home Audience 5 Pain relief with Morphine: instructions for use. Relief of pulmonary edema Opioid for relief of pulmonary edema

Pain relief with Morphine: instructions for use. Relief of pulmonary edema Opioid for relief of pulmonary edema

Treatment of patients with pulmonary edema should be aimed at eliminating or significantly reducing the effect of the main causes that led to the development of this complication. Therefore, first of all, measures are needed to reduce blood flow to the lungs, which can be achieved by using vasodilators, diuretics, using tourniquets or bloodletting. If there are indications, conditions should be simultaneously provided to improve the outflow of blood from the pulmonary circle, which is achieved by means that increase the contractility of the heart and improve metabolic processes in the myocardium, as well as reduce peripheral vascular resistance and, thereby, facilitating the work of the heart.

Measures should also be taken aimed at compacting the alveolar-capillary membranes, increasing the filtration back pressure, increasing the surface tension of the foam, providing the body with oxygen, and reducing the effect of biologically active substances.

It is most advisable to begin treatment of conscious patients with pulmonary edema by applying measures aimed at normalizing the patient’s emotional background, eliminating the reaction to a stressful situation, which, as already mentioned, often becomes a trigger for the development of pulmonary edema.

The importance of sedative therapy in relieving pulmonary edema is very great. When using sedatives, the content of catecholamines in the blood is normalized, and consequently, peripheral vascular spasm is reduced, blood flow to the lungs is reduced and the work of the heart is facilitated, which improves the outflow of blood from the pulmonary circle and reduces the filtration of tissue fluid through the alveolar-capillary membrane.

When using these drugs, shortness of breath decreases, which contributes, in particular, to both a decrease in blood flow to the lungs (the action of a thoracic pump) and the normalization of filtration backpressure in the lungs, since the significant vacuum that develops at the height of inspiration in the alveoli is reduced. In addition, against the background of the action of sedatives, the intensity of metabolic processes decreases, which makes it easier to tolerate the lack of oxygen.

The oldest drug in this group, the significance of which has not been lost to this day, is morphine. Slow intravenous administration of 1 - 1.5 ml of 1% morphine solution in 10-15 ml of 0.9% sodium chloride solution or 5% glucose solution can significantly improve the patient's condition and even completely stop pulmonary edema.

However, morphine should not be used in patients with chronic cor pulmonale, since cardiac decompensation may develop, as well as in patients in whom pulmonary edema has developed due to toxicosis of pregnancy, due to the possible adverse effect of the drug on the fetus. In addition, under the influence of morphine, significant respiratory depression is possible, aggravating hypoxia. Narcotic analgesics are contraindicated in cases of cerebrovascular accident and cerebral edema.

The best means that normalize the emotional background in patients with pulmonary edema can be considered diprazine (pipolfen), droperidol and seduxen. Intravenous administration of 2 ml of a 2.5% solution of diprazine, 2-4 ml of a 0.25% solution of droperidol or 2 ml of a 0.5% solution of seduxen (Relanium) can cause the same sedative effect as the use of morphine, but will not be accompanied by the inherent side effects of this drug. Droperidol and seduxen can be used for both hemodynamic types of pulmonary edema.

In patients with a tendency to lower blood pressure, it is preferable to use sodium hydroxybutyrate. To do this, 4-6 g of the drug (20-30 ml of 20% solution) should be administered intravenously very slowly, over 6-10 minutes. The advantage of sodium hydroxybutyrate is that it stabilizes blood pressure and helps normalize it.

Less commonly, barbituric acid preparations - hexenal or sodium thiopental - can be used to normalize the emotional background (their negative inotropic effect on the heart and the possibility of developing arterial hypotension limit the use of these drugs in most patients with pulmonary edema).

To reduce blood volume, unload the pulmonary circulation and dehydrate the pulmonary parenchyma, diuretics should be used. The best drug in this group is Lasix (furosemide), which should be administered intravenously at a dose of 20–40 mg.

The therapeutic effect of furosemide is explained by its diuretic activity: the effect develops within a few minutes and lasts 2-3 hours with the release of up to 2 liters of urine. A distinct decrease in plasma volume and an increase in colloid osmotic pressure due to blood thickening cause the transition of edematous fluid into the vascular bed, leading to a decrease in pressure in the pulmonary artery and blood filling in the lungs, thereby reducing effective filtration pressure. Ethacrynic acid (uregit) has a similar property - 50-100 mg. In case of a sharp disturbance of hemodynamics (shock, paroxysmal tachycardia), the use of diuretics is indicated only after normalization of blood pressure.

It is not recommended to use osmotic diuretics for dehydration during pulmonary edema, since in the first phase of their action they increase the volume of blood volume, which creates an increased load on the pulmonary circulation and can contribute to the progression of pulmonary edema.

A powerful way to relieve pulmonary edema are vasodilators. The mechanism of their beneficial effect is a decrease in vascular tone, a decrease in intrathoracic blood volume due to a decrease in blood flow to the small circle and in facilitating the outflow of blood from the lungs due to their effect on peripheral vascular resistance.

The most widely used gangil blocking drugs are ar-fonad (hygronium), as well as pentamine or benzohexonium.

The short-acting ganglion blocker arfonad (or the domestic drug gigroniy) is used in the form of a 0.1% solution. In this case, 250 mg of the drug is dissolved in 250 ml of 0.9% sodium chloride solution or 5% glucose solution. Intravenous administration of hygronium begins at a rate of 80-100 drops/min, and then as blood pressure decreases, the rate of administration decreases. To maintain systemic pressure at the desired level (approximately 80-100 mm Hg), it is sufficient to administer the drug at a rate of 10 - 15 drops/min.

The intermediate-acting ganglion blocker pentamine is best administered intravenously in fractional syringes. To do this, 50-100 mg of the drug (1-2 ml of a 5% solution) is diluted in a 0.9% sodium chloride solution to 20 ml and 3-5 ml of this mixture is injected into a vein at intervals of 5-10 minutes until the desired effect is obtained. .

With the help of gangliolytics, it is especially possible to quickly stop pulmonary edema if systolic blood pressure exceeds 180-200 mm Hg. Art. Within 10 - 20 minutes after administration of the drug and blood pressure reaching 110-120 mm Hg. Art. shortness of breath decreases, moist wheezing in the lungs disappears, breathing becomes even and calm.

Patients can take a horizontal position, excitement is relieved, and they sometimes fall asleep. Benzohexonium at a dose of 10–40 mg has an even more rapid and pronounced effect.

With the help of drugs of this group in patients with an initial normal level of blood pressure, it can be safely reduced to 80 - 70 mm Hg. Art. In this case, the clinical picture of pulmonary edema can be completely stopped.

A similar effect can be achieved by prescribing vasodilators from the nitrate group. Nitrosorbide (20 - 30 mg) or nitroglycerin (1-2 tablets) is given under the tongue. If appropriate dosage forms are available, intravenous administration of nitrates is possible. The advisability of prescribing aminophylline for pulmonary edema of any etiology is questionable. The moderate antispasmodic, vasodilating and diuretic effect of xanthines does not compensate for the adverse effects on metabolism in the heart muscle, pronounced tachycardia, which is manifested under their influence by stimulation of the respiratory center. Intravenous administration of 5-10 ml of a 2.4% solution of this drug is indicated only with concomitant bronchiolospasm and cerebral edema with the development of bradycardia. In addition to the listed pharmacological agents, the use of other therapeutic measures can also contribute to the relief of pulmonary edema.

Thus, reducing blood flow to the lungs can be achieved by applying venous tourniquets to all extremities. In this case, it is necessary to avoid erroneous application of an arterial tourniquet, since clamping of the arteries turns off significant vascular volumes, which can lead to increased blood flow to the lungs and the progression of edema.

The resolution of pulmonary edema is also facilitated by exfusion of venous blood, the volume of which should be at least 400 - 600 ml. However, it often seems more appropriate to use so-called pharmacological exfusion using ganglion-blocking drugs according to the methods described above to reduce blood flow to the small circle. The advantage of this method of unloading the pulmonary circulation is obvious and consists in the possibility of preserving the patient’s own blood. In the absence of medications, moderate unloading of the small circle can be achieved with the help of hot sitz foot baths. In this case, the patient’s legs up to the middle of the legs are placed in a basin or bucket of hot water, and due to the development of local hyperemia, blood is deposited in the dilated vessels of the legs, more intense in a sitting position.

A very important component of intensive care for pulmonary edema are measures aimed at increasing the filtration backpressure in the alveoli and thereby complicating the passage of blood transudate from the capillaries of the small circle into them. This can be achieved by spontaneous breathing with expiratory resistance or mechanical ventilation with positive end-expiratory pressure (PEEP). Breathing against dosed resistance is achieved by exhaling the patient through a water seal, which creates an obstacle to exhalation of 5-6 cm of water. Art. Assisted or artificial ventilation in the PEEP mode can be achieved by creating an end-expiratory pressure (using a bag or bellows of a manual ventilator) of 5 - 6 cm of water. Art.

During intensive care, measures should be taken to increase the oxygen content in the air inhaled by the patient (using inhalation through a mask), as well as to reduce foaming, which in emergency care is called defoaming. The latter can be done using ethyl alcohol or a 10% aqueous (alcohol) solution of antifomsilane.

Alcohol vapor can be introduced into the respiratory tract by passing oxygen through it, enriching the respiratory mixture. Intratracheal (percutaneous puncture of the trachea) administration of 1 - 3 ml of alcohol or intravenous administration of 5 ml of absolute alcohol mixed with 15 ml of glucose solution are possible. It should be emphasized that the therapeutic effect of defoaming with ethyl alcohol (disappearance of bubbling breathing) begins to affect no earlier than after 10 - 15 minutes of inhalation. The irritating effect of the drug on the respiratory tract forces patients to often refuse to inhale an oxygen-alcohol mixture, even when it is administered through nasopharyngeal catheters. After intratracheal infusion of alcohol, the amount of foam decreases immediately, although the difficulties of carrying out this measure (puncture of the trachea) in an excited patient and the possibility of burns to the mucous membrane of the trachea and bronchi with a small amount of foam require this measure to be carried out according to strict indications. Antifomsilane solution is administered into the respiratory tract by spraying over the larynx or using a nebulizer built into an oxygen inhaler. Experimental and clinical data indicate low toxicity and greater effectiveness of antifomsilan in both hemodynamic and toxic forms of pulmonary edema. For defoaming, inhalation of 2 - 3 ml of a 10% alcohol solution of antifomsilane for 10-15 minutes is sufficient, which in many cases allows you to stop swelling within 20-45 minutes from the start of inhalation. Mandatory conditions include cleansing the oral cavity, emergency aspiration of foam from the upper respiratory tract, and gradual (1-2 minutes) adaptation of patients to inhalation of the antifoam agent. Inhibited patients tolerate inhalation of the defoamer more easily than with severe psychomotor agitation (mandatory preliminary sedation!). Antifoam therapy is compatible with any method of decongestant therapy and has no absolute contraindications.

The sequence of treatment measures for pulmonary edema can be presented as follows:

use of sedatives;
defoaming - inhalation of oxygen with alcohol, antifomsilane;
use of vasodilators;
prescription of diuretics;
application of venous tourniquets;
the use of cardiac glycosides, vitamins and glucocorticoid hormones;
blood exfusion;
after the patient’s condition improves, hospitalization is carried out in a hospital department specialized in the main disease.

Ed. V. Mikhailovich

eyeballs. Appetite is sharply reduced, nasal breathing is difficult, and there is widespread hyperemia in the throat. Presumable diagnosis +++a) influenza

92 A 32-year-old patient complains of severe weakness, malaise, lethargy over the past 3
weeks There is no fever or catarrhal symptoms. Periodically, I experience pain. large joints.
Objectively: pain in the right epigastric region, liver at the edge of the costal arch. From the anamnesis
It became known that approximately 4 months ago the woman was treated by a dentist. About what
disease can be assumed?

c) viral hepatitis A

D) viral hepatitis B
e) viral hepatitis E

93 A fire victim in the back has burn wounds with blisters filled with
serous fluid and areas of desquamated epidermis. Determine the total area and depth of the lesion
by degree.

A) 18%, II degree

b) 36%, II degree

B) 45%, ShB degree
-d) 27%, xxx degree
e) 40%, ShB degree

94 A 60-year-old patient suffering from diabetes mellitus complains of pain in the neck and swelling.
On the back surface of the neck there is hyperemia, swelling, severe pain, multiple necrotic
rods. What disease can you think about?

95 The patient complains of nausea, vomiting, pain in the right side of the abdomen. Temperature rises to
37.50 C. Upon examination, the tongue is coated. The abdomen is tense in the right iliac region. Positive
Shchetkin-Blumberg symptom. What disease can you think of? 1. Acute appendicitis 2. Acute
cholecystitis 3. Perforation of a stomach ulcer. 4. Acute pancreatitis 5. acute paraproctitis
First aid A) lay the patient down, wrap him warmly, place a heating pad on his stomach B) put the patient in
comfortable position give analgesics C) place the patient in a comfortable position, cold on the stomach D)
put the patient in a comfortable position, give antispasmodics D) do nothing before arrival
doctor

96 Male 25 years old. Complaints: after sexual intercourse, 4 weeks later I felt that I started faster
get tired, increased fatigue. After 5 weeks I began to lose weight. The temperature remains high
diarrhea. Acute respiratory infections last longer than usual, muscle pain, arthralgia. Memory loss has been noticed. ABOUT
what disease do you think: 1. HIV infection 2. dysentery 3. acute respiratory
viral infection 4. vegetative-vascular dystonia 5. gonorrhea This disease is not
transmitted: A) sexually B) through blood transfusion C) through the placenta D) through
household items D) when using the same tools with an infected person

97 A 48-year-old patient, a livestock specialist, complains of fever, weakness, headache, chest pain,
shortness of breath. Objectively: the condition is serious, 1: - 390C, injection of scleral vessels, the face is puffy. Tones
hearts are deaf. In the lungs in the left upper lobe there are moist fine rales. Stands out
foamy sputum with blood. From the anamnesis: the patient helped a neighbor slaughter a sick camel.
Presumable diagnosis

C) anthrax +++p) brucellosis -e) pneumonia

98 The child poured an unknown liquid from a bottle. There were sharp pains in the mouth, abdomen, lips.
The mucous membrane of the oral cavity is inflamed, covered with loose whitish-gray films,
repeated vomiting with blood. Breathing is difficult. What substance was the child poisoned with?

A) alkali - b) acid

^ch The patient complains of g.plLogchch. malaise, Lol and chest, cough for three weeks.

OO"ective: the skin is thin, there is an increase in regional lymph nodes. About what
disease you might think? 1. bronchitis 2. pneumonia 3. bronchial asthma 4. tuberculosis 5.
cardiac asthma Specify the priority method of examination for this disease A)

X-ray 1>) fluorological B) serological D) bacterioscopic E)

electrocardiographic ---a) 2 - B -b) 3 - L -i) 1 - I"

100 A young woman developed acute pain in her lower abdomen four hours ago. Then it appeared

dizziness, “flickering spots” before the eyes, feeling of lack of air. It is known that the patient
delay of menstruation by 2-3 weeks. On examination, the patient is very pale, the pulse is 110 beats per minute.
The abdomen is tense, palpation of the lower parts is painful. What pathology can be suspected in this
sick? 1. acute appendicitis 2. anemia 3. ectopic pregnancy 4. urolithiasis

disease b. intussusception First aid measures A) rest, cold

stomach C) cleansing enema, antispasmodics C) warm bath, heat on the stomach D) cold on
stomach, antispasmodics D) cold on the stomach, analgesics
---a) 1 ■ A
--b) 2 - B
NPO 1 L
d) -1 I"

101 In what cases when determining the groups of crops do they use serum of LI (IV) group

a) in cases where, when determining blood groups, agglutination is absent in all test tubes

+ 116) in cases where agglutination occurred with sera of O (I), A (II), B (III) blood groups

c) in cases where agglutination occurred with sera of these groups after the 10th minute

-e) in cases where agglutination occurred with serum of only the first group O (I)

102 Components of the test for individual compatibility of donor and recipient blood
a) donor plasma and recipient plasma

B) recipient plasma and donor serum

c) donor plasma and recipient blood

neither 1) recipient serum and donor blood

k) recipient and donor serum

^ 103 Complicated fractures of the spine are fractures
-a) vertebral body

---o) spinous and transverse processes

c) fractures with damage to the sacrum

+++d) fractures with spinal cord damage

e) fractures with damage to the intervertebral disc

104 A constant sign of spinal cord damage is *
a) springy fixation in the joints

+*b) dysfunction of the pelvic organs

c) disorders of the cardiovascular system

-e) facial paresis

105 Nature and localization of pain in perforated gastric ulcer
-a) constant, strong in the right iliac region

b) constant, sharp pain in the right hypochondrium

m) girdling, dull in nature

(| I g) "dagger", n inigistrllmy areas
d) sharp (in the hypochondrium.

KI" Nature of pain in acute cholecystitis

158 Antibiotics for influenza are prescribed
course of the disease 3. in severe cases
high risk groups
a) 1, 2, 3

1. in any case 2. for mild to moderate severity

4. in case of complications 5. patients from

1. corticosteroids 2. antihistamines

159 Means of symptomatic treatment of influenza can be
antipyretic and anti-inflammatory 3. antibiotics
vitamins

B) 2, 3, 4 -c) 3, 4, 5 +++d) 2, 4, 5 -e) 1, 4, 5 ;

160 Sources of infection for botulism are all of the above,
-a) home-canned mushrooms

B) home canned vegetables

C) fruits, milk, dairy products

D) homemade salted and smoked fish

D) homemade ham, lard, sausage

161 The main clinical symptoms of tetanus are all except
a) trismus

b) tonic tension of the muscles of the face, neck, back, abdomen and limbs, intercostal muscles

c) increase in body temperature

162 Meningococcal infection is characterized by everything except
-a) acute onset

B) severe headache

D) vomiting that does not bring relief

The main food sources of vitamin A and carotene are all of the listed products,

fish oil potatoes

D) red pepper,

sorrel, tomatoes

164 The most important sources of vitamin C are all of the following
+++a) butter

b) dill, cabbage, parsley

c) lemon, black currant

165 Hepatic swelling is not a complication
a) acute hepatitis

D) hepatocellular cancer
e) chronic pyelonephritis

The following foods help normalize intestinal activity during diarrhea:

blueberries --d) oak bark decoctions -e) rice water

All of the listed drugs contribute to disruption of the normal composition of the intestinal microflora,

May be accompanied by all of the above except

168 Menopause

B) chills with high fever

B) pain in the heart

d) feeling of lack of air

169 Antigen is
-a) bacteria

B) any substance that causes an immune response

170 The basic principles of treatment of iron deficiency anemia are reduced to 1. timely
whole blood transfusion 2. to long-term

The sequence of treatment measures for acute acute illness, regardless of the cause and hemodynamic state, should be as follows (Fig. 4):

1. Place in 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. Inhalation of oxygen with alcohol vapor

When prescribing Morphine and determining its dose, it is necessary to take into account age, state of consciousness, breathing pattern, and heart rate. Bradypnea or irregular breathing rhythm, the presence of signs of cerebral edema, severe bronchospasm are contraindications to its use. For bradycardia, the administration 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 t every 15-20 minutes) or spraying Isoket (Isosorbide dinitrate) in the mouth. In the conditions of a medical team, and even more so an intensive care unit or a cardiology team, intravenous drip use of Perlinganite or Isoket is advisable, which allows for controlled peripheral vasodilation. The drug is administered in 200 ml of isotonic solution. The initial rate of administration is 10-15 mcg/min with a sequential increase every 5 minutes by 10 mcg/min. The criterion for dose effectiveness is the achievement of clinical improvement in the absence of side effects. Systolic blood pressure should not be reduced to less than 90 mmHg.

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.

The use of diuretics, for example Lasix, Furosemide, in a dose of 60-80 mg (up to 200 mg) as a bolus, is effective for OA. Within a few minutes after administration, venous vasodilation occurs, which leads to a decrease in blood flow into the pulmonary circulation system. After 20-30 minutes, the diuretic effect of Furosemide begins, which leads to a decrease in blood volume and an even greater decrease in the hemodynamic load.

If hypertension and mental agitation persist, a quick effect can be achieved by intravenous injection of Droperidol. This drug has pronounced internal α-adrenolytic activity, the implementation of which helps to reduce the load on the left ventricle by reducing total peripheral vascular resistance. Droperidol is administered in a dose of 2-5 ml depending on the patient’s blood pressure level and weight.

Eufillin should not be used for pulmonary edema, even if there are signs of bronchial obstruction, because this obstruction is not associated with bronchospasm, but with swelling of the peribronchial space, and the risk of increasing myocardial oxygen demand with the introduction of Eufillin is much higher than the possible beneficial effect.

Against the background of low blood pressure numbers Pulmonary edema most often occurs in patients with widespread post-infarction cardiosclerosis, with extensive repeated myocardial infarctions. Hypotension can also be the result of inappropriate 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 included in therapy.

With 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 exception is ventricular unidirectional paroxysmal tachycardia, relieved by lidocaine or ventricular paroxysmal tachycardia of the “pirouette” type, which can be successfully interrupted by intravenous administration of magnesium sulfate (see section “Heart rhythm disturbances”).

Drug therapy for bradysystolic arrhythmias (atrioventricular or sinoatrial block, sinus node failure) in patients with pulmonary edema also appears dangerous: the use of atropine and β-adrenergic stimulants to increase heart rate can lead to the development of fatal cardiac arrhythmias. The treatment of choice in these cases is temporary prehospital pacing.

The use of cardiac glycosides for pulmonary edema is permissible only in patients with tachysystole against the background of a permanent form of atrial fibrillation.

If, after stopping the arrhythmia, signs of left ventricular failure persist, it is necessary to continue treatment of pulmonary edema, taking into account the hemodynamic state.

Treatment of pulmonary edema due to acute myocardial infarction is carried out in accordance with the stated principles.

The criteria for relieving pulmonary edema, in addition to subjective improvement, are the disappearance of moist rales and cyanosis, a decrease in shortness of breath to 20-22 per minute, and the patient’s ability to take a horizontal position.

Patients with relieved pulmonary edema are hospitalized by the medical team independently in the cardiac intensive care unit (department). Transportation is carried out on a stretcher with a raised head end.

Indications for self-call intensive care or cardiology teams for a linear medical team are:

lack of clinical effect from the treatment measures;

pulmonary edema due to low blood pressure;

pulmonary edema due to acute myocardial infarction;

arrhythmogenic pulmonary edema;

in cases of complications of therapy.

A 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 available in accordance with these recommendations.

1) in case of methanol poisoning;(?) Ethanol

Spiritus aethylici (sol) 70%

D.s for root canal treatment

Warming, astringent (conc), antimicrobial (↓conc), 20% w/v, antidote for poisoning with methyl alcohol

2) H2 – histamine blocker for gastric ulcer;

Cordiamine

Cordiamini 1 ml D.t.d. N. 10 in ampull.

S. 1 ml subcutaneously

Analeptic, mixed mechanism

1. Dependence of the pharmacological effect on the dose of the active substance. Types of doses. The breadth of therapeutic action of drugs. Biological standardization.

11. Dependence of the pharmacological effect on the dose of the active substance. Types of doses. The breadth of therapeutic action of drugs. Biological standardization.

Doses of pharmacological substance

Pulmonary edema due to high blood pressure. Treatment of pulmonary edema and cardiac asthma

Treatment of pulmonary edema and cardiac asthma

#image.jpgIn the treatment of pulmonary edema and cardiac asthma, it is necessary to distinguish between urgent measures to relieve edema or asthma and measures that are not of an emergency nature and are used only to enhance the effectiveness of the first group of drugs and to prevent pulmonary edema.

The drugs of the first group include blood glucose blockers (with a systolic blood pressure of at least 100 mm Hg), morphine, antipenal therapy, and cardiac glucosides.

Intravenous administration of Novurpt or other fast-acting diuretics, as well as prednisolop, diaphylline, etc. should be classified as drugs of the second group.

One of the first places among the drugs that relieve pulmonary edema and cardiac asthma should be given to ganglion blockers (pentamine, hexonium, arfonade, etc.). Ganglion blockers for the treatment of pulmonary edema were used back in 1952 (cited by A. Lazaris and I. A. Serebrovsky), but entered into widespread practice only in recent years (R. N. Lebedeva, V. P. Osipov, 1965; O. B. Rudneva, 1965; A. V. Vinogradov, T. D. Tsibekmacher, 1966 ; E. V. Zemtsovsky, Ya-L. Segal, 1967; G. M. Tsygankov,

N. M. Shutova, 1967; S.V. Shestakov, I. Ya-Pevzner, 1967). With the action of ganglion blockers, systolic and diastolic pressure decreases, venous pressure decreases, and cardiac output increases without increasing cardiac work (A. V. Vinogradov, T. D. Tsibekmakher, 1966; E. V. Zemtsovsky, Ya. L. Segal, 1967 ). Due to the dilation of the blood vessels of the internal organs, blood is redistributed, the mass of circulating blood and venous return decreases. In this regard, it turns out to be possible to completely abandon bloodletting, which was previously recommended in all guidelines. We only had to resort to bloodletting once. The so-called “bloodless bloodletting” with the help of ganglion blockers differs favorably from true bloodletting in that there is no reflex vascular spasm, and the deposited blood is again included in the circulation after the cessation of the ganglion blockade. In addition, pharmacological blockade of the chromaffin substance of the adrenal glands reduces the secretion of adrenaline, the excess content of which in the blood during pulmonary edema occurs due to developing hypoxia. Pentamin (5%) or hexonium (2.5%) is used by intravenous administration from 0.5 to 1.0 ml (slowly) or the same doses are administered intramuscularly. Arfonad is administered intravenously in the form of a 0.1% solution in 5% glucose at a rate of 40-60 drops per G. When using ganglion blockers, blood pressure is sought to be reduced to 90-80 mm Hg, if the initial pressure is normal, or by 40% of the initial one, if it is increased, i.e. up to 100-120 mm Hg.

Ganglioblockers can be used for pulmonary edema or cardiac asthma only with elevated or normal initial blood pressure. If the initial systolic pressure is below 100 mm Hg, the use of ganglion blockers is unacceptable, as it can lead to collapse, from which the patient cannot be recovered. When using ganglion blockers, it is necessary to pre-establish a slow intravenous drip infusion of 5-10% glucose (for the use of vasopressor therapy in case of prolonged hypotension in response to ganglion blockers). When the pressure decreases to the target numbers (90-80 mmHg with normal initial systolic pressure or to 100-120 with high systolic pressure), vasopressors should not be used immediately (this is an error

It is often assumed that it deprives the procedure of meaning). If within one hour the systolic pressure does not reach 90-110 mm Hg, i.e., values at which sufficient filtration of urine occurs, it is necessary to begin drip administration of vasopressors. In the vast majority of cases, this does not have to be resorted to, since systolic pressure reaches normal values within the next 30-60 minutes. When administering ganglion blockers, the patient must be placed in a horizontal position in advance to avoid disruption of the blood supply to the brain and heart. After administration of ganglion blockers, frequent (approximately every 5 minutes) blood pressure measurements are necessary for approximately 30 minutes, i.e., during the period of development of hypotension. If the patient's condition dictates urgent care, intravenous administration of the drug is preferable, but if the patient's condition does not require immediate intervention, the ganglion blocker can be administered intramuscularly. In the latter case, the effect does not occur in the first minutes, but after 15-30 minutes. We used this therapy (in combination with other measures) in 19 patients with pulmonary edema due to normal or high blood pressure. An immediate effect was noted in 18 patients, and in 15 people the effect was persistent; almost all patients were subsequently discharged. However, we did not observe any complications associated with ganglion blockade. The hapglionic block was shallow, since the pupil dilation was insignificant and the hypotension was slight. (In the presence of hypertension 150/90 - 190/120 mm Hg, the pressure decreased to 105/80 mm Hg, and with normal pressure 120/80-130/80 mm Hg - to 90/70-100/80 mm Hg.)

Blood deposition against the background of hypotension can be safely performed by applying tourniquets to the limbs.

Another effective remedy for relieving cardiac asthma and pulmonary edema (before the use of ganglion blockers is the most effective remedy) is morphine (S. G. Weisbein, 1957; Luisada, Rosa, 1964, etc.). Morphine is administered subcutaneously in the form of a 1% solution of 1-2 ml or intravenously 1 ml. The therapeutic effect occurs within a few minutes. Despite the frequent use of morphine, the mechanism of its action in pulmonary edema and cardiac asthma remains unclear. It is assumed that the beneficial effect of morphine in these conditions is associated with a decrease in basal metabolism and depression of the respiratory center (Luisada, Rosa, 1964), a decrease in total peripheral resistance, circulating blood mass and venous return (Nenney et al. 1966; Messer. 1966; Pur- Shariari et al. 1967), a decrease in blood pressure in some cases (Thomas et al. 1965). In this regard, there is a certain risk of using morphine for low blood pressure. Along with morphine, a solution of atropine (0.1% 0.5-1.0) is usually administered to prevent its vagotropic effect and excessive depression of the respiratory center. In addition, atropine has an antispasmodic effect on the bronchial muscles and relieves bronchospasm, in some cases accompanying cardiac asthma.

Considering the side effects associated with the use of morphine (respiratory depression, nausea, vomiting, gastrointestinal paresis), the use of ganglion blockers (in the absence of hypotension) should be given preference.

The drug that is certainly effective during an attack of cardiac asthma or pulmonary edema is strophanthin (or other fast-acting cardiac glucosides) (A. S. Smetnev et al. 1964; A. V. Vinogradov, 1965, etc.). Clinical experience indicates the effectiveness of strophanthin in myocardial infarction complicated by acute heart failure, although experimental observations cast doubt on the appropriateness of its use (Luisada, Rosa, 1964). Strophanthin is administered intravenously, preferably by drip (0.05% 0.25 in 100-200 ml of 5-10% glucose solution once a day or repeatedly at intervals of 8-12 hours). We used strophanthin in this way, at intervals of 8-12 hours, in 33 people with pulmonary edema or cardiac asthma (simultaneously with other drugs - ganglion blockers, morphine, etc.) and did not see any complications from such therapy. Considering the need for a quick effect in pulmonary edema and cardiac asthma, in these cases strophanthin sometimes has to be administered not as a drip, but as a stream.

Antifoam therapy, proposed by Luisada in 1950, has a pronounced effect in the treatment of pulmonary edema. Most often, alcohol and silicone preparations, which have antifoaming properties, are used for this purpose. In addition, alcohol has the ability to tan, which leads to a decrease in the permeability of the alveolar walls. Alcohol can be supplied to the alveoli in three ways: intravenous administration, inhalation, and introduction into the trachea.

To combat foaming, other substances are also used - a 10% colloidal solution of silicone in water, a 10% alcohol solution of antifomsilone (A.P. Zysko et al. 1966; A.P. Zysko, M. Ya-Ruda, 1968; Luisada, Rosa , 1964). In this case, the effect occurs much faster than from inhalation of alcohol. Antifoam therapy is indicated in all cases of pulmonary edema.

Medical Instructions

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

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

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

stopping foaming.
correction of emerging hemodynamic disorders.
reducing TPVR - total peripheral vascular resistance.
correction of acid-base disorders.

Pulmonary edema due to arterial hypertension.

the patient's position is sitting, with legs down.
nitroglycerin 1% mg per minute, increasing the dose until systolic blood pressure decreases by 10-15% of the original. At very high blood pressure levels, instead of nitroglycerin, sodium nitroprusside is administered at a dosage of µg per minute.
short-acting ganglion blocker pentamin 5% - 1-2 ml diluted in 20 ml NaCl, 3-5 ml solution intravenously every 5-10 minutes.
with high blood pressure numbers and moderate clinical manifestations of pulmonary edema - clonidine 0.01% - 1 ml IV bolus.
furosemide mg IV bolus. If there is no effect, repeat administration after an hour.
droperidol 0.25% ml intravenous bolus.

Pulmonary edema against the background of normal blood pressure.

nitroglycerin 1% - 10 mg/min.
furosemide mg IV.
droperidol 0.25% ml i.v.
Prednisolone 90 mg IV bolus.

Constant monitoring of blood pressure, not allowing it to drop below 90 mm Hg.

Pulmonary edema with moderately low blood pressure.

dobutamine 5 – 10 mcg/kg/min intravenously until a normal blood pressure level is achieved.

Pulmonary edema with severe arterial hypotension.

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

Pulmonary edema due to mitral stenosis.

promedol 2% -1ml intravenously.
furosemidemg IV p.
aminophylline 2.4% - 10ml IV p.
strophanthin 0.05% - 0.5 ml intravenously.

Pulmonary edema due to central nervous system damage due to stroke.

furosemidemg IV p.
aminophylline 2.4% - 10 ml i.v.
promedol 2% -1ml intravenously.
reopolyglucin 400 ml intravenous drip.
strophanthin 0.05% solution - 0.5 ml intravenously.
for arterial hypertension - pentamin 5% - 1 ml intravenously.
mannitol 30-60 ml diluted in 200 ml NaCl intravenously.

Criteria for relieving pulmonary edema.

Reduction in respiratory rate to 22 or less per minute.
No foamy sputum.
No 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.

Morphine for pulmonary edema

granules for the preparation of suspension for oral administration, capsules, extended-release capsules, solution for intramuscular administration, solution for injection, rectal suppositories, tablets, film-coated tablets of extended release

Narcotic analgesic. Opioid receptor agonist (mu-, kappa-, delta-). Inhibits the transmission of pain impulses to the central nervous system, reduces the emotional assessment of pain, causes euphoria (increases mood, causes a feeling of mental comfort, complacency and bright prospects, regardless of the real state of affairs), which contributes to the formation of drug dependence (mental and physical). In high doses it has a hypnotic effect. Inhibits conditioned reflexes, reduces the excitability of the cough center, causes excitation of the center of the oculomotor nerve (miosis) and n.vagus (bradycardia). anov (including bronchi, causing bronchospasm), causes spasm of the sphincters of the biliary tract and the sphincter of Oddi, increases the tone of the sphincters of the bladder, weakens intestinal motility (which leads to the development of constipation), increases gastric motility, accelerates its emptying (promotes better detection ulcers of the stomach and duodenum, spasm of the sphincter of Oddi creates favorable conditions for x-ray examination of the gallbladder). May stimulate the chemoreceptors of the vomiting center trigger zone and cause nausea and vomiting.

Severe pain syndrome (trauma, malignant neoplasms, myocardial infarction, unstable angina, postoperative period), as an additional drug to general or local anesthesia (including premedication), spinal anesthesia during childbirth, cough (if non-narcotic, etc. are ineffective). narcotic antitussive drugs), pulmonary edema due to acute LV failure (as an additional therapy), X-ray examination of the stomach and duodenum, gall bladder.

Stuttering in a Child: What to Do.2009

What to do if mom doesn’t have enough.

What to do if you have a child.

DENTAL TREATMENT UNDER ANESTHESIA IN CHILDREN: ALL PROS AND CONS - president.org.ua

But what to do if every trip to the doctor turns into hysterics that are almost impossible to stop? Some will say: treat your teeth under general conditions.

What to do if your child is in pain.

"The child has a cough. What should I do?" - 5.

Examination of a patient with bronchial asthma has several goals. Firstly, respiratory functions are examined to identify the degree of their impairment, since.

Exercises for Pneumonia

Depending on the stage of the disease, localization of the inflammatory process, dysfunction of external respiration and the general condition of the patient, the most are selected.

Help with Pulmonary Edema

Quincke's edema (angioedema, giant urticaria) is an acute allergic reaction that is expressed in rapidly developing subcutaneous edema.

Among respiratory tract diseases, bronchitis occurs very often. Bronchitis is an inflammation of the bronchial mucosa. If at the same time it stands out profusely.

Good day, dear reader. We continue to introduce you to the results of treatment with the Life Energy Universal device and today we present it to you.

@Kostya Kolyvanov. The little one has bronchitis, she called me, she coughs so badly, but such a sweet, dear, hoarse voice - she almost burst into tears! DO NOT BE ILL. GET NO ONE SICK

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Cardiogenic pulmonary edema

In the world of medicines »» No. PROFESSOR A.E. RADZEVICH, HEAD OF THE DEPARTMENT OF THERAPY, FACULTY OF POSTGRADUATE EDUCATION, MOSCOW MEDICAL DENTAL INSTITUTE

A.G. EVDOKIMOVA, ASSOCIATE PROFESSOR OF THE DEPARTMENT, DOCTOR OF MEDICAL SCIENCES

Pulmonary edema is an acute condition based on the pathological accumulation of extravascular fluid in the lung tissue and alveoli, leading to a decrease in the functional abilities of the lungs. The etiology of pulmonary edema is varied: it develops with infections, intoxications, anaphylactic shock, damage to the central nervous system, drowning, at high altitudes, as a side effect of the use of certain medications (beta blockers; vasotonics that increase the load on the heart), with transfusion of excess plasma substitutes, rapid evacuation of ascitic fluid, removal of large amounts of plasma, aggravates the course of acute (thromboembolism of the pulmonary artery and its branches) and chronic “pulmonary heart”.

In the clinic of internal diseases, we can distinguish the main nosological forms that most often lead to the development of pulmonary edema:

1. Myocardial infarction and cardiosclerosis.

2. Arterial hypertension of various origins.

3. Heart defects (usually mitral and aortic stenosis).

The pathogenesis of pulmonary edema is complex and not completely clear.

Normally, blood plasma is kept in the lumen of the capillary from filtering through its wall into the interstitial space by the force of colloid-osmotic pressure, which exceeds the hydrostatic pressure of the blood in the capillaries. Currently, there are three main conditions in which 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 leading 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 leaving the pulmonary circulation system into the lung tissue.

2. Increased permeability of the capillary wall.

3. A significant decrease in plasma oncotic pressure (under normal conditions, its value allows the 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). Thus, the most important reason for the increase in hydrostatic pressure in the capillaries of the lungs is left ventricular failure, which causes an increase in the diastolic volume of the left ventricle, an increase in diastolic pressure in it and, as a consequence, an increase in pressure in the left atrium and pulmonary vessels, including capillaries. When it reaches mm Hg. Art. and is compared with the value of oncotic pressure, active sweating of plasma into the lung tissue begins, significantly exceeding in volume its subsequent reabsorption into the vascular bed, 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 disrupted due to narrowing of the left atrioventricular orifice, and the appearance of pulmonary edema is not caused by left ventricular failure.

During the development of pulmonary edema, its pathogenesis (according to the principle of the formation of a “vicious” circle) may include other mechanisms: activation of the sympathetic-adrenal system, renin-angiotensin vasoconstrictor and sodium-sparing systems. Hypoxia and hypoxemia develop, leading to an increase in pulmonary vascular resistance. The components of the kallikrein-kinin system are turned on, with the transition of their physiological effect to pathological.

Pulmonary edema is one of the conditions that can be diagnosed at a distance, right from the threshold of the room 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 respirations is more than 30 per minute; profuse cold sweat; cyanosis of mucous membranes and skin; a lot of wheezing in the lungs; tachycardia, gallop rhythm, accent of the second tone over the pulmonary artery. Clinically, there are 4 stages:

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

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

3 - advanced clinical stage, wheezing can be heard at a distance, orthopnea is pronounced;

4 - extremely severe stage: a lot of wheezing of various sizes, 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 infiltrates the entire lung tissue, including the 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 surfactant, collapse of the alveoli, and flooding of them 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 (similar to 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, tries to go to the window, is agitated, fears of death appear, answers questions with difficulty, sometimes nodding his head, is not distracted by anything, completely devoting himself to the struggle for air. The duration of an attack of cardiac asthma is from several minutes to several hours.

When auscultating the lungs, as an early sign of interstitial edema, one can listen to weakened breathing in the lower sections, dry wheezing, indicating swelling of the bronchial mucosa. In cases of chronic hypervolemia of the pulmonary circulation (mitral stenosis, chronic heart failure), of the additional research methods for diagnosing interstitial pulmonary edema, X-ray is of greatest importance. In this case, a number of characteristic signs are noted:

Curley septal lines “A” and “B”, reflecting swelling of the interlobular septa;

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

Subpleural edema in the form of compaction along the interlobar fissure.

Acute alveolar pulmonary edema is a more severe form of left ventricular failure. Characteristic is bubbling breathing with the release of flakes of white or pink foam (due to the admixture of red blood cells). Its quantity can reach several liters. In this case, blood oxygenation is particularly severely disrupted and asphyxia may occur. The transition from interstitial pulmonary edema to alveolar edema sometimes occurs very quickly - within a few minutes. Most often, violent 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 clear 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 number of moist rales of different sizes appear. In some cases, along with wet wheezing, dry wheezing is heard, and then differential diagnosis with an attack of bronchial asthma is necessary. Like cardiac asthma, alveolar pulmonary edema is more often observed at night. Sometimes it is short-lived and goes away on its own, in some cases it lasts several hours. With strong foaming, death from asphyxia can occur very quickly - within minutes after the onset of clinical manifestations.

The X-ray picture of alveolar pulmonary edema in typical cases is determined by the symmetrical impregnation of both lungs with transudate with a predominant localization of edema in the hilar and basal parts. Laboratory data are scarce, reduced to sharp changes in the gas composition of the blood and the acid-base state (metabolic acidosis and hypoxemia), and have no clinical significance. The ECG shows tachycardia, a change in the terminal 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 scar fields after myocardial infarction), pulmonary edema more often occurs with increased blood pressure or with cardiac arrhythmias, leading to a decrease in minute volume of blood.

Therapeutic measures for interstitial and alveolar forms of pulmonary edema in cardiac patients are in many ways 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 pulmonary vessels . In case of alveolar pulmonary edema, measures are added aimed at destroying the foam, as well as more vigorous correction of secondary disorders.

When treating pulmonary edema, the following tasks are solved:

A. Reducing hypertension in the young circulation by:

Decreased venous return to the heart;

Decrease in circulating blood volume (CBV);

B. Increased contractility of the left ventricular myocardium when prescribed:

Antiarrhythmic drugs (if necessary).

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

D. Supporting activities.

Oxygen inhalation is prescribed through nasal cannulas or a mask in a concentration sufficient to maintain arterial blood pO2 more than 60 mmHg. Art. (can be done through alcohol vapor).

A special place in the treatment of pulmonary edema is occupied by the use of morphine hydrochloride intravenously, 2-5 mg, if necessary, again after a minute. Morphine relieves psychoemotional arousal, reduces shortness of breath, has a vasodilator effect, and reduces pressure in the pulmonary artery. It should not be administered if there is low blood pressure or 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 prescribed intravenously at the initial dose, if necessary, the dose is increased to 200 mg; or ethacrynic acidumg, bumetamide or Burinex 1-2 mg (1 mg = 40 mg Lasix). Diuresis occurs within minutes and lasts about 2 hours.

The administration of peripheral vasodilators (nitroglycerin) helps limit inflow to the heart, reduce total peripheral vascular resistance (TPVR), and increases the pumping function of the heart. It must be used carefully. The initial dose is 0.5 mg under the tongue (the mouth must be moistened first: there is wheezing in the lungs, dryness in the mouth!). Then, a 1% solution of nitroglycerin is injected intravenously at an initial rate of µg/min, followed by an increase in dose after 5 minutes, achieving a reduction in systolic blood pressure by 10-15% of the original, but not less than mm Hg. Art. Sometimes the dose is increased domkg/min depending on the level of initial arterial hypertension.

For high blood pressure, sodium nitroprusside is prescribed, which reduces pre- and afterload. Initial dose kg/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 ml of isotonic NaCl solution and administered intravenously under blood pressure control, hygronium mg in ml of 5% glucose solution or isotonic NaCl solution; pentamine 5% - 0.5-0.1 or benzohexonium 2% - 0.5-0.1 mL of isotonic NaCl solution or 5% glucose solution intravenously in a bolus with blood pressure monitoring through 1-2 ml of solution. Sometimes it is enough to administer until blood pressure normalizes. You need to keep mezaton or norepinephrine at the ready.

Cardiac glycosides are recommended for severe tachycardia and atrial fibrillation. Strophanthin 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 slowly intravenously in an isotonic NaCl solution or 5% glucose solution. After 1 hour, administration can be repeated until the full effect is achieved. Glycosides should not be administered in case of atrioventricular orifice stenosis, 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 circle 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 the emergency treatment of pulmonary edema should be recognized. However, after the acute phenomena of pulmonary edema have been 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 reduce the heart rate, beta blockers are sometimes used (propranolol - 1-2 mg intravenously in an isotonic NaCl solution or 5% glucose solution).

If pulmonary edema develops against the background of paroxysmal rhythm disturbances (atrial fibrillation, atrial flutter, ventricular tachycardia), emergency electrical pulse therapy is recommended.

With concomitant bronchospasm, aminophylline can be administered intravenously, and then intermittently every hour. The administration of aminophylline in patients with acute myocardial infarction is not recommended.

When pulmonary edema develops against the background of cardiogenic shock, dobutamine is used. This is a biological precursor of norepinephrine, stimulates alpha and to a lesser extent beta adrenergic receptors, specific dopamine receptors, increases cardiac output, and 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. 175 mcg/min is administered dropwise, gradually increasing the dose to 300 mcg/min. Side effects: extrasystole, tachycardia, angina.

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

In case of severe hypoxemia and hypercapnia, artificial pulmonary 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, if equipment is available, using isolated ultrafiltration at a rate of about 2000 ml/hour.

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

Bloodletting currently has more of a historical and medical significance 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 measures.

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

The method is implemented using the commercially produced device “NIMB-1”. A plastic bag of sufficient size (at least 40 x 50 cm) is connected to a flexible air tube to supply any breathing mixture or air. The second plastic tube connects the cavity of the bag with a pressure gauge with a scale from 0 to + 60 cm water column. From the source, compressed oxygen is supplied under ATI-5-7 atm to the injector of the “NIMB-1” apparatus, from where it is sent into the cavity of the bag in the form of a 1:1 oxygen-air mixture. After the mixture begins to be supplied 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 between the patient’s body and the wall of the bag there is a “leaks” gap that bleeds the supplied flow.

In patients with psychomotor agitation, a negative attitude towards the beginning of the session disappears after 1-2 minutes without the use of sedative therapy. This fact is quite clear: after stopping the session in the event of a repeated recurrence of respiratory failure, all patients asked for a repeat session, noting a rapid improvement in their subjective state during SD PPD. An increase in intrathoracic pressure during SD PPD sessions is used as the main factor that relieves pulmonary edema, limiting the flow of venous blood to the heart as a result of a decrease in the suction effect of the chest cavity, with a decrease in venous return and preload of the right parts of the heart. In addition, excess pressure + 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 SD 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 arterial blood increases along with the effect of obstructing the collapse of the alveoli, which manifests itself 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 SD PPD method in patients in the complex therapy of cardiogenic pulmonary edema. In this case, rapid normalization of central hemodynamic parameters occurs (in minutes). According to rheopulmonography, with the use of SD PPD in all patients, hypervolemia of the pulmonary circulation decreases, blood oxygenation improves, acid-base balance normalizes, cyanosis and shortness of breath are relieved more quickly, and within minutes diuresis appears. The alveolar phase of pulmonary edema resolves within minutes in most patients without the use of antifoam agents. In the control group this figure was minutes.

To prevent recurrence of alveolar edema, stopping SD PPD should be done gradually, with a stepwise decrease in pressure by 2-3 cm aq. Art. for a minute with exposure at each level for 5-15 minutes.

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

1. Respiratory regulation disorders - bradypnea or Cheyne-Stokes type breathing with long periods of apnea (over seconds), when artificial ventilation is indicated.

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

3. Severe disturbances in the contractile function of the right ventricle.

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

1. Alpert J., Francis G. Treatment of myocardial infarction. Per. from English M. "Practice". 1994, p. 255.

2. Guide to cardiology. (Edited by E.I. Chazov) M., 1982.

3. Radzevich A.E., Evdokimova A.G., Bezprozvanny A.B. and others. A method of treating pulmonary edema in patients with cardiovascular pathology. Materials of the 1st Congress of CIS Cardiologists. 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 scientific degree of Doctor of Science. honey. Sci. M., 1995, p. 33.

6. Belousov Yu.B., Moiseev V.D., Lepakhin V.K. Clinical pharmacology and pharmacotherapy. M., 1993, p..

7. Popov V.G., Topolyansky V.S., Lepakhin V.K. Pulmonary edema. M.: Medicine, 1975, p. 167.

Morphine for pulmonary edema

Pulmonary edema is a disease characterized by sudden onset due to the accumulation of fluid in the lungs. For this reason, a disruption of gas exchange processes in the body occurs, which causes hypoxia, cyanosis of the skin and severe suffocation.

Drugs

Pulmonary edema is an emergency condition, so at the first symptoms it is necessary to call an ambulance. Treatment is carried out in the intensive care unit, under the constant supervision of the doctor on duty.

A patient with pulmonary edema needs emergency medical care, which is provided during transportation to the hospital:

Place the patient in a semi-sitting position;
Oxygen therapy: applying a mask with oxygen or, if necessary, intubation of the lungs with artificial ventilation;
Apply venous tourniquets to the upper third of the thighs, but so that the pulse does not disappear (for no more than 20 minutes), the tourniquets are removed with gradual relaxation. This is done in order to reduce the flow to the right side of the heart to prevent further increases in pressure in the pulmonary circulation;
Nitroglycerin tablet under the tongue;
To relieve pain, intravenous administration of narcotic analgesics (Morphine 1% 1 ml);
Diuretics: Lasix 100 mg IV.

Treatment in the emergency department, treatment is carried out under strict constant monitoring of hemodynamics (pulse, blood pressure) and breathing. The attending physician prescribes treatment individually, depending on the clinic and the cause of pulmonary edema. The administration of almost all drugs is carried out through a catheterized subclavian vein.

Groups of drugs used for pulmonary edema:

Inhalation of oxygen in combination with ethyl alcohol is used to extinguish the foam that forms in the lungs;
Intravenous, drip administration of Nitroglycerin, 1 ampoule diluted with saline, the number of drops per minute depending on the level of blood pressure. Used in patients with pulmonary edema accompanied by high blood pressure;
Narcotic analgesics: Morphine - 10 mg IV, fractionally;
In case of pulmonary edema, accompanied by a decrease in blood pressure, Dobutamine or Dopamine drugs are administered to increase the force of heart contraction;
For pulmonary edema caused by pulmonary embolism, Heparin 5000 units is administered intravenously, then 1 unit per hour, diluted in 10 ml of saline, for an anticoagulant effect;
Diuretics: Furosemide initially 40 mg, repeat the dose if necessary, depending on diuresis and blood pressure;
If pulmonary edema is accompanied by a low heartbeat, Atropine up to 1 mg, Eufillin 2.4% - 10 ml are administered intravenously;
Glucocorticoids: Prednisolone mg IV infusion, for bronchospasm;
If there is insufficient protein in the blood, patients are prescribed an infusion of fresh frozen plasma;
For infectious processes (sepsis, pneumonia or others), broad-spectrum antibiotics (Ciprofloxacin, Imipenem) are prescribed.

How to treat

The treatment algorithm itself can be divided into 7 stages:

sedative therapy;
defoaming;
vasodilator therapy;
diuretics;
cardiac glycosides for cardiogenic edema and glucocorticoids for non-cardiogenic edema;
blood exfusion;
after relief of edema, hospitalization for treatment of the underlying disease.

To relieve 80% of cases of pulmonary edema, morphine hydrochloride, furosemide and nitroglycerin are sufficient.

Then therapy for the underlying disease begins:

The prognosis after pulmonary edema is rarely favorable. Survival requires observation for a year. Effective therapy for the underlying disease that caused pulmonary edema significantly improves the patient’s quality of life and prognosis.

Therapy for pulmonary edema primarily comes down to the removal of the edema itself. Therapy in a hospital is aimed at treating the disease that caused the swelling.

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Folk remedies

It should be noted that traditional medicine for pulmonary edema is advisable to use in the case when a person has undergone hospital treatment and is at home during rehabilitation.

Pulmonary edema can be effectively eliminated with the help of a decoction made from flax seeds. This tea is prepared from four tablespoons of flax, which should first be filled with one liter of boiled water. The entire mixture should be boiled over fire for three minutes. It can be consumed only after the decoction is cold. Next, you should strain it and drink half a glass two hours before meals. This procedure must be repeated at least six times a day.
Cardiogenic pulmonary edema can be eliminated with a decoction of cyanosis. This plant should be filled with hot, clean water. For the first preparation, he recommends taking one tablespoon of cyanosis. It should be cooked in a water bath. Don't forget to strain the broth before drinking. You should drink one sip after meals.

Complications such as pulmonary edema can be avoided by using medicinal herbs that have a positive effect on the body’s condition. Also, some decoctions are used for prophylactic purposes, in order to prevent the development of the disease at the initial stage. For this purpose, tea made from flax seeds and cherry stalks is often used. This composition should be taken four times a day for at least three months.

Remember that any traditional medicine can cause an allergic reaction in your body. This process can negatively affect the patient’s health and only worsen it.

Emergency care for swelling

Before the doctor arrives, you can do the following on your own:

Place the patient in a sitting or half-sitting position with legs down
Provide reliable access to a large peripheral vein (for subsequent catheterization)
Organize access to fresh air
Allow the patient to inhale alcohol vapors (96% for adults, 30% for children)
Take a hot foot bath
Use venous tourniquets on the limb (from 30 minutes to 1 hour)
Constantly monitor your breathing and pulse
In the presence of nitroglycerin and not low blood pressure - 1-2 tablets under the tongue.

Emergency care for pulmonary edema, provided by the ambulance team before arriving at the hospital, is as follows:

Oxygen therapy (active oxygen saturation)
Foam suction and anti-foam therapy (oxygen inhalation through ethyl alcohol solution)
Diuretic therapy (Lasix, Novurit) – removes excess fluid from the body; for low blood pressure, reduced doses of drugs are used
If there is pain, take painkillers (analgin, promedol)

Other drugs depending on blood pressure level:

high – ganglion blockers (promote blood outflow from the heart and lungs and flow to the extremities: benzohexonium, pentamine), vasodilators (dilate blood vessels: nitroglycerin)
normal – reduced doses of vasodilators
low – inotropic agents (increase myocardial contractility: dobutamine, dopmin).

Defoamers

With developing pulmonary edema (an increase in the number of moist rales, the appearance of bubbling breathing), antifoam agents can be used. Inhalation of ethyl alcohol vapor has a beneficial effect (the patient inhales oxygen from a cylinder through a catheter or mask inserted into the nose; instead of water, 96° alcohol is placed in the humidifier; the rate of oxygen administration is initially 2-3 l/min, then up to 9-10 l /min (procedure duration 30-40 minutes); if necessary, after a short break (10-15 minutes), the procedure can be repeated. The antifoam agent antifomsilan has proven itself well, giving an effect after 3-5 minutes.

In particularly severe cases of treatment of pulmonary edema with profuse discharge of foam from the mouth, alcohol can be urgently administered intratracheally by puncturing the trachea in the 1-2 interannular space (1 ml of 96° alcohol is administered, after which in most cases the release of foamy liquid decreases sharply). The question of the rationality of suctioning edematous fluid from the trachea remains controversial, since along with the release of the airways in this case, negative pressure is created in the airways and, as it were, a new influx of fluid into the alveoli is caused.

Morphine

For pulmonary edema, morphine is effective - 1 ml of a 1% solution intravenously as a bolus: it has a calming effect on the central nervous system, relieves pathological impulses of the overexcited respiratory center, and relieves the pulmonary circulation. The side effects of morphine - activation of the vomiting center and increased bronchospasm - are eliminated to some extent by a combination with 2 ml of droperidol. The administration of morphine is contraindicated in case of bronchospasm and in patients with low breathing volume (hypoventilation).