Pulmonary edema is cardiogenic and noncardiogenic considered as the immediate cause of death in every fourth deceased person.
Pathogenesis. In a healthy person, the hydrostatic pressure in the pulmonary capillaries is 7-9 mm Hg. Art. it slightly exceeds that in interstitium. The liquid is retained in the capillaries due to its viscous properties, high enough oncotic pressure figures. Alveolar-no-capillary membranes are semipermeable; the minimal fluid flow from the pulmonary capillaries into the interstitium to the pulmonary edema does not lead, since excess fluid immediately flows down the lymphatic vessels.
For the development of pulmonary edema, the following factors are necessary:
• High hydrostatic pressure (more than 20-30mm Hg. in the capillaries of the lungs. This hemodynamic situation is possible in acute left ventricular failure (myocardial infarction, post-infarction scars, tachyarrhythmias, etc.), mitral stenosis, large transfusions (transfusion of large quantities of liquids in intensive care, surgical practice, in pregnant women).
• Low, less than 15 mm Hg. Art. oncotic plasma pressure. This more rare cause of pulmonary edema is caused by hypoproteinemia after blood loss, with alimentary dystrophy, liver failure.
• High permeability of alveolar-capillarymembranes for infectious-toxic, anaphylactic, enzymatic (pancreatic) shock, chemical and thermal trauma of the lungs, "neurogenic" edema of the lungs with strokes, severe craniocerebral trauma.
• Negative (less than 20 mm Hg) intra-alveolar pressure with severe obstruction of the upper respiratory tract in patients with sublingual laryngitis, asphyxiation of foreign tracheal bodies;
when drowning; excessively active mode of mechanical ventilation.
When there is a pulmonary edema, a self-sustaining thanatagonal vicious circle begins to work:
The variety of causes of pulmonary edema allowsconsider it a typical pathological process. Modern science has not answered the question of A. Sop-heim: whether pulmonary edema is the cause of death, or pulmonary edema occurs because the patient is about to die (ie, the patient "dies through the mechanism of pulmonary edema").
Sharp left-handed ud ocular failure -cardiogenic interstitial and alveolar pulmonary edema - occurs with myocardial infarction, postinfarction cardiosclerosis, cardiomyopathies, acquired and congenital heart defects. The probability of acute left ventricular failure sharply increases with maximal and systolic paroxysmal arrhythmias, hypertensive crises.
The left ventricle loses its ability"Pumping" all the blood entering it during diastole, hence increasing the final diastolic pressure in the left ventricle, hydrostatic pressure in the pulmonary veins, then in the capillaries and arteries. Due to a sharp increase in hydrostatic pressure in the pulmonary capillaries, the fluid transudation in the interstitium increases, the resorptive mechanisms become untenable. Interstitial pulmonary edema develops into the alveolar. If the vicious cycle of pulmonary edema (see above) does not succeed in breaking, a lethal outcome occurs.
Clinic, diagnosis. Interstitial pulmonary edema has a clinical equivalent in the form of paroxysm of mixed dyspnea ("cardiac asthma"). The situation of the patient is forced, semisid. Ak-rotsianoz. Tachypnea, tachycardia. In the lungs, breathing is weakened or stiff, scattered dry wheezes. Patients with chronic heart failure under the scapula can listen to unsmooth, finely bubbly, wet rales.
Alveolar pulmonary edema is characterized byby joining to the described symptomatology of wet wheezing starting from the roots of the lungs (interblade spaces), then through all the pulmonary fields. Breathing becomes bubbling, sometimes heard from a distance. A foamy whitish-pink sputum is allocated with a cough. With auscultation of the heart - g-lopopodobnye rhythms. Tachycardia.
Radiographically with interstitial edemaThe pulmonary pattern appears to be fuzzy, "blurry". In the basal regions, a decrease in transparency, an expansion of the inter-frontal partitions. In the basal no-lateral and basal areas, the Curly lines, peribronchial and perivascular shadows due to the accumulation of transudate in interstitial tissue.
Alveolar pulmonary edema from the position of X-raymethod has several forms: central (with a symmetric homogeneous darkening of high intensity in the central sections of pulmonary fields); diffuse (with shadows of different intensity); focal (with limited or draining roundness, seizing several segments or a fraction of the lung).
The course of pulmonary edema can be acute (up to 4 hours)with myocardial infarction, mitral stenosis, anaphylactic shock, cerebral stroke; subacute (4-12 h) - with myocardial infarction, acquired and congenital heart defects, pneumonia; protracted (over 12 hours) - in patients with myocardial diseases, postinfarction cardiosclerosis, atrial fibrillation.
In the structure of the clinical diagnosis of pulmonary edema cardiogenic and non-cardiogenic always carried into the heading "complication of the main disease."
• IHD; Transmural anteroporeurotic myocardial infarction (date, hour).
Complication. Cardiogenic alveolar edema of the lungs, acute course (date, hour).
• Rheumatism, inactive phase. Combined mitral defect with predominance of stenosis of the left atrioventricular orifice. Atrial fibrillation, tachysystolic form.
Chronic heart failure 3 f. cl. (H 2 A).
Complication. Interstitial pulmonary edema, prolonged course (date, hour).
- if blood pressure is increased or normal - give the patient a semi-sitting position;
- inhalation of moistened oxygen through the nasal cannula. The mask is less acceptable, because in a state of suffocation, it is poorly tolerated;
- Defoamers: inhalation of 30% aqueous solution of ethyl alcohol or 2-3 ml of 10% alcohol solution of antifosilane. In severe cases, endotracheal administration of 2-4 ml of a 96% solution of ethyl alcohol;
- increase in resistance to breathing - exhale through the tube, lowered into a jar with water;
- Elimination of hypercatecholamineemia by inserting into the vein of droperidol or Relanium, or narcotic analgesics.
• With toxic pulmonary edema (inhalationphosgene, ozone, nitric oxide, cadmium oxide, monochloromethane, etc .; endotoxicosis in sepsis, peritonitis, meningococcal and nonclostridial anaerobic infections, pancreatitis, hantavirus lung syndrome, severe allergies, inhalation of toxic aerosols and fumes in a fire) at the pre-hospital stage, prednisolone is injected into the vein with a bolus of 90-120 mg, up to 1.2-2 g / day. With inhalation lesions - bekotid or other inhaled glucocorticoid steroid for 4 breaths every 10 minutes to complete emptying of the inhaler, calculated for 200-250 doses (V. Alekseev, V. Yakovlev, 1996).
To create a redundant gradient with a view tothe direction of the fluid flow from the interstitium to the vascular bed should increase the oncotic pressure of the plasma. In a vein, 10-20% albumin solution is administered up to 200-400 ml / day. Immediate call of resuscitation team of First Aid. Intubation, artificial ventilation can save even patients with hantavirus lung syndrome (OA Alekseev, VI Roshchupkin, 1997).
• In case of cardiogenic pulmonary edema, measures are determined by figures of arterial pressure (BP).
- If blood pressure is increased, sublingually repeatednitroglycerin, intravenously injected clonidine 0,25% 1-1,5 ml on isotonic solution, lasix in a dose of 40-80 mg, if necessary re-morphine or Relanium. In severe cases, sodium nitroprusside 30 mg or nitroglycerin 5-10 mg is intravenously drip. Sodium nitroprusside (naprus, nipride) 30 mg in 400 ml of glucose begins to enter at a rate of 6 cap / min with a gradual increase. A permanent control of blood pressure is mandatory, which should not be reduced to figures below 90/60 mm Hg. Art. Side effects can be (except for hypotension) vomiting, abdominal pain, arrhythmias. The most convenient form of nitroglycerin for drip in the vein is perligenite - ampoules containing 10 ml of a 0.1% solution of nitroglycerin in glucose (1 mg in 1 ml). A 0.01% solution is introduced with an initial rate of 25 μg / min, which corresponds to 1 ml of 0.01% solution in 4 minutes. Constant blood pressure control is mandatory!
- With normal BP numbers: nitroglycerin sublingually repeatedly, lasix intramuscularly or intravenously at a dose of 40-80 mg, relanium or morphine in a vein. In severe cases, nitroglycerin is intravenously drip.
- The most severe clinical situation - swellinglungs with low blood pressure. Position of patient lying down. Dopamine is intravenously drip: ampoules containing 5 ml of a 0.5% solution (25 mg of dry matter) or 5 ml of a 4% solution (200 mg of dry matter) are used. For 400 ml of 5% glucose, 200 mg of dopamine are added, the initial rate of administration is 2-10 cap / min.
An alternative option is the administration of dobutamine. Dobutamine is produced in 20 ml vials and 5 ml ampoules containing 250 mg of dry matter. The contents of the vial or ampoule are diluted in 400 ml of 5% glucose. The introduction of a drop, the initial injection rate of 5-10 cap. / Min. If long administration of dobutamine or dopamine is required, additionally norepinephrine (400 ml of liquid 1 ml of 0.1% solution of the drug) is added.
If you can raise blood pressure, you enter lasix, nitroglycerin.
• With myocardial infarction, goodanesthesia (fentanyl 0.005% 1-2 ml in jet in a vein in combination with 2-4 ml of 0.25% solution of droperidol). If blood counts are allowed, the isoket is injected into the vein (each ampoule contains 10 mg of dry matter in 10 ml of isotonic sodium chloride solution). 500 ml of the infusion solution is added the contents of 5 ampoules, the drug is injected into the vein, the initial speed is 3-7 cap / min, followed by a gradual increase. Constant blood pressure control is mandatory!
• In case of paroxysmal tachyarrhythmia, universalantiarrhythmic drugs (etmozin, etatsizin, kordaron, novokainamid, with ventricular tachycardia - 10-15 ml of 1% lidocaine solution, drip into the vein panangin 20 ml, 4 units of simple insulin per 250 ml of 5% glucose). If the single injection of the antiarrhythmic drug into the vein is ineffective - electrical depolarization of the heart!
• With mitral stenosis, the method of choice -intravenous administration of morphine or its analogues, with normal or elevated blood pressure - 0.3-0.5-1 ml of pentamine or benzohexonium, depending on the figures of blood pressure. At low BP figures, it is advisable to inject 30-90 mg of prednisolone into the vein.
Criteria for patient transportability,who underwent pulmonary edema: disappearance of foamy sputum, wet wheezing above all pulmonary fields, absence of a repeated attack of suffocation in the horizontal position of the patient, stabilization of the number of breaths 22-26 per 1 min. In the course of transportation-oxygen vapors.
Acute left ventricular failure is interstitial and alveolar pulmonary edema. Noncardiogenic pulmonary edema.
- CARDIOGENE TYPE OF LUNGS
Cardiogenic pulmonary edema occurs as a result ofa significant increase in hydrostatic pressure in the left atrium, pulmonary veins and the pulmonary artery system. Its main sign is acute left ventricular failure, accompanied by an increase in the pressure gradient in the pulmonary vessels and interstitial space and the release of part of the fluid from the vessels into the lung tissue. Weak left
- PULMONARY EDEMA
Under the puffiness of the lungs understand the increasedsweating of the liquid part of the blood into the lung tissue - interstitium and alveoli. According to the etiology, there are 4 variants of pulmonary edema: 1) hydrostatic - with increasing pressure in a small circle of circulation; the main cause is a decrease in the contractility of the left heart; 2) neurogenic - pathogenesis similar to hydrostatic; The
- Edema of the brain
Increase the water content in the brain can beis due to several mechanisms. Most often there is vasogenic edema caused by an increase in the permeability of the blood-brain barrier, which is accompanied by the release of plasma into the brain tissue. Elevated blood pressure promotes vaso-genic edema. The causes of vasogenic edema: mechanical trauma, inflammatory diseases of the brain, brain tumors, arterial
- OTECE OF LUNGS IN CHANGES OF COLLOID-OSMOTIC PRESSURE
The COD produced by plasma proteins is 25 mmHg. which corresponds to a plasma protein level of 74 g / l. This indicator is the most important force that keeps water in the vascular space. DZLK, i.e. The hydrostatic pressure in the capillaries of the lungs is normally 8 mm Hg. (the force of "pushing" water). The difference between the parameters of RCD and DZLK is normally 17 mm Hg. what protects
- Abstract. Internal Diseases, 2007
Emergency care in a polyclinicAspiration pneumonia in children Colon's disease Crohn's disease Glomerulonephritis Bronchial asthma IHD. Angina pectoris Infectious myocarditis Edema Quincke Pulmonary edema Pneumoconiosis Pneumonia Gout Renal failure Cirrhosis Stomach ulcer Ulcerative
- Electropulse therapy
Indications for electropulse therapy onprehospital stage with the suppression of supraventricular tachycardia with narrow QRS complexes (paroxysmal reciprocal AV node tachycardia and ortodromic paroxysmal reciprocal AV tachycardia involving additional atrioventricular connections) are clinical signs of acute left ventricular failure (stable arterial
- Typical violations of gas exchange function of the lungs.
The following typical violations of gas exchangelung function? 1. Violation of alveolar ventilation? a) alveolar hypoventilation b) alveolar hyperventilation c) uneven ventilation 2. Violation of lung perfusion. 3. Violation of ventilation-perfusion relations. 4. Diffusion of the lungs. Mixed
They can develop from the first days of the disease andare the leading cause of death in acute glomerulonephritis. 1. Acute left ventricular failure: more often in the elderly, especially in the previous cardiovascular pathology. Its causes: a sharp volumetric overload of the ventricles, a sudden rapid increase in blood pressure (the heart is not ready); the defeat of the myocardium (dystrophy, toxic
Complications of AH and the main complications arisingagainst the background of hypertensive crises are presented in Tables 11 and 12. Table 11 COMPLICATIONS OF ARTERIAL HYPERTENSION 1. On the part of the cardiovascular system: angina and myocardial infarction, acute heart failure / cardiac asthma and pulmonary edema /, Respiratory acidosis
By respiratory acidosis we mean the primaryincrease in PaCO2, which is accompanied by a shift to the right of the reaction H2O + CO2 "- * H2CO3 * - * H + + + HCO3 ', and, respectively, an increase in [H +] and a decrease in the pH of the arterial blood. For the reasons discussed above, the concentration of HCO3 "does not change significantly: PaCO2 reflects the equilibrium between the formation and elimination of CO2 (Chapter 22): _ Formation of CO2 PaCO2