 - moderate hypoxia, acrocyanosis, decreased saturation (oxygen saturation in the blood), dry wheezing against the background of hard breathing, increased pulmonary pattern on the x-ray.

Grade 2 - shortness of breath, cyanosis, fine wheezing. Oxygen therapy without effect. The X-ray shows snow patches across all fields.

Stage 3 - “hysterical” breathing with auxiliary muscles, often foamy sputum mixed with blood. Auscultation: against the background of hard breathing, there are foci of sharply weakened breathing and a mass of moist rales. The radiograph shows a large number of large focal shadows.

Stage 4 - the state can be regarded as agonal. There is no consciousness, breathing is arrhythmic, practically unlistenable. The image shows total darkening of the lung fields.

Treatment: the syndrome is easier to prevent than to treat.

1. Transfer the patient to mechanical ventilation with PEEP (positive end expiratory pressure) with sputum drainage and aerosol therapy.

2. Infusion therapy. Colloids: crystalloids in a 2:1 ratio. Reopolyglucin 400 ml, albumin 10%-20% solution - 200 ml, CES 6% 400 ml, fresh frozen plasma, amino acids 500 ml, glucose-potassium mixture 800 ml, Ringer's solution 400 ml.

3.Heparin 5 thousand units IV 4 times a day.

4. Hormones: prednisolone 60 mg 4 times a day i.v.

5.Trental 5ml 3-4 times a day i.v.

6. Euphyllin 2.4% - 10 ml, papaverine 2 ml IV 2-3 times a day.

7IV antibiotics.

8. Vitamins: “E” – 3 ml i.m. (warm up!), “C” – 5-10 ml i.v., “B” – 3-5 ml i.v.

9. For pulmonary edema - treatment of pulmonary edema.

10. Compensation for blood loss.

11. Stimulation of diuresis: furosemide, lasix.

12. Treatment of the underlying disease.

Severe pneumonia (destructive, aspiration).

Pneumonia is a serious disease that affects lung tissue. Caused by microbes, viruses, protozoa. With a sharp decrease in immunity or concomitant diseases, extremely severe forms occur that are not amenable to conventional therapy. Treatment:

1. Infusion therapy: glucose-potassium mixture 800 ml, albumin 100-200 ml, rheopolyglucin 400 ml, fresh frozen plasma 300 ml.

2. Antibiotics.

3. Heparin 5 thousand units IV 4 times a day.

4. Prednisolone 30 mg 3-4 times a day i.v.

5. Eufillin 2.4% - 10 ml IV, drops, 3-4 times a day.

6. Gordox 300 thousand units 3 rubles/day i.v.

7. Immunoglobulin 6-10 g/day.

8. Retabolil 1g IM.

9. Expectorants: ACC, fluimucil, acetylcysteine, bromhexine.

10. Oxygen therapy or transfer to mechanical ventilation with PEER and sputum drainage.

LECTURE No. 5.

ACUTE CARDIOVASCULAR

FAILURE

The main features of emergency cardiac conditions are that they occur frequently, can develop rapidly, be severe and threaten the patient’s life. The causes of acute severe circulatory disorder include myocardial infarction, acute tachycardia and bradyarrhythmia, hypertensive crisis, cardiac tamponade, PE (pulmonary embolism).

Vascular insufficiency is manifested by atony of the vascular bed, increased permeability of the vascular wall. Often expressed in septic, neurogenic (spinal), toxic-allergic shock.

Acute heart failure is a complication of various diseases or conditions of the body. Blood circulation is impaired due to a decrease in the pumping function of the heart or a decrease in its filling with blood.

Sudden coronary death.

Sudden cardiac death is cardiac arrest, most likely caused by ventricular fibrillation and not associated with anything other than ischemic heart disease. In almost 50% of cases, sudden death is the first manifestation of coronary heart disease. Ventricular fibrillation always occurs suddenly. After 15-20 seconds from its onset, the patient loses consciousness, after 40-50 seconds characteristic convulsions develop - a single tonic contraction of skeletal muscles. At the same time, the pupils begin to dilate. Breathing gradually decreases and stops at the 2nd minute of clinical death. In case of ventricular fibrillation, emergency care is limited to immediate defibrillation. In the absence of a defibrillator, a single blow to the sternum (precordial blow) should be applied with a fist, which sometimes interrupts fibrillation. If it is not possible to restore the heart rhythm, then it is necessary to immediately begin mechanical ventilation and closed cardiac massage.

Acute lesions are a frequent and severe complication of a number of diseases. First of all, we are talking about viral-bacterial pneumonia, which sometimes takes a malignant course and is accompanied by massive, sometimes total, bilateral damage to the respiratory parenchyma with severe, difficult-to-correct respiratory failure, which within a few days and sometimes hours can lead to death . Against this background, destructive processes and even gangrene of the lungs can develop.

The next group is represented by acute lung lesions, united by the term “shock lungs”, developing in patients with severe trauma who have undergone surgical interventions, including with artificial circulation on the open heart (post-perfusion pulmonary syndrome), hemorrhagic, septic or anaphylactic shock, massive blood transfusions ("homologous blood" syndrome ).

In addition, the lungs are affected by various exogenous intoxications and poisoning. In obstetric practice, lung lesions develop with eclampsia, amniotic fluid embolism, and disseminated intravascular coagulation syndrome (DIC syndrome). Many types of endogenous intoxications, especially those that develop with acute pancreatitis, are also accompanied by lung damage.

All these types of acute lesions respiratory parenchyma of the lungs usually united by the general term - (RDS). In foreign literature, it was usually called “adult respiratory distress syndrome,” or ARDS, where the first letter corresponded to the word adult, which did not satisfy everyone, since a similar complication is typical not only for adults, but also for children. Therefore, in 1994, the Consensus Commission of scientists from European and American countries dealing with this problem revised this terminology and, leaving the same abbreviation ARDS, introduced into it a new and closer to reality concept - acute respiratory distress syndrome, and the first the letter in the abbreviation comes from the word acute.

In our literature, the term most often used was simply " respiratory distress syndrome" - RDS, and we will also continue to adhere to it, since this syndrome cannot be anything other than acute.

Due to such a large group of diseases accompanied by respiratory distress syndrome, there is practically no summary statistical information on its frequency, although in 1980 such data were provided for the United States - about 150,000 patients with RDS per year. It is interesting that the materials of the mentioned Conciliation Commission provide exactly the same figures for the United States for 1994. Considering the difficulties in treating this complication, which is accompanied by high mortality (from 10 to 90% depending on the severity of the lesion), this problem seems extremely urgent.

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 drugs;

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;

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.