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Pulmonary edema with increased permeability of the vascular wall

In many conditions called acute RDSV, the ultrastructure of the lungs is damaged and vascular permeability increases, which leads to the redistribution of water into the lung tissue. The concentration of protein in the interstitial fluid and in the alveoli increases. One of the main signs of RDSV is a large amount of protein in the pulmonary extravascular fluid and alveoli.

Diagnostics. Cardiogenic pulmonary edema most often occurs with acute myocardial infarction, left ventricular failure, arrhythmias, mitral defect. The disease is diagnosed on the basis of clinical, radiological and laboratory data.

Clinical signs:

• the earliest symptom of pulmonary edema is shortness of breath, in the advanced stage - suffocation;

• cough with clear, watery sputum, sometimes with traces of blood;

• during auscultation - wet rales, sometimes bubbling breathing;

• tachycardia, arrhythmia is possible;

• Blood pressure is often increased, but may be normal or decreased;

• possible swelling on the legs, an increase in the size of the liver;

• decrease in urine output;

• identification of cardiac pathology (myocardial infarction, CHD, mitral defect, etc.).

X-ray signs:

• changes in the configuration of the heart, cardiomegaly are often observed;

• an increase in the size of the pulmonary vessels, the vagueness of their outlines;

• the presence of fluid in the pleural cavities does not indicate pulmonary, but systemic venous hypertension.

Laboratory signs:

• blood pH in the late stage is reduced;

• RaO2 reduced;

• respiratory alkalosis, followed by respiratory acidosis.

The most reliable signs of cardiogenic pulmonary edema:

• high DZLK (18–20 mm Hg);

• increased CVP (12 cm aq);

• decrease in SV.

Stages of cardiogenic pulmonary edema:

Stage I - interstitial pulmonary edema, shortness of breath (first, sometimes the only symptom), tachycardia, hard breathing;

Stage II — alveolar pulmonary edema, increased shortness of breath, wheezing, arterial hypoxemia, the appearance of small bubbling rales in the lungs;

Stage III - manifest pulmonary edema, shortness of breath, suffocation, cyanosis of the face and upper half of the body, puffiness of the face, swollen neck veins, sweating, separation of foamy sputum, a large number of wet rales, severe arterial hypoxemia.

Treatment of cardiogenic pulmonary edema (Scheme 13.1). The main task is to restore the normal pressure gradient in the pulmonary capillaries and alveoli, relieve mental stress and eliminate hypoxia.

1. Oxygen therapy. In mild cases, oxygen therapy is carried out using nasal catheters, in more severe cases, masks are used with the creation of positive pressure. In the most severe cases, tracheal intubation, removal of edematous fluid from the respiratory tract, mechanical ventilation with high IFC (up to 100%) in the PDKV mode are indicated. If mechanical ventilation is not performed, the patient must be given a sitting position in bed, because it, due to the postural effect, reduces intravascular pressure in the upper parts of the lungs. Inhalation of oxygen under positive pressure increases intra-alveolar pressure and prevents the transudation of fluid from the alveolar capillaries, limiting the venous return to the chest.

2. Relieve mental stress. Diazepam (seduxen) 5 mg, droperidol 5-7.5 mg intramuscularly or intravenously are used, morphine is from 2 to 5 mg, which reduces motor excitation and adrenergic vasoconstrictor reaction.

3. Reduction of hydrostatic pressure in the pulmonary capillaries. Reduce venous flow to the heart by applying venous turnstiles on 3 or 4 limbs for 15 minutes. Lasix or ethacrylic acid is administered intravenously. The initial dose of Lasix is ​​20–40 mg (up to 80–100 mg). Every 2-3 hours, the dose is doubled to obtain the effect. A single dose of Lasix should not exceed 240 mg. These diuretics, reducing bcc, contribute to the rapid restoration of diuresis. With intravenous administration, furosemide also has a venodilating effect, reduces venous return to the heart and stops the progression of pulmonary edema even before the appearance of the diuretic effect. It is necessary to monitor CVP, diuresis, plasma osmolality, concentration of protein, electrolytes and glucose in the blood.

4. Reduced after-load. If blood pressure exceeds 100 mm Hg, sodium nitroprusside is administered at a dose of 20-30 μg / min intravenously to reduce afterload. Nitrates affect mainly large vessels, lead to redistribution of blood, a significant decrease in pressure in the pulmonary artery system and some increase in MOS.
However, if there is no central overflow, nitrates can significantly reduce MOC. Therefore, nitroprusside is indicated at high DZLK (more than 12-16 mm Hg) under constant monitoring of blood pressure.

5. The use of drugs with positive inotropic effects. Sympathomimetic amines contribute to an increase in myocardial contractility. With reduced blood pressure, dopamine is most effective, and with normal or high blood pressure, dobutamine. Both drugs are administered intravenously under the control of SV and other hemodynamic parameters. After stabilization, amrinone and aminophylline are shown, with atrial fibrillation and supraventricular tachycardia - digoxin.

Non-stopping pulmonary edema is an indication for surgery.

Scheme 13.1. Algorithm for cardiogenic pulmonary edema

• Furosemide at 0.5-1 mg / kg intravenously;

• morphine - 2-5 mg intravenously;

• nitroglycerin - 0.005 mg under the tongue;

• tracheal intubation (oxygenation);


• nitroglycerin - at 0.3 μg / kg / min (with blood pressure> 100 mmHg) intravenously;

• dopamine - 5-15 mcg / kg / min (with blood pressure <100 mm Hg) intravenously;

• dobutamine - 5–10 mcg / kg / min (at BP> 100 mmHg) intravenously;

• PEEP (constant positive pressure at the end of expiration);

• СРАР (forced ventilation with PEEP);


• amrinone - 0.75 mg / kg simultaneously intravenously, then drip 5-15 μg / kg / min;

• aminophylline - 3-5 mg / kg intravenously for 20 minutes;

• digoxin - intravenously in 1 ml of a 0.025% solution (for atrial fibrillation and supraventricular tachycardia);

• thrombolytic therapy (if there is no shock);

• surgical intervention.

Treatment of non-cardiogenic pulmonary edema. Hyperhydration (hypertonic, isotonic and hypotonic) leads to the accumulation of water in the lungs. The most important condition for successful treatment is the creation of a negative balance of water, and with hypotonic and isotonic hyperhydration, a negative balance of sodium, an increase in the content of which leads to tissue edema. To diagnose the type of violation of the water-electrolyte balance, an accurate calculation of all income and loss of fluid is carried out, the CVP and diuresis are determined. With hyperhydration, the rate of diuresis is often reduced, signs of renal failure are possible. In these cases, it is necessary to stimulate diuresis by the introduction of Lasix, achieving the release of at least 50 ml of urine per hour.

It is necessary to maintain normal colloidal hydrostatic gradients with adequate cardiac activity. With hypoalbuminemia and general hypoproteinemia, the use of albumin, dry and native plasma is indicated. The use of protein and colloidal solutions gives the greatest effect at an early stage of treatment, i.e. before the development of shock and increased vascular permeability. In this case, an increase in COD leads to the return of fluid from the interstitial space of the lungs to the vessels. At a COD below 19 mmHg, which corresponds to a plasma content of 55 g / l, administration of protein or colloidal media is indicated. At the same time, they are taking measures to reduce the DZLK. Maintain hydrostatic pressure as low as possible, since even a slight increase in it under conditions of increased vascular permeability leads to pulmonary edema.

The most important diagnostic criteria: pressure in the pulmonary vessels, determined using a Svan-Ganz catheter, MOS, direct blood pressure measurement, determination of PaO2 and PaCO2, osmolality and plasma COD, CVP (the latter does not always correspond to the parameters of DZLK). With RDSV, sepsis, shock, and other critical conditions, the effect of albumin transfusion may be insufficient or completely absent, since albumin passes from the vessels to the pulmonary interstitium. It should be emphasized the danger of using massive doses of albumin or large molecular compounds for the treatment of non-cardiogenic pulmonary edema. You can recommend moderate doses of albumin (100 ml of a 20% solution) with a very slow rate of administration under the control of other indicators, including CODE. The latter in patients with non-cardiogenic edema, as a rule, is significantly lower than in patients with cardiogenic pulmonary edema. With the infusion of crystalloid solutions against a background of reduced COD, edema increases. Measures that increase COD prevent the transmission of fluid from the pulmonary vessels. The value of COD is a kind of diagnostic criterion for pulmonary edema and the likelihood of a fatal outcome: a decrease in COD to 12.5 mm Hg. - extremely dangerous!
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Pulmonary edema with increased permeability of the vascular wall

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