Basic principles of pharmacotherapy of pulmonary edema. Pulmonary edema: types, signs, diagnosis, emergency care and treatment. Medical care for pulmonary edema

»» №1 1998 PROFESSOR A.E. RADZEVICH, HEAD OF THE DEPARTMENT OF THERAPY, FACULTY OF POSTGRADUATE EDUCATION, MOSCOW MEDICAL DENTAL INSTITUTE
A.G. EVDOKIMOVA, ASSOCIATE PROFESSOR, DOCTOR OF MEDICAL SCIENCES

Pulmonary edema is an acute condition, which is based on the pathological accumulation of extravascular fluid in the lung tissue and alveoli, leading to a decrease in the functional capacity of the lungs. The etiology of pulmonary edema is diverse: it develops with infections, intoxications, anaphylactic shock, CNS lesions, drowning, in high altitude conditions, as a side effect of the use of certain medications (beta-blockers; vasotonic agents that increase the load on the heart), with transfusion of excess plasma substitutes, rapid evacuation of ascitic fluid, removal of a large amount of plasma, aggravates the course of acute (thromboembolism of the pulmonary artery and its branches) and chronic "cor pulmonale".

In the clinic of internal diseases, the main nosological forms can be distinguished, most often leading to the development of pulmonary edema:

1. Myocardial infarction and cardiosclerosis.
2. Arterial hypertension of various origins.
3. Heart defects (often mitral and aortic stenosis).

The pathogenesis of pulmonary edema is complex and not fully understood.

Normally, blood plasma is kept in the lumen of the capillary from filtration through its wall into the interstitial space by the force of colloid osmotic pressure, which exceeds the hydrostatic pressure of blood in the capillaries. Currently, there are three main conditions in which the penetration of the liquid part of the blood from the capillaries into the lung tissue is observed:

1. An increase in hydrostatic pressure in the pulmonary circulation system, and any reason that leads to an increase in pressure in the pulmonary artery is important. It is believed that the level of average pressure in the pulmonary artery should not exceed 25 mm Hg. Art. Otherwise, even in a healthy body, there is a threat of fluid exit from the pulmonary circulation system into the lung tissue.

2. Increase in the permeability of the capillary wall.

3. A significant decrease in plasma oncotic pressure (under normal conditions, its value allows filtration of the liquid part of the blood into the interstitial space of the lung tissue within physiological limits, followed by reabsorption in the venous section of the capillary and drainage into the lymphatic system). So, the most important reason for the increase in hydrostatic pressure in the capillaries of the lungs is the insufficiency of the left ventricle, which causes an increase in the diastolic volume of the left ventricle, an increase in diastolic pressure in it and, as a result, an increase in pressure in the left atrium and small circle vessels, including capillaries. When it reaches 28-30 mm Hg. Art. and is compared with the value of oncotic pressure, active leakage of plasma into the lung tissue begins, significantly exceeding its subsequent reabsorption into the vascular bed in volume, and pulmonary edema develops. This seems to be the main mechanism for the development of cardiogenic pulmonary edema in acute myocardial infarction, cardiosclerosis, arterial hypertension, some defects, myocarditis and other vascular diseases. It should be noted that with mitral stenosis, the outflow of blood is disturbed due to narrowing of the left atrioventricular orifice, and the appearance of pulmonary edema is not based on left ventricular failure.

In the process of development of pulmonary edema in its pathogenesis (according to the principle of the formation of a "vicious" circle), other mechanisms may also be included: activation of the sympathetic-adrenal system, renin-angiotensin-vasoconstrictor and sodium-saving systems. Hypoxia and hypoxemia develop, leading to an increase in pulmonary vascular resistance. The components of the kallikrein-kinin system are switched on with the transition of their physiological effect into a pathological one.

Pulmonary edema is one of the conditions that can be diagnosed at a distance, right from the threshold of the ward where the patient lies. The clinical picture is very characteristic: shortness of breath, often inspiratory, less often - mixed; cough with phlegm; orthopnea, the number of breaths is more than 30 per minute; profuse cold sweat; cyanosis of mucous membranes, skin; mass of wheezing in the lungs; tachycardia, gallop rhythm, accent II tone over the pulmonary artery. Clinically conditionally distinguish 4 stages:

1 - dyspnoetic - characterized by dyspnea, an increase in dry rales, which is associated with the onset of edema of the lung (mainly interstitial) tissue, there are few wet rales;

2 - stage of orthopnea - when moist rales appear, the number of which prevails over dry ones;

3 - stage of the expanded clinic, wheezing is heard at a distance, orthopnea is pronounced;

4 - an extremely difficult stage: a lot of different-sized wheezing, foaming, profuse cold sweat, progression of diffuse cyanosis. This stage is called the "boiling samovar" syndrome.

In practical work, it is important to distinguish between interstitial and alveolar pulmonary edema.

With interstitial pulmonary edema, which corresponds to the clinical picture of cardiac asthma, fluid infiltration occurs throughout the lung tissue, including perivascular and peribronchial spaces. This sharply worsens the conditions for the exchange of oxygen and carbon dioxide between the air of the alveoli and the blood, and contributes to an increase in pulmonary, vascular and bronchial resistance.

Further flow of fluid from the interstitium into the cavity of the alveoli leads to alveolar pulmonary edema with the destruction of the surfactant, the collapse of the alveoli, and their flooding with transudate containing not only blood proteins, cholesterol, but also formed elements. This stage is characterized by the formation of an extremely persistent protein foam that blocks the lumen of the bronchioles and bronchi, which in turn leads to fatal hypoxemia and hypoxia (like asphyxia during drowning). An attack of cardiac asthma usually develops at night, the patient wakes up from a feeling of lack of air, takes a forced sitting position, tends to go to the window, is excited, fear of death appears, answers questions with difficulty, sometimes with a nod of the head, is not distracted by anything, completely surrendering to the struggle for air. The duration of an attack of cardiac asthma is from several minutes to several hours.

During auscultation of the lungs, as an early sign of interstitial edema, one can listen to weakened breathing in the lower sections, dry rales, indicating swelling of the bronchial mucosa. In cases of chronic course of hypervolemia of the pulmonary circulation (mitral stenosis, chronic heart failure), of the additional research methods for diagnosing interstitial pulmonary edema, X-ray is of the greatest importance. At the same time, a number of characteristic features are noted:

Kerli's septal lines "A" and "B", reflecting the swelling of the interlobular septa;

Strengthening of the lung pattern due to edematous infiltration of the perivascular and peribronchial interstitial tissue, especially pronounced in the root zones due to the presence of lymphatic spaces and an abundance of tissue in these areas;

Subpleural edema in the form of a seal along the interlobar fissure.

Acute alveolar pulmonary edema is a more severe form of left ventricular failure. Bubbling breathing is characteristic with the release of flakes of white or pink foam (due to the admixture of erythrocytes). Its quantity can reach several liters. In this case, oxygenation of the blood is especially sharply disturbed and asphyxia may occur. The transition of interstitial pulmonary edema to alveolar edema sometimes occurs very quickly - within a few minutes. Most often, rapid alveolar pulmonary edema develops against the background of a hypertensive crisis or at the onset of myocardial infarction. The detailed clinical picture of alveolar pulmonary edema is so bright that it does not cause diagnostic difficulties. As a rule, against the background of the above-described clinical picture of interstitial pulmonary edema in the lower sections, and then in the middle sections and over the entire surface of the lungs, a significant amount of different-sized moist rales appears. In some cases, along with wet rales, dry rales are heard, and then differential diagnosis with an attack of bronchial asthma is necessary. Like cardiac asthma, alveolar pulmonary edema is more common at night. Sometimes it is short-term and goes away on its own, in some cases it lasts for several hours. With strong foaming, death from asphyxia can occur very quickly - in the next few minutes after the onset of clinical manifestations.

The X-ray picture in alveolar pulmonary edema in typical cases is due to symmetrical soaking of the transudate of both lungs with the predominant localization of edema in their basal and basal sections. Laboratory data are scarce, reduced to sharp shifts in the gas composition of the blood and acid-base state (metabolic acidosis and hypoxemia), they have no clinical significance. The ECG shows tachycardia, a change in the end part of the QT complex in the form of a decrease in the ST segment and an increase in the amplitude of the P wave with its deformation - as manifestations of acute atrial overload.

In patients with signs of congestive heart failure, the cause of which is a decrease in the contractility of the left ventricle (large cicatricial fields after myocardial infarction), pulmonary edema is more likely to occur with an increase in blood pressure or with heart rhythm disturbances leading to a decrease in minute blood volume.

Therapeutic measures for interstitial and alveolar forms of pulmonary edema in cardiac patients are largely similar: they are primarily aimed at the main mechanism of edema development with a decrease in venous return to the heart, a decrease in afterload with an increase in the propulsive function of the left ventricle and a decrease in increased hydrostatic pressure in the vessels of the small circle . With alveolar pulmonary edema, measures are added to destroy the foam, as well as a more energetic correction of secondary disorders.

In the treatment of pulmonary edema, the following tasks are solved:

A. Reducing hypertension in the pulmonary circulation by:
- decrease in venous return to the heart;
- decrease in the volume of circulating blood (BCC);
- dehydration of the lungs;
- normalization of blood pressure;
- anesthesia.

B. Increased contractility of the myocardium of the left ventricle when administered:
- inotropic agents;
- antiarrhythmic drugs (if necessary).

B. Normalization of the acid-base composition of blood gases.

D. Ancillary activities.

Doctor tactics

Oxygen inhalation is prescribed through nasal cannulas or a mask in a concentration sufficient to maintain arterial blood pO2 of more than 60 mm Hg. Art. (possible through alcohol vapor).

A special place in the treatment of pulmonary edema is the use of morphine hydrochloride intravenously at 2-5 mg, if necessary, again after 10-25 minutes. Morphine relieves psycho-emotional arousal, reduces shortness of breath, has a vasodilating effect, reduces pressure in the pulmonary artery. It should not be administered with low blood pressure and respiratory distress. When signs of depression of the respiratory center appear, opiate antagonists - naloxone (0.4-0.8 mg intravenously) are administered.

In order to reduce congestion in the lungs and provide a powerful venodilating effect that occurs after 5-8 minutes, furosemide is administered intravenously at an initial dose of 40-60 mg, if necessary, the dose is increased to 200 mg; or ethacrynic acid 50-100 mg, bumetamide or burinex 1-2 mg (1 mg = 40 mg lasix). Diuresis occurs in 15-30 minutes and lasts about 2 hours.

The appointment of peripheral vasodilators (nitroglycerin) helps to limit inflow to the heart, reduce total peripheral vascular resistance (OPVR), and increase the pumping function of the heart. It must be applied carefully. The initial dose is 0.5 mg under the tongue (the mouth must first be moistened: in the lungs - wheezing, in the mouth - dry!). Then intravenous drip of a 1% solution of nitroglycerin at an initial rate of 15-25 mcg / min, followed by an increase in dose after 5 minutes, reaching a decrease in systolic blood pressure by 10-15% of the original, but not less than 100-110 mm Hg. Art. Sometimes the dose is increased to 100-200 mcg / min, depending on the level of initial arterial hypertension.

With high blood pressure figures, sodium nitroprusside is prescribed, which reduces pre- and afterload. The initial dose is 15-25 mcg / min. The dose is selected individually until blood pressure normalizes, then it is recommended to switch to intravenous nitroglycerin.

Short-acting ganglion blockers are especially effective when the cause of pulmonary edema is an increase in blood pressure: arfonad 5% - 5.0 is diluted in 100-200 ml of isotonic NaCl solution and administered intravenously under the control of blood pressure, hygronium 50-100 mg in 150-250 ml of 5% glucose solution or isotonic NaCl solution; pentamine 5% - 0.5-0.1 or benzohexonium 2% - 0.5-0.1 in 20-40 ml of isotonic NaCl solution or 5% glucose solution intravenously with blood pressure control through 1-2 ml of solution. Sometimes it is enough to enter before the normalization of blood pressure. At the ready, you need to keep mezaton or norepinephrine.

Cardiac glycosides are recommended for severe tachycardia, atrial tachyarrhythmia. Strofantin is used at a dose of 0.5-0.75 ml of a 0.05% solution, digoxin at a dose of 0.5-0.75 ml of a 0.025% solution intravenously slowly in isotonic NaCl solution or 5% glucose solution. After 1 hour, the introduction can be repeated until the full effect. Glycosides should not be administered with stenosis of the atrioventricular orifice, with acute myocardial infarction and against the background of high blood pressure. It must be remembered that cardiac glycosides can lead to a paradoxical effect, stimulating not only the left but also the right ventricle, which contributes to an increase in hydrostatic pressure in the pulmonary circulation and increased pulmonary edema. It is important to consider that the worse the functional state of the myocardium, the closer the values of therapeutic and toxic concentrations of glycosides. In 31% of cases, patients develop digitalis arrhythmias. The limited role of cardiac glycosides in emergency treatment of pulmonary edema should be recognized. However, after the acute effects of pulmonary edema are stopped, with clinical signs of chronic left ventricular decompensation, cardiac glycoside preparations should also be used, which help stabilize hemodynamics and prevent relapses of pulmonary edema.

In order to more quickly slow down the heart rate, beta-blockers are sometimes used (propranolol - intravenously 1-2 mg in isotonic NaCl solution or 5% glucose solution).

If pulmonary edema develops against the background of paroxysmal arrhythmias (flickering, atrial flutter, ventricular tachycardia), emergency electropulse therapy is recommended.

With concomitant bronchospasm, you can enter eufillin intravenously 250-500 mg, and then 50-60 mg every hour. It is not recommended to administer aminophylline in patients with acute myocardial infarction.

With the development of pulmonary edema against the background of cardiogenic shock, dobutamine is used. It is a biological precursor of norepinephrine, stimulates alpha and, to a lesser extent, beta-adrenergic receptors, specific dopamine receptors, increases cardiac output, increases blood pressure. It has a unique property: along with a powerful inotropic effect, it has a dilating effect on the vessels of the kidneys, heart, brain, intestines and improves their blood circulation. The drug is administered intravenously at a dose of 50 mg in 250 ml of isotonic NaCl solution. Administered drip at 175 mcg / min, gradually increasing the dose to 300 mcg / min. Side effects: extrasystole, tachycardia, angina pectoris.

In addition, phosphodiesterase inhibitors are used, which increase the contraction of the heart and dilate the peripheral vessels. These include amrinone - used intravenously (bolus) at a dose of 0.5 mg / kg, then infusion at a rate of 5-10 mcg / kg / min continues to be administered until a persistent increase in blood pressure. The maximum daily dose of amrinone is 10 mg/kg.

In severe hypoxemia, hypercapnia, artificial lung ventilation (ALV) is effective, but its implementation requires special equipment and anesthesia.

In case of refractory pulmonary edema, when the administration of saluretics is not effective, they are combined with an osmotic diuretic (mannitol - 1 g per kg of the patient's weight). Dehydration can be carried out with the availability of equipment using isolated ultrafiltration at a rate of about 2000 ml/hour.

Mechanical methods are widely used in real practice at the prehospital stage (venous tourniquets on limbs) to reduce venous return to the heart and pulmonary congestion, but the effect of this is short-lived.

Bloodletting of 250-500 ml is currently of historical and medical importance in the practice of treating pulmonary edema, but it can be life-saving in a situation where there are no other options.

In some cases, alveolar pulmonary edema develops so rapidly that it does not leave time for the doctor and the patient to carry out all of the above activities.

We have tested and introduced into clinical practice the use of the method of spontaneous breathing under constant positive pressure (SPPP) + 10 cm of water column in the complex therapy of pulmonary edema in patients with acute myocardial infarction, hypertensive crises, and heart defects.

The method is implemented using a commercially available apparatus "NIMB-1". A polyethylene bag of sufficient size (at least 40 x 50 cm) is connected to an airway flexible tube to supply any respiratory mixture or air. The second plastic tube connects the cavity of the bag with a manometer with a scale from 0 to + 60 cm w.c. From the source, compressed oxygen enters under ATI-5-7 atm into the injector of the "NIMB-1" apparatus, from where it is directed into the cavity of the bag in the form of an oxygen-air mixture 1:1. After the start of the mixture supply with a flow of about 40 l / min, the bag is put on the patient's head and fixed on the shoulder girdle with a wide foam tape so that there is a "leak" gap between the patient's body and the wall of the bag, which bleeds the supplied flow.

In patients with psychomotor agitation, a negative attitude to the beginning of the session disappears after 1-2 minutes without the use of sedative therapy. The following fact is quite clear: after stopping the session in case of recurrence of respiratory failure, all patients asked for a second session, noting a rapid improvement in the subjective state during PPD DM. As the main factor stopping pulmonary edema, an increase in intrathoracic pressure during PPD sessions is used, which limits the flow of venous blood to the heart as a result of a decrease in the suction action of the chest cavity, with a decrease in venous return and preload of the right heart. In addition, overpressure + 10 cm of water. Art., created in the bronchi, promotes the reverse movement of fluid from the alveoli into the interstitial space, followed by resorption into the lymphatic and venous systems.

During PPD sessions, the functional residual capacity of the lungs increases, the degree of dissociation of the ventilation-blood flow ratio decreases, intrapulmonary venous-arterial shunting decreases, oxygen tension in the arterial blood increases along with the effect of preventing the collapse of the alveoli, which is manifested as a result of a decrease in the phenomena of alveolar and interstitial edema. The SD PPD method can also be used for prophylactic purposes in patients with cardiovascular pathology that threatens the development of acute left ventricular failure and pulmonary edema. We use the DM PPD method in patients in the complex therapy of cardiogenic pulmonary edema. In this case, there is a rapid normalization of central hemodynamic parameters (after 20-30 minutes). According to rheopulmonography, against the background of the use of DM PPD, hypervolemia of the pulmonary circulation decreases in all patients, blood oxygenation improves, acid-base balance normalizes, cyanosis, shortness of breath stop faster, diuresis appears after 12-20 minutes. The alveolar phase of pulmonary edema in most patients resolves within 10-20 minutes without the use of defoamers. In the control group, this figure was 20-60 minutes.

To prevent the recurrence of alveolar edema, it is necessary to stop DM PPD gradually, with a stepwise decrease in pressure by 2-3 cm aq. Art. within a minute with exposure at each stage for 5-15 minutes.

We consider the following contraindications to the use of SD PPD:

1. Violations of the regulation of breathing - bradypnea or Cheyne-Stokes breathing with long periods of apnea (over 15-20 seconds), when mechanical ventilation is indicated.

2. A stormy picture of alveolar pulmonary edema with large foamy secretions in the oropharynx and nasopharynx, requiring removal of the foam and intratracheal administration of active defoamers.

3. Severe violations of the contractile function of the right ventricle.

Thus, the use of DM PPD in the complex therapy of cardiogenic pulmonary edema contributes to its faster resolution and creates a reserve of time for all therapeutic measures.

Literature

1. Alpert J., Francis G. Treatment of myocardial infarction. Per. from English. M. "Practice". 1994, p. 255.
2. Guide to cardiology. (Under the editorship of E.I. Chazov) M., 1982.
3. Radzevich A.E., Evdokimova A.G., Bezprozvanny A.B. and other Method for the treatment of pulmonary edema in patients with cardiovascular pathology. Materials of the 1st Congress of Cardiologists of the CIS. M., 1997.
4. Dzhanashiya P.Kh., Nazarenko V.A., Nikolaenko S.A. Pharmacotherapy of cardiovascular diseases. M., 1997, p. 273.
5. Evdokimova A.G. Hypervolemia of the pulmonary circulation and methods of its compensation in patients with coronary heart disease, hypertension and heart defects. Abstract of the dissertation for the degree of Dr. honey. Sciences. M., 1995, p. 33.
6. Belousov Yu.B., Moiseev V.D., Lepakhin V.K. Clinical pharmacology and pharmacotherapy. M., 1993, p. 97-138.
7. Popov V.G., Topolyansky V.S., Lepakhin V.K. Pulmonary edema. M.: Medicine, 1975, p. 167.
8. Guidelines. Orlov V.N. The use of intrapulmonary pressure in the complex therapy of pulmonary edema in emergency cardiology. M., 1985, p. 13.

Primary actions for the treatment of pulmonary edema, regardless of its etiology.

Ensure airway patency. According to indications - tracheal intubation.
Inhalation with 100% oxygen.
Oxygen inhalation through a solution of 96% alcohol. With abundant foaming, the introduction of 2-3 ml of 96% alcohol into the trachea.
Intravenous administration of morphine 1% solution - 1 ml. For the treatment of pulmonary edema, it is of particular importance. It calms, relieves emotional stress, has a vasoconstrictive effect, reduces shortness of breath, and, most importantly, reduces pressure in the small circle, thereby combating the signs of edema. Morphine is contraindicated in low blood pressure. In case of depression of the respiratory center - immediate intravenous administration of naloxone.

Treatment of acute pulmonary edema is primarily aimed at normalizing pulmonary pressure. And also on:

stop foaming.
correction of emerging hemodynamic disorders.
reduction of OPSS - total peripheral vascular resistance.
correction of violations of the acid-base state.

Pulmonary edema in arterial hypertension.

the patient's position is sitting, with legs lowered.
nitroglycerin 1% - 15-30 mg per minute, increasing the dose until systolic blood pressure decreases by 10-15% of the original. At very high blood pressure figures, sodium nitroprusside is administered instead of nitroglycerin at a dosage of 15-25 mcg per minute.
short-acting ganglionic blocker pentamine 5% - 1-2 ml diluted in 20 ml NaCl, 3-5 ml solution intravenously every 5-10 minutes.
with high blood pressure figures, and a moderately severe clinic of pulmonary edema - clonidine 0.01% - 1 ml intravenously.
furosemide 40-60 mg IV bolus. If there is no effect, re-introduction after an hour.
droperidol 0.25% - 2-4 ml intravenous bolus.

Pulmonary edema against the background of normal blood pressure.

nitroglycerin 1% - 10 mg / min.
furosemide 40-60 mg IV.
droperidol 0.25% - 2-4 ml IV.
prednisolone 90 mg IV bolus.

Constant control of blood pressure, preventing it from falling below 90 mm Hg.

Pulmonary edema with moderately low blood pressure.

dobutamine 5 - 10 mcg / kg / min intravenously drip until a normal level of blood pressure is reached.

Pulmonary edema with severe arterial hypotension.

dopamine 5-10 mcg/kg/min, slowly increasing to 50 mcg/kg/min maximum. BP control.
with a simultaneous increase in pressure and an increase in symptoms of pulmonary edema - nitroglycerin 15 mg / min.
furosemide 40 mg IV once.

Pulmonary edema on the background of mitral stenosis.

promedol 2% -1ml intravenously.
furosemide 90-120 mg IV p.
eufillin 2.4% - 10ml i.v.
strophanthin 0.05% - 0.5 ml intravenously.

Pulmonary edema on the background of CNS damage in stroke.

furosemide 90-120 mg IV p.
eufillin 2.4% - 10ml i.v.
promedol 2% -1ml intravenously.
reopoliglyukin 400ml intravenous drip.
strophanthin 0.05% solution - 0.5 ml intravenously.
with arterial hypertension - pentamine 5% - 1 ml intravenously drip.
mannitol 30-60ml diluted in 200ml NaCl intravenously drip.

Criteria for relief of pulmonary edema.

Reducing the respiratory rate to 22 or less per minute.
Absence of frothy sputum.
Absence of wheezing on auscultation.
Normalization of skin color.
Absence of symptoms of pulmonary edema when the patient is transferred to a horizontal position.
Normalization of blood pressure, heart rate.

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Cardiogenic pulmonary edema is an extremely dangerous medical emergency resulting from acute left ventricular failure.

Definition

Cardiogenic pulmonary edema is an extremely dangerous medical emergency resulting from acute left ventricular failure. Rapidly increasing hydrostatic pressure in the pulmonary circulation leads to pathological leakage of fluid into the lung tissue, and then into the alveoli.
Most often, cardiogenic pulmonary edema develops against the background of:
arterial hypertension (hypertensive crisis);
acute myocardial infarction;
extensive postinfarction cardiosclerosis;
heart rhythm disturbances;
heart defects.
There are 2 phases of acute left ventricular failure (OLZh).
1. INTERSTITIAL pulmonary edema is characterized by infiltration of the entire lung tissue. Swelling of the perivascular and peribronchial spaces sharply impairs gas exchange between the air of the alveoli and the blood. Clinically, this phase corresponds to cardiac asthma (CA) and is manifested by a feeling of lack of air, the patient's need to take a sitting position, dry cough, severe inspiratory dyspnea. On auscultation, increasing dry rales are heard in the lungs, there are few or no wet rales.
2. The development of ALVEOLAR pulmonary edema is promoted by the remaining elevated hydrostatic pressure in the pulmonary circulation system, which leads to further leakage of fluid from the interstitial tissue into the alveoli. This stage is characterized by the formation of an extremely persistent protein foam, literally flooding the alveoli, bronchioles and bronchi. The clinic of alveolar pulmonary edema is characterized by orthopnea, inspiratory (rarely mixed) shortness of breath; the number of respiratory movements is more than 30 per minute, cough with frothy sputum, in especially severe cases, stained by erythrocytes in the transudate; widespread cyanosis of the mucous membranes and skin, an abundance of moist rales in the lungs, often audible at a distance. The skin is covered with profuse cold sweat, tachycardia is detected, the gallop rhythm is heard.
Basic principles of the treatment of pulmonary edema

Having established the diagnosis of pulmonary edema, it is necessary to immediately begin intensive care. At the same time, it is important to understand that the approach to the treatment of cardiac asthma and alveolar pulmonary edema does not have fundamental differences, because they are based on the same mechanism. In all cases of acute left ventricular failure, therapeutic measures are aimed at solving the following problems:
elimination of "respiratory panic";
reduction of hydrostatic pressure in the pulmonary circulation by:
- decrease in blood flow to the pulmonary circulation;
- reduction of hypervolemia.
correction of blood pressure;
correction of the heart rhythm (in the presence of arrhythmia);
normalization of the acid-base composition of blood gases;
foam destruction measures;
increase in myocardial contractility (according to indications).
In addition, with alveolar pulmonary edema, it is necessary to carry out measures to destroy the resulting foam. In some cases, it is necessary to resort to such auxiliary measures as tracheal intubation, auxiliary and artificial ventilation of the lungs.

Fig.4. Treatment of pulmonary edema in the prehospital stage depending on the level of blood pressure
Treatment of pulmonary edema
The sequence of therapeutic measures in AL, regardless of the cause and the state of hemodynamics, should be as follows (Fig. 4):
1. Give a sitting position (moderate hypotension is not a contraindication);
2. Provide permanent access to the vein (catheter);
3. Morphine 1% 0.5-1.0 IV
4. Oxygen inhalation with alcohol vapor

When prescribing Morphine and determining its dose, it is necessary to take into account age, state of consciousness, breathing patterns, and heart rate. Bradypnea or a violation of the rhythm of breathing, the presence of signs of cerebral edema, severe bronchospasm are a contraindication to its use. With bradycardia, the introduction of Morphine should be combined with Atropine 0.1% 0.3-0.5 ml.
With elevated or normal blood pressure numbers along with general measures, therapy should begin with sublingual application of Nitroglycerin (1-2 tons every 15-20 minutes) or Isoket (Isosorbide dinitrate) spray in the mouth. In the conditions of a medical team, and even more so an ICU or a team of a cardiological profile, it is advisable to drip intravenous use of Perlinganite or Isoket, which allows for controlled peripheral vasodilation. The drug is administered in 200 ml of isotonic solution. The initial rate of administration is 10-15 µg/min, with a gradual increase every 5 minutes by 10 µg/min. The criterion for the effectiveness of the dose is the achievement of clinical improvement in the absence of side effects. Systolic blood pressure should not be reduced below 90 mm Hg.
When prescribing nitrates, it should be remembered that they are relatively contraindicated in patients with isolated mitral stenosis and aortic stenosis, and should be used only as a last resort and with great caution.
Effective in OL is the use of diuretics, for example, Lasix, Furosemide, at a dose of 60-80 mg (up to 200 mg) as a bolus. Within a few minutes after administration, venous vasodilation occurs, which leads to a decrease in blood flow to the pulmonary circulation system. After 20-30 minutes, the diuretic effect of Furosemide is added, which leads to a decrease in BCC and an even greater decrease in hemodynamic load.
With persistent hypertension and mental agitation, a rapid effect can be achieved by intravenous injection of Droperidol. This drug has a pronounced internal α-adrenolytic activity, the implementation of which helps to reduce the load on the left ventricle by reducing the total peripheral vascular resistance. Droperidol is administered at a dose of 2-5 ml, depending on the level of blood pressure and the weight of the patient.
Eufillin should not be used for pulmonary edema, even with the presence of signs of bronchial obstruction, tk. this obstruction is not associated with bronchospasm, but with swelling of the peribronchial space, and the risk of increased myocardial demand, with the introduction of Eufillin, in oxygen, is much higher than the possible beneficial effect.
Against the backdrop of low blood pressure Pulmonary edema most often occurs in patients with widespread postinfarction cardiosclerosis, with extensive repeated myocardial infarctions. Hypotension can also be the result of incorrect drug therapy. In these cases, there is a need to use non-glycoside inotropic agents (see Fig. 7).
After stabilization of systolic blood pressure at a level not lower than 100 mm Hg. diuretics and nitrates are connected to therapy.
In ARRHYTHMOGENIC pulmonary edema, the first priority is to restore the correct heart rhythm. In all cases of tachysystolic arrhythmias, relief should be carried out only by electrocardioversion. The exceptions are ventricular unidirectional paroxysmal tachycardia, which is stopped by Lidocaine or ventricular paroxysmal tachycardia of the "pirouette" type, which can be successfully interrupted by intravenous administration of magnesium sulfate (see section "cardiac arrhythmias").
Drug therapy for bradysystolic arrhythmias (atrioventricular or sinoatrial blockade, sinus node failure) in patients with pulmonary edema also seems dangerous: the use of atropine and β-agonists to increase heart rate can lead to the development of fatal cardiac arrhythmias. The treatment of choice in these cases is temporary pacing at the prehospital stage.
The use of cardiac glycosides in pulmonary edema is permissible only in patients with tachysystole against the background of a constant form of atrial fibrillation.
If signs of left ventricular failure persist after arresting arrhythmia, it is necessary to continue treatment of pulmonary edema, taking into account the state of hemodynamics.
Treatment of pulmonary edema associated with acute myocardial infarction is carried out in accordance with the principles outlined.
The criteria for relief of pulmonary edema, in addition to subjective improvement, are the disappearance of wet rales and cyanosis, a decrease in dyspnea to 20-22 per minute, the patient's ability to take a horizontal position.
Patients with stopped pulmonary edema are hospitalized by the medical team on their own in the block (department) of cardioreanimation. Transportation is carried out on a stretcher with a raised head end.
Indications for the call "on yourself" intensive care or cardiology teams for a linear medical team are:
lack of clinical effect from ongoing therapeutic measures;
pulmonary edema due to low blood pressure;
pulmonary edema against the background of acute myocardial infarction;
arrhythmogenic pulmonary edema;
in cases of complications of therapy.
The paramedic, when independently providing assistance to a patient with pulmonary edema, in all cases calls "on himself", while carrying out therapeutic measures to the maximum extent possible in accordance with these recommendations.

In recent decades, significant advances have been made in the treatment of patients with acute myocardial infarction (AMI) and chronic heart failure (CHF) in industrialized countries.

This circumstance has led to a noticeable increase in the life expectancy of patients suffering from diseases of the cardiovascular system, and a natural increase in the number of calls to ambulance teams for patients with cardiogenic pulmonary edema (CEP). As a result, the frequency of hospitalization significantly increased.

Despite some differences in statistics between the US and Western European countries, acute heart failure is a common indication for hospitalization in people over 65 years of age. Approximately 50% of patients from this group are admitted to the emergency department with a clinical picture of POL.

For patients admitted to the hospital with a diagnosis of COL, the prognosis is serious. Already during the first hospitalization for acute left ventricular failure, 10 to 20% of patients die, and about half of them die on the first day of hospitalization.

In addition, about 50% of those admitted to a hospital with a COL and successfully discharged from it will be re-hospitalized over the next six months with the same diagnosis and with the same chances of an unfavorable outcome. Two years after the first hospitalization for KOL, no more than half of the patients remain alive.

Interestingly, life expectancy in patients with pulmonary edema due to AMI is slightly higher than in patients with COL due to other causes. By the way, AMI among patients hospitalized with KOL is detected in approximately 1/3 of cases. Five years after the first hospitalization for pulmonary edema, less than one third of patients will still be alive.

In contrast to the fairly clear and well-reasoned standards for the provision of medical care to patients with CHF, most of the currently existing recommendations for the intensive care of patients with COL have not been tested that meet the criteria of evidence-based medicine.

Perhaps, at present, only two directions in the provision of emergency care for PKC do not raise doubts about their effectiveness:

early start of non-invasive ventilation in CPAP or BiLevel mode;
prescribing drugs with a vasodilatory effect to the patient.

Many studies have shown the insufficient effectiveness of the routine use of drugs such as narcotic analgesics, diuretics, and inotropic drugs for pulmonary edema. The use of these drugs should be limited to situations where there are direct indications for their use.

Some aspects of the pathogenesis of cardiogenic pulmonary edema

In acute heart failure, the left ventricle is unable to adequately pump the blood that enters it through the pulmonary veins. Stagnation of blood in the pulmonary capillaries and an increase in hydrostatic pressure in them (an increase in the preload of the heart) is accompanied by the penetration of the liquid part of the blood into the lumen of the alveoli and the development of a clinical picture of pulmonary edema.

Filling a significant part of the alveoli with edematous fluid negatively affects the processes of gas exchange in the lungs and is accompanied by the development of hypoxia, which, in turn, contributes to the release of catecholamines, which cause an increase in the resistance of the arterial vessels of the systemic circulation. This mechanism increases the afterload of the heart.

Thus, simultaneously with the deterioration of the gas exchange process in the alveoli, there is an increase in the load on the myocardium, accompanied by an increase in its oxygen demand, as a result, myocardial ischemia occurs or increases.

A decrease in myocardial contractility due to progressive ischemia of the heart muscle leads to a decrease in stroke volume, which causes a progressive increase in diastolic pressure in the left ventricle. A vicious circle is closing.

In his publication, A. Nohria notes that in 67% of patients with KOL there were no pronounced signs of impaired perfusion of peripheral tissues, and the clinical picture was represented mainly by manifestations of respiratory failure. Such patients are called "warm and sweaty". The group of patients with obvious perfusion disorders of peripheral tissues is about 28% (“cold and sweaty”). Finally, the remaining 5% of patients were assigned A. Nohria to the group, which received the conditional name "cold and dry".

In patients of the first group, high pressure in the pulmonary artery is detected, and peripheral vasoconstriction was moderately expressed.
In the second group of patients, there was a decrease in cardiac output in combination with severe vasoconstriction of the vessels of the systemic circulation.
Finally, in patients from the smallest third group, peripheral vasoconstriction significantly prevailed over the increase in pressure in the pulmonary artery.

It must be remembered that patients with other diseases and conditions are often delivered to the hospital under the “mask” of COL. The frequency of diagnostic errors is about 23%.

Approaches to the provision of emergency medical care at the prehospital stage

At the prehospital stage of emergency medical care, it includes three main areas:

preload reduction;
afterload reduction;
increased contractility of the heart.

Providing respiratory care to patients with cardiogenic pulmonary edema

Over the past decade, a huge number of publications have appeared in English-language medical journals demonstrating the high effectiveness of non-invasive mechanical ventilation (nIVL) as a component of intensive care for PKOL.

It should be recalled that NIVL refers to artificial lung ventilation, without tracheal intubation or tracheostomy (conicostomy). Usually, various masks are used to perform NIV, less often - devices in the form of a light plastic helmet worn on the patient's head and hermetically attached to the body at the level of the shoulder girdle.

The obvious advantage of NIV over the invasive option is the relative ease of use, the absence of the risk of developing a number of specific complications associated with tracheal intubation (for example, ventilator-associated pneumonia), greater comfort for the patient - the absence of discomfort in the throat, maintaining the ability to verbal communication, receiving water, etc.

The most significant negative features of NIV are the increased risk of regurgitation and aspiration of gastric contents, as well as the objective difficulty of sealing the mask on the face in many patients, leading to the release of part of the air sent to the lungs into the atmosphere.

The latter circumstance makes it highly desirable to use ventilators already at the prehospital stage, which allow controlling not only the tidal volume (VT) introduced into the lungs, but also the volume of air exhaled by the patient (VTE).

The difference between VT and VTE makes it possible to evaluate losses (“leaks”) caused by incomplete sealing of the breathing circuit and compensate for them due to changes in ventilation parameters. Some modern high-quality transport ventilators are able to automatically calculate the amount of leakage and make the necessary adjustments to the NIV parameters (increase in VT with subsequent breaths by the amount of leakage).

It should be noted that NIV has a number of contraindications for use, including in patients with acute left ventricular failure.

Among non-invasive ventilation modes for patients with cardiogenic pulmonary edema, CPAP has received the most recognition. Until recently, research on the effectiveness of other ventilation modes continues (of particular interest in this regard are BIPAP and PSV). However, according to most experts, they do not have significant advantages over CPAP.

When performing NIV in CPAP mode in patients with COL, it is usually recommended to use an airway pressure of 10-15 cm H2O with an initial fraction of oxygen in the inhaled air (FiO2) equal to 1.0 (i.e. 100%). Correction of FiO2 in the direction of lowering the oxygen content is possible and even desirable with an improvement in the general condition of the patient, stabilization of hemodynamic parameters, and a clear trend towards normalization of SpO2.

In cases where CPAP mode is not available, but it is possible to use BiLevel mode, Phigh = 15 cmH2O and Plow = 5 cmH2O are recommended. NIVL in CPAP or BIPAP mode with KOL lasts from 2 to 32 hours, on average - about 5 hours, i.e. respiratory support can be continued not only on the way to the hospital, but also at the initial stage of inpatient care.

Conducting NIV in the CPAP mode leads to a rapid decrease in the clinical manifestations of pulmonary edema, a noticeable improvement in the general condition of patients. Unfortunately, the assessment of the impact of this type of respiratory support on the prognosis in patients with COL in the medium and long term is not so unambiguous, but, nevertheless, most researchers point to a significant decrease in the frequency of tracheal intubation at the hospital stage, a decrease in the length of stay both in the ICU, as well as in the hospital.

A high immediate result of the use of CPAP in KOL is observed in more than 87% of patients. A similar therapeutic effect was found in severe exacerbations of chronic obstructive pulmonary disease (COPD). For this reason, this type of respiratory support is increasingly found in ventilators designed for emergency care.

There are also simplified devices that are able to create a constant positive pressure in the patient's airways and thereby have a therapeutic effect in cardiogenic pulmonary edema. One example of such devices is the Boussignac valve.

Some aspects of drug therapy for cardiogenic pulmonary edema

Morphine have been widely used to treat patients with KOL for many decades. Its introduction allows you to quickly achieve a decrease in shortness of breath, reduce the feeling of respiratory discomfort in a significant part of patients in this group. It has been suggested that the therapeutic effect of the drug is due to the expansion of the veins in the systemic circulation and, due to this, a decrease in blood flow to the heart (reduction of preload).

However, studies of past and recent years have shown that the effect of varicose veins under the influence of morphine is rather insignificant and ensures the sequestration of only a small volume of blood, which is not able to have a significant effect on pulmonary artery pressure and cardiac preload. At the same time, it was clarified that the decrease in dyspnea in KOL after the administration of this drug is due to the effect on the central nervous system.

Retrospective clinical studies in groups of patients with KOL who received morphine showed a significant increase in the number of hospitalizations in the ICU, as well as an increase in the frequency of tracheal intubations at the hospital stage of intensive care. It is indicated that morphine has many side effects, among which for patients with KOL the most significant is the inhibition of myocardial contractility.

It is important that the administration of morphine potentiates the risk of vomiting in the patient, which, in turn, causes the release of catecholamines into the blood and further increases the afterload. For these reasons, most publications concerning studies of the therapeutic possibilities of morphine note the inappropriateness of including this drug among the recommended drugs in the provision of emergency care to patients with COL.

Nitroglycerine is a drug that can quickly and effectively reduce the wedge pressure in the pulmonary capillaries. Thus, one of the tasks of providing emergency care to patients with COL, i.e., preload reduction, has been fulfilled.

Studies have shown a fairly high efficacy of sublingual administration of nitroglycerin at a dose of 0.4 mg every 5 minutes until a clear clinical improvement occurs. The purpose of the drug according to this scheme is recognized as equivalent to intravenous administration of nitroglycerin at a rate of 60 µg/min.

There are marked national differences in the frequency of prescribing intravenous and other forms of nitroglycerin for POL. The leaders in prescribing the intravenous form of the drug are the countries of Eastern Europe, where this route of administration of nitroglycerin is used in a third of patients, in Western Europe the frequency of intravenous administration of nitroglycerin does not exceed 25%, in the USA - in 2.5% of patients.

Positive properties of nitroglycerin:

the speed of onset and controllability of vasodilation;
ease of prescribing the drug (availability of sublingual, intravenous and other dosage forms);
higher therapeutic effect than other drugs often prescribed for cardiogenic pulmonary edema (for example, furosemide);
enhancing the effect of loop diuretics when co-administered;
satisfactory tolerability, especially in patients with preserved perfusion of peripheral tissues ("warm and wet");
rather late development of tolerance in the patient to the introduction of nitroglycerin (usually not earlier than after 12 hours).

Restrictions to the appointment of nitroglycerin in cardiogenic pulmonary edema. Limitations are situations when cardiogenic pulmonary edema is caused by mitral valve insufficiency, aortic valve stenosis, pulmonary hypertension, right ventricular infarction. The patient is taking Viagra or other drugs with a similar mechanism of action, since their interaction with nitroglycerin can cause deep arterial hypotension.

Loop diuretics have been used in COL for a long time. In the past, drugs in this group were often prescribed as monotherapy, while counting on both their vasodilatory effect and diuretic effect (preload reduction).

Recent studies have somewhat changed the notion of the appropriateness of the routine appointment of loop diuretics in KOL. Taking into account the identification of many side and negative effects associated with the introduction of these drugs, they no longer belong to the priority means in the provision of emergency medical care in this group of patients.

Adverse events with the use of diuretics. With severe systolic dysfunction of the left ventricle, the appointment of loop diuretics in moderate doses causes an increase in the number of fatal arrhythmias.

From 40% to 50% of patients with clinical manifestations of KOL are in a state of normovolemia or even hypovolemia.

The introduction of furosemide leads to an increase in diuresis only after 45-120 minutes. The immediate effect of the drug administration is reduced to increased vasoconstriction, increased pulmonary capillary wedge pressure and increased afterload.

The decrease in the pulmonary capillary wedge pressure, which increased against the background of the administration of furosemide, coincides in time with an increase in diuresis, i.e. observed after several tens of minutes. This circumstance can be fatal for patients with severe pulmonary edema. An increase in vascular tone at an early stage of furosemide action led to the recommendation to use this drug only after the administration of nitroglycerin and captopril to the patient.

Angiotensin-converting enzyme inhibitors are the "second line" drugs used for the intensive care of COL. The drugs of this group in this pathology can be administered sublingually or, much less frequently, intravenously. Publications summarizing the experience of using angiotensin-converting enzyme inhibitors in COL suggest that these drugs are quite effective and relatively safe.

Some features of angiotensin-converting enzyme inhibitors that make their use desirable in this group of patients are discussed below. The possibility of prescribing to the patient a single dose of the drug with a good effect. As a rule, there is a need for repeated doses of the drug or its long-term administration.

Captopril. The therapeutic effect of one of the most common representatives of the group of angiotensin-converting enzyme inhibitors, captopril, when taken sublingually, occurs quite quickly, usually within the next 5 minutes. The onset of action of captopril can be further accelerated by moistening the tablet with water (improving the absorption of the drug in the gastrointestinal tract).

Captopril has a dose-dependent hypotensive effect, which makes it possible to control its action in patients with different blood pressure values. In patients with pulmonary edema having a systolic pressure below 110 mm Hg. Art., the dose of captopril should not exceed 12.5 mg. In patients with higher systolic blood pressure, a dose of 25 mg is recommended.

Captopril can be successfully combined with nitroglycerin, especially in cases where the patient's blood pressure remains consistently high or with individual intolerance to conventional therapeutic doses of nitroglycerin (i.e. the possibility of reducing the dose of nitroglycerin when combined with captopril). The combined use of these drugs leads to an increase and lengthening of the vasodilating effect.

Early administration of captopril in KOL can significantly increase urine output without additional diuretics. For this reason, there are recommendations to wait 30 minutes after taking captopril by the patient and only in the absence of an increase in diuresis to introduce diuretic drugs. Subject to this recommendation, spasm of the vessels of the lungs and kidneys, which occurs shortly after the administration of furosemide, is simultaneously prevented.

A decrease in the length of stay in the ICU in patients with KOL treated with captopril was shown. In addition, these patients were significantly less likely to require tracheal intubation.

cardiac glycosides currently not recommended for use in patients with KOL. Occasionally, recommendations continue to be made to use digoxin to reduce the number of ventricular contractions in patients with tachysystolic atrial fibrillation, but at present, other groups of drugs are used much more often for this purpose.

Milrinone, a phosphodiesterase inhibitor, and other inotropic agents are used in patients with low cardiac output and poor peripheral tissue perfusion. The results of the use of drugs of these groups are very controversial. There are reports of achieving stabilization of hemodynamics against the background of their use, improvement of the general condition.

However, the duration of hospital stay in patients treated with inotropic drugs was generally higher than in a similar group of patients in which vasodilators were used without the addition of inotropic agents.

The use of inotropic drugs indicated in patients with acute left ventricular failure, combined with arterial hypotension, and contraindicated in patients with a satisfactory level of systolic blood pressure and acceptable perfusion of peripheral tissues.

When prescribing inotropic drugs, the circumstances outlined below should be borne in mind. Of the catecholamines, dobutamine appears to be the most recommended for use in COL, as it moderately reduces both preload and afterload. This effect is absent in patients taking beta-blockers on a regular basis.

In the case of progressive arterial hypotension, it may be necessary to administer dobutamine in high doses (calculation for the appearance of an a-adrenergic effect). At the same time, along with the stabilization of blood pressure, there is an increase in myocardial oxygen consumption, the appearance of severe arrhythmias and myocardial ischemia. At the earliest opportunity, the introduction of vasodilators to the patient should be resumed, which will reduce pre- and afterload.

The therapeutic effect of milrinone does not depend on whether the patient is taking beta-blockers. This drug has a more pronounced effect on cardiac output, pulmonary capillary wedge pressure, and peripheral vascular tone. However, studies have not proven the benefits of prescribing milrinone to patients with KOL (length of stay in the hospital, mortality) compared to dobutamine.

Finally, the cost of dobutamine is several times lower than the cost of milrinone, which makes it more affordable for prehospital use.

Thus, when providing emergency care to patients with KOL at the prehospital stage, the following should be used:

non-invasive ventilation in the CPAP mode (10 cm H2O), - a "first line" remedy;
the appointment of nitroglycerin sublingually or intravenously, - a means of "first line";
the appointment of captopril sublingually (the dose is determined taking into account the magnitude of blood pressure), - a means of "second line". Captopril should be prescribed while maintaining adequate perfusion of peripheral tissues, in the presence of individual contraindications to taking nitroglycerin, as well as with an insufficiently pronounced vasodilating effect with the isolated administration of nitroglycerin;
furosemide should be administered 30 minutes after the start of vasodilatory therapy in the absence of a diuretic effect from previous therapy. This drug belongs to the means of the "third line";
dobutamine may be prescribed in combination of left ventricular failure with arterial hypotension. When blood pressure is stabilized at a satisfactory level with dobutamine, vasodilators can be used with caution;
Morphine should be avoided in cardiogenic pulmonary edema. If necessary, sedative therapy is more rational to prescribe benzodiazepines.

Morphine is an opioid receptor agonist pain reliever.

Release form and composition

Morphine is available as:

Tablets, each containing 10 mg of morphine hydrochloride as the active substance;
Injection solution with an active substance content of 10 mg / ml (in ampoules and syringe tubes);
Powder in a dosage of 300 mg.

Indications for use

The use of Morphine is indicated for the elimination of high-intensity pain, which is a consequence of cancer, serious injury, myocardial infarction, surgery, unstable angina, etc.

As an additional remedy, Morphine is prescribed:

For premedication;
With general or local anesthesia;
For spinal anesthesia during childbirth.

The instructions for Morphine indicate that the drug is also advisable to use:

With pulmonary edema that has developed against the background of acute left ventricular failure (as an addition to the main therapy);
With a cough that cannot be stopped with the use of antitussive drugs;
If necessary, an x-ray examination of the duodenum, stomach, gallbladder.

Contraindications

The use of Morphine is contraindicated:

With hypersensitivity to the drug;
When the respiratory center is depressed (including conditions that develop against the background of drug or alcohol poisoning);
With depression of the central nervous system;
With paralytic ileus of the intestinal tract.

In cases where Morphine is used as an adjunct to anesthesia with other drugs, and in particular when performing epidural or spinal anesthesia, it is contraindicated in people who have impaired hemocoagulation function (including people undergoing anticoagulant therapy). Also, it is not prescribed if the patient is diagnosed with an infectious disease, because. the use of Morphine increases the risk of infection in the central nervous system.

According to the instructions, Morphine is prescribed with caution in the following conditions:

An attack of bronchial asthma;
Arrhythmia;
Pain in the abdomen of unknown origin;
COPD (chronic obstructive pulmonary disease);
Increased convulsive activity;
Drug dependence (including those noted in the anamnesis);
Alcohol addiction;
Predisposition to suicidal ideation;
emotional lability;
Surgical operations on the organs of the digestive tract and urinary system;
Cholelithiasis;
brain injury;
Increased intracranial pressure;
Liver and / or renal failure;
epileptic syndrome;
Hypothyroidism;
BPH;
Severe inflammatory diseases of the intestinal tract;
Urethral strictures;
Pregnancy;
Breast-feeding;
The general serious condition of the patient;
Advanced age.

In pediatric practice, the use of Morphine is allowed no earlier than from the age of two.

Method of application and dosage

Morphine tablets are taken orally at a dose selected by the doctor, taking into account the intensity of pain and the patient's individual sensitivity to the drug.

A single dose for tablets is from 10 to 100 mg. The highest daily dosage should not exceed 200 mg, respectively.

For children, the drug is prescribed at the rate of 0.2-0.8 mg per kilogram of body weight.

A dose of 60 mg taken by mouth once, or 20-30 mg taken repeatedly, is equivalent to 10 mg of Morphine injected into the muscle.

If it is necessary to relieve postoperative pain syndrome, the drug is prescribed no earlier than 12 hours after surgery. The dose is calculated depending on the weight of the patient:

People weighing less than 70 kg are indicated to take 20 mg every 12 hours;
Patients weighing more than 70 kg are prescribed 30 mg every 12 hours.

Single dose for Morphine injection solution:

1 mg - if subcutaneous injection is indicated;
10 mg - for intravenous or intramuscular administration of the drug.

The highest daily dose for intramuscular or intravenous administration is not more than 50 mg.

Patients suffering from acute and chronic pain are allowed to inject Morphine epidurally (ie through a catheter into the epidural space of the spine). The recommended dose is 2 to 5 mg in 10 ml of isotonic sodium chloride solution.

Side effects

Like other opioid drugs, the drug provokes a large number of side effects. The instructions for Morphine indicate that the drug can have a sedative or, conversely, stimulant effect, and also cause:

Bradycardia, tachycardia, decrease or increase in blood pressure;
Nausea, constipation, vomiting, cholestasis in the main bile duct, spasms of the biliary tract or stomach, gastralgia, hepatotoxicity, intestinal atony, toxic megacolon;
Intracranial hypertension, which can result in circulatory disorders in the brain;
Dizziness, general weakness, unusual fatigue, drowsiness, fainting, headache, involuntary muscle twitching, tremor, incoordination of muscle movements, confusion, depression, paresthesia, nervousness, restless sleep, decreased ability to concentrate, hallucinations, delirium;
Respiratory depression, atelectasis, bronchospasm;
Violation of the outflow of urine, decreased libido and potency, spasm of the ureters;
Wheezing, rash, urticaria, flushing of the face, swelling of the trachea and face, chills, laryngospasm;
Burning, swelling at the injection site.

special instructions

The drug should be used with caution in patients who are simultaneously undergoing treatment with MAOIs (monoamine oxidase inhibitors). Morphine potentiates the effect of hypnotics, local anesthetics and sedatives, as well as anxiolytics and general anesthesia.

Analogues

Morphine analogues are Morfilong, MCT continus, DHA continus, Codeine + Paracetamol, Nurofen, Codelmixt.

Terms and conditions of storage

Morphine should be stored in a dark place at temperatures up to 25 ºC. Its shelf life is 3 years.