Pulmonary edema is pathological condition, which occurs suddenly and is accompanied by exudation of fluid from the capillaries into the interstitial tissue of the lungs and alveoli. This pathology leads to disruption of gas exchange and oxygen starvation of tissues and organs. It is manifested by severe suffocation, cough (at first dry, and then with copious amounts of pink frothy sputum), shortness of breath and cyanosis of the skin. In case of failure to provide emergency care, it can lead to death.

Pulmonary edema may debut with difficulty breathing and chest pain.

Pulmonary edema can be provoked by physical exertion, the transition of the body from a vertical to a horizontal position, or psycho-emotional arousal. In some cases, it can begin with precursors: rapid breathing, increasing shortness of breath and coughing with moist rales.

According to the rate of development, pulmonary edema can be:

• acute: develops within 2-3 hours;
• lightning fast: the death of the patient is caused by suffocation in a few minutes;
• protracted: develops over several hours or days.

At the beginning of an attack in a patient, fluid accumulates in the interstitial tissue of the lungs: interstitial pulmonary edema. This condition is accompanied by the following symptoms:

• pain or pressure in the chest;
• quickening of breathing;
• frequent cough without sputum;
• bronchospasm may occur;
• increasing with difficulty inhaling and exhaling;
• feeling of lack of air;
• tachycardia;
• increased blood pressure;
• cold clammy sweat;
• severe pallor;
• growing weakness;
• increased sweating;
• anxiety.

The patient seeks to take a forced position: he sits on the bed, his legs dangling, and rests on outstretched arms. With the transition of fluid into the alveoli and the onset of alveolar pulmonary edema, the patient's condition worsens significantly:

• shortness of breath increases, breathing becomes bubbling;
• suffocation increases;
• the skin acquires a bluish-gray tint;
• the cough gets worse;
• foamy pink sputum appears;
• veins in the neck swell;
• increases (up to 140-160 beats per minute);
• the pulse becomes weak and thready;
• possible decrease in blood pressure;
• the patient is afraid of death;
• confusion appears;
• in the absence of adequate assistance, the patient may fall into a coma.

During an attack, a violation of the integrity of the respiratory tract can occur and death can occur.

After stopping an attack of pulmonary edema, the patient may develop severe complications:

• pneumonia and bronchitis (due to the addition of a secondary infection);
• disorders of cerebral circulation;
• segmental atelectasis;
• pneumofibrosis;
• ischemic lesions of organs and systems.

First aid emergency

1. At the first signs of pulmonary edema, the patient or his environment should call ambulance.
2. Give the patient a semi-sitting or sitting position with legs down.
3. Ensure sufficient flow fresh air, open windows and air vents, remove clothing that restricts breathing from the patient.
4. Constantly monitor breathing and pulse.
5. Measure (if possible) arterial pressure.
6. Immerse the patient's legs in hot water.
7. Apply a tourniquet to the thigh for 30-50 minutes, then apply it to the other thigh.
8. Carry out inhalation of alcohol vapors (for adults 96%, for children 30%).
9. At a pressure not lower than 90 mm. rt. Art. give the patient a Nitroglycerin tablet under the tongue.
10. Have the patient take a Furosemide (Lasix) tablet.

Emergency medical care

After the arrival of the ambulance, the patient is injected intravenously with a narcotic analgesic (Morphine, Promedol), Lasix and Nitroglycerin. During transport to the hospital, the following activities are performed:

Emergency care and treatment in a hospital setting

Treatment of pulmonary edema in the emergency department is carried out under constant monitoring of blood pressure, pulse and respiratory rate. Most drugs are administered through a catheter into subclavian vein. The treatment regimen is determined for each patient individually, depending on the causes that caused pulmonary edema.

The complex of treatment may include such drugs and activities:

During the treatment of pulmonary edema, the patient must adhere to a restricted diet. table salt, liquids and fats, completely exclude respiratory and physical stress. After the course of treatment of the underlying disease, the patient must be under outpatient medical supervision.

ALGORITHM FOR PROVIDING EMERGENCY AID. ACUTE LEFT VENTRICULAR FAILURE

Acute left ventricular failure (ALHF) manifests itself in the form of cardiac asthma and pulmonary edema. First, fluid accumulates in the interstitial tissue of the lung (in the interstitial gaps) - cardiac asthma. and then the edematous fluid sweats into the alveoli - pulmonary edema. In this way, cardiac asthma and pulmonary edema are two successive phases of acute left ventricular failure.

The cause of acute left ventricular failure may be heart disease (cardiac OLZHN). It develops in connection with a decrease in the contractility of the left ventricular myocardium with coronary artery disease, mitral stenosis, arrhythmias, aortic heart disease, cardiomyopathies, and severe myocarditis.

extracardiac acute left ventricular failure occurs due to overload of the heart with increased BCC and blood pressure in hypertension, symptomatic hypertension, chronic renal failure.

Factors that provoke an attack: 1. psycho-emotional stress, 2. inadequate physical activity, 3. weather change 4. geomagnetic disturbances, 5. excess salt in food 6. drinking alcohol, 7. taking corticosteroids, anti-inflammatory non-steroids, sex hormones, 8. pregnancy, 9. premenstrual syndrome, 10. violation of urodynamics, 11. exacerbation of any chronic disease, 12 cancellation of cardiotonic, b-blockers.

Clinic: paroxysm of cardiac asthma occurs more often at night or during the day in the supine position. Inspiratory dyspnea appears (RR up to 30-40 per minute), turning into suffocation, which makes the patient sit or stand up. The face is pale and then bluish, covered with sweat, contorted with fear. The attack is accompanied by a cough with copious liquid sputum. Speech is difficult due to coughing. Hand tremors and hyperhidrosis are observed. On auscultation, moist rales over the entire surface of the lungs. The appearance of bubbling breath and cough with pink frothy sputum indicates the onset of pulmonary edema.

Complications: 1. cardiogenic shock, 2. asphyxia.

Differential Diagnosis carried out with an attack bronchial asthma and other variants of broncho-obstructive syndrome.

EMERGENCY AID ALGORITHM

Pulmonary edema, emergency care

Pulmonary edema- severe pathological condition sweating of plasma, blood into lung tissue. leads to respiratory failure.

It is observed in acute and chronic heart failure, pneumonia, coma, brain tumors, anaphylactic shock, Quincke's edema, poisoning, head and chest injuries, intracranial hemorrhages, plague and other infectious diseases.

Clinic

Shortness of breath, cough, bubbling breath, frothy sputum with blood, a feeling of constriction and pain in the heart, anxiety, agitation, pale skin, cold sticky sweat, cyanosis, auscultatory - an abundance of moist rales in the lungs, dullness of percussion sound.

Urgent care

1. Give the patient a semi-sitting position.

2. Suction mucus from the upper respiratory tract.

3. Carry out inhalation with vapors of 70% ethyl alcohol.

4. Apply a tourniquet to the lower limbs.

5. According to the doctor's prescription, enter: 1% solution of lasix - 4.0 intravenously or intramuscularly, if there is no effect, again after 20 minutes, increasing the dose, 2.4% solution of aminophylline - 10 ml intravenously by stream, 0.05% solution of strophanthin - 0 5-1 ml in an isotonic solution of sodium chloride intravenously bolus slowly.

6. Prednisolone 60 mg intravenously.

7. 5% solution arfonade- 100 ml per 200 ml of isotonic solution intravenously drip slowly.

8. 0.25% solution of droperidol - 2.0 in 20% glucose solution intravenously by bolus.

9. 2.5% solution of a mixture of chlorpromazine - 0.5 ml, 2.5% solution of pipolfen - 1.0 ml intravenously by bolus in 20 ml of 40% glucose solution.

10. 5% solution of ascorbic acid - 4 ml, 1% solution nicotinic acid- 1 ml.

11. 4% sodium bicarbonate solution - 2 mg/kg intravenously by bolus.

12. 7.5% solution of potassium chloride - 15-20 ml intravenously drip.

Pulmonary edema

Pulmonary edema is an excessive accumulation of fluid in the extravascular space of the lungs, accompanied by a violation of gas exchange and acute respiratory failure.

Classification

The modern classification of pulmonary edema is based on differences in its pathogenesis. Two main types can be distinguished:

• cardiogenic or hydrostatic
• non-cardiogenic, or edema due to increased permeability of the alveolar membrane
• mixed forms of edema (usually neurogenic)
• pulmonary edema due to other, rarer causes

The reasons

Increased pulmonary capillary transmural pressure.

• Left ventricular failure, acute or chronic.
• Myocardial infarction or ischemia.
• Severe hypertension.
• Aortic stenosis or insufficiency.
• Hypertrophic cardiomyopathy.
• Myocarditis.
• Mitral valve stenosis or severe mitral regurgitation.
• Over-infusion therapy.

Increased permeability of the endothelium of the pulmonary capillaries.

• Infection (bacteremia, sepsis).
• Inflammation.
• Disseminated intravascular coagulation.
• Allergic reaction.
• Iatrogenic damage (opiates, salicylates, chemotherapy, radiopaque drugs).
• ARDS.

Increased permeability of the alveolar epithelium.

• Inhalation of toxic substances.
• Allergic reaction.
• Aspiration, drowning.
• Surfactant deficiency.

Decreased plasma oncotic pressure.

• Hypoalbuminemia.
• nephrotic syndrome.
• Liver failure.

Impaired outflow of plasma.

• Lymphangitis.
• After lung transplant.

mixed mechanism.

• Neurogenic pulmonary edema.
• Altitude sickness.
• Postoperative pulmonary edema.

Knowing the cause of pulmonary edema is important when choosing priority treatments. Questions clinical physiology, diagnosis and treatment of non-cardiogenic pulmonary edema are similar to those of ARDS.

Clinical physiology of pulmonary edema

According to Starling's law, the movement of fluid from the capillaries to the interstitium and vice versa depends on the difference in hydrostatic and oncotic pressures on both sides of the vascular wall, as well as on the permeability of the wall itself.

Initially, when the CVL increases due to the interstitium of the lungs, hypoxia occurs without hypercapnia, which is easily eliminated by oxygen inhalation, since it is associated only with a thickening of the alveolo-capillary membrane and a violation of the diffusion of gases through it. If, despite the inhalation of oxygen, hypoxemia persists, then this is due to the onset of alveolar shunting of the blood.

Due to mucosal edema, the lumen of the respiratory tract narrows, and the bronchioles lose their elasticity, an alveolar shunt develops, which increases respiratory failure.

In addition, increased muscle effort is required to open the blood-filled, edematous lungs. At the same time, the work of the respiratory muscles increases and the oxygen price of respiration increases. Hypoxia intensifies, therefore, the permeability of the alveolocalillary membrane increases even more, and fluid extravasation may occur, i.e. pulmonary edema. Hypoxemia-associated catecholaminemia blocks lymphatic drainage - lung stiffness increases even more.

In all patients with decompensated left ventricular failure, a functional study reveals signs of obstructive and restrictive disorders:

• static volumes of the lungs, including their total capacity, are reduced;
• forced expiratory volume is usually no more than half of the proper value;
• indicators of the curve "flow - maximum expiratory volume" are sharply reduced.

As pulmonary edema develops, plasma extravasation occurs, and then the main mechanism of respiratory failure is the blockage of the airways by foam, which is formed when plasma foams in the atveoli. The same pricing serves as the main physiological mechanism for respiratory failure in normal (non-cardiogenic) pulmonary edema, although intensive care for these respiratory forms varies significantly.

Emergency Diagnostics

Pulmonary edema may be due to various reasons, but it is not easy to differentiate them due to similar symptoms.

Symptoms of pulmonary edema are not specific. Most often, pronounced shortness of breath is noted as a manifestation of interstitial edema, tachypnea, cyanosis, participation of auxiliary muscles inhalation, i.e. Clinical signs respiratory failure. At the first stage of pulmonary edema, auscultation reveals dry rales of narrowing of the airways against the background of peribronchial edema. As the edema develops, moist rales appear, more pronounced in the basal regions.

Chest x-ray should be performed for everyone with pulmonary edema, it allows you to identify the phases of interstitial and alveolar edema, changes in the size of the heart.

The diagnostic accuracy of chest x-ray in pulmonary edema is limited for a number of reasons. First, swelling may not be visible until the amount of fluid in the lungs has increased by 30%. Secondly, many of the X-ray signs are not specific, and may be characteristic of other pulmonary pathologies. Finally, one cannot ignore the technical difficulties, including respiratory movements, patient position, positive pressure ventilation.

Echocardiography evaluates myocardial function, the condition of the valves, helping to determine the cause of pulmonary edema. Doppler echocardiography can assess diastolic pressure and reveal diastolic dysfunction.

Diagnostic algorithm for pulmonary edema

We present a diagnostic algorithm for managing a patient with pulmonary edema in emergency pulmonology.

Stage I - Anamnesis, physical examination, laboratory examination

Stage II - Chest X-ray

If the diagnosis is not clear

Stage III - Transthoracic or transesophageal echocardiography

emergency therapy

Elimination of the factors that cause pulmonary edema is an obligatory component of treatment tactics.

Elimination of feelings of fear, catecholaminemia with the help of neuroleptics is an important universal measure. intensive care with pulmonary edema.

Intensive care measures can be divided into the following groups:

• defoaming;
• elimination of plethora;
• increase in cardiac output;
• stimulation of diuresis;
• respiratory therapy.

Since pulmonary edema is a critical condition requiring urgent life support measures, the listed measures sometimes have to be performed against the background of mechanical ventilation and oxygen therapy.

Defoaming

If foaming in the lungs and airways is severe, defoaming is considered the most urgent measure. The most studied means for this purpose is inhalation of ethyl alcohol vapors.

Since ethyl alcohol can cause bronchospasm, oxygen is first given, which "bubbles" through 96% ethyl alcohol and is added through a catheter to the mixture inhaled by the patient. If there is no negative reaction, you can try aerosol inhalation of 30-60% alcohol for 2-3 minutes with monitoring of effectiveness after each session.

Defoaming can also be achieved by intravenous administration of 30-40% ethanol (15-30 ml). Alcohol is released into the alveoli and quenches the foam.

Eliminate pulmonary congestion and increase cardiac output

To do this, it is necessary to increase the output of the left ventricle: normalize the levels of plasma and cellular potassium, eliminate metabolic acidosis, and use cardiac glycosides already against this background.

Morphine is used to reduce peripheral resistance. At the same time, the configuration of the left ventricle changes, which makes its contractions more efficient, and the volume of blood is redistributed from the pulmonary circulation to the large one. However, this effect of morphine occurs at significant doses that depress respiration.

In intensive care, the initial level of blood pressure is of particular importance. The choice of inotropic support in patients with pulmonary edema directly depends on the level of blood pressure.

The level of arterial pressure serves both as an indicator of the effectiveness of treatment and as a prognostic indicator. When it is elevated, the efficacy of treatment is high, and a positive result occurs quite quickly with the infusion of sodium nitroprusside and other vasodilators. Baseline low blood pressure is an unfavorable prognostic sign, since the use of dopamine in these patients to maintain sufficient tissue perfusion may exacerbate left ventricular failure.

Stimulation of diuresis

Furosemide is used, which helps to reduce VOVL, which reinforces the beneficial effect of previous measures.

The lungs become less rigid, their opening requires less effort of the respiratory muscles, oxygen homeostasis improves, which means that the permeability of the alveolo-capillary membrane and interstitial pulmonary edema decrease.

Respiratory Therapy

The primary measure is the inhalation of oxygen in combination with spontaneous ventilation in the PEEP mode. These regimens increase intrapulmonary pressure, decrease lung congestion, and improve lung compliance. The gas exchange area increases, sputum evacuation is facilitated, i.e. the main mechanisms of respiratory failure are eliminated.

If the PEEP mode is ineffective during spontaneous ventilation for 30-60 minutes, mechanical ventilation should be performed. The level of PEEP during mechanical ventilation with pulmonary edema must be at least 8 cm of water.

Emergency Help - Algorithm

When foaming in the lungs, inhalation of ethyl alcohol vapors is indicated, and if bronchiolospasm does not occur on them, short-term (2-3 minutes) inhalation of an aerosol of 30-60% ethyl alcohol is carried out.

To reduce the plethora of the lungs, cardiac glycosides are shown after the normalization of the acid-base and electrolyte state, dobutamine.

To lower peripheral vascular resistance - morphine, nitrates under the control of blood pressure.

PEEP mode during spontaneous breathing - early non-invasive respiratory support.

With its insufficient efficiency - IVL through an endotracheal tube in a moderate PEEP mode.

Call a doctor to provide qualified assistance.

Assume a sitting position with legs lowered to facilitate breathing.

Provide suction of sputum to facilitate breathing.

Provide inhalation of oxygen through ethyl alcohol vapors in order to reduce hypoxia and foaming.

Apply venous tourniquets to 3 limbs to reduce blood flow to the heart and lungs (as prescribed by a doctor).

Provide sublingual nitroglycerin every 7-10 minutes to reduce pressure in pulmonary artery(under the control of blood pressure).

According to the doctor's prescription, prepare lasix, morphine, strophanthin, nitroglycerin for intravenous administration (in order to stop pulmonary edema).

Control of appearance sick; Respiratory rate, pulse, blood pressure according to the manipulation algorithm.

1.7 Features of treatment

I-initial

healthy lifestyle

dieting

II-expressed clinical manifestations

exclusion of physical education and physical work.

digitalis preparations

prescribe thiazide diuretics or non-thiazide sulfonamides

III-terminal

home mode shown

limit salt intake

cardiac glycosides

angiotensin-converting enzyme inhibitors

Assign a set of measures aimed at creating living conditions that help reduce the load on cardiovascular system, as well as muscle and disturbed water-salt metabolism. The volume of activities carried out is determined by the stage chronic insufficiency circulation.

Common measures include limiting exercise and dieting.

With CHF stage I exercise stress not contraindicated, light physical work is acceptable, including physical education without significant stress. With CHF stage II, physical education and physical work are excluded. A reduction in working hours and the introduction of extra day recreation. Patients with stage III CHF are shown at home, and with the progression of symptoms, half-bed rest. Sufficient sleep is very important (at least 8 hours a day).

With CHF stage II, you should limit the intake of table salt with food (the daily dose should not exceed 2-3 g). A salt-free diet (no more than 0.5-1.0 g per day) is prescribed for stage III CHF. With the development of CHF, alcohol, strong tea and coffee are excluded - drugs that stimulate the work of the heart.

Drug therapy is aimed at enhancing contractile function and removing excess water and sodium ions from the body.

To enhance the contractile function of the heart, cardiac glycosides are prescribed (digital preparations, strophanthin, corglicon). Strofantin and corglicon are administered intravenously only in cases of exacerbation of CHF, when the effect must be obtained immediately. In other cases, it is better to treat with digitalis preparations (isolanide, digoxin), appointing them inside. In stage III CHF, it is also preferable to administer intravenously strophanthin, corglicon, since the drug taken orally is poorly absorbed from gastrointestinal tract and exacerbates dyspepsia.

To facilitate the work of the heart, the so-called angiotensin-converting enzyme inhibitors are successfully used (it was previously indicated that drugs of this group are also used in the treatment of hypertension). In chronic heart failure, the drugs of this group (enalapril, ramipril, lisinopril) are used in doses of 2.5-40 mg per day (in this case, the possibility of a significant decrease in blood pressure should be taken into account, which makes it necessary to reduce the dose of the drug). In addition, these drugs are not used for some heart defects (mitral stenosis, aortic stenosis).

Removal of excess water and sodium from the body is achieved by using a salt-restricted diet. However, the most important means of achieving this goal is the use of various diuretic drugs. There are various groups of drugs, the use of which depends on the severity of CHF and the patient's individual response to them. In stage I CHF, diuretics are not prescribed. In stage II, thiazide diuretics (gripothiazide) or non-thiazide sulfonamides (brinaldix) are prescribed. Frequent use of these drugs can disrupt electrolyte metabolism (hypokalemia and hyponatremia), and therefore they should be combined with triamterene, a diuretic agent that retains potassium in the body. The combined drug triamnur containing triamterene and hypothiazide is quite suitable in terms of its strength for patients with stage II CHF. If such diuretic therapy is not very effective, then strong diuretics are prescribed - furosemide or uregit. Doses of diuretics should not be too high, so as not to cause a large release of fluid from the body.

More with CHF stage I are able-bodied, with stage II, the ability to work is limited or lost. Patients with stage III CHF need constant care, the use of medications and the need for timely information about them from medical personnel.

1.8 Prevention, prognosis

Prevention of CHF includes three aspects:

1) primary prevention of diseases leading to the development of heart failure (meaning the primary prevention of rheumatism, hypertensive disease, coronary disease etc.);

2) prevention of the development of CHF with existing heart diseases (heart disease, hypertonic disease, ischemic disease);

3) prevention of repeated decompensations in already developing heart failure.

Disease prognosis.

The prognosis of patients with heart failure is still one of the worst, although this is rarely recognized by practitioners. According to the Framingham study in 1993, the average 5-year mortality in the entire population of patients with CHF (taking into account the initial and moderate stages) remains unacceptably high and amounts to 65% for men and 47% for women. Among patients with severe stages of CHF, mortality is even higher and ranges from 35-50% for one year, 2-year-old is 50-70%, and 3-year-old exceeds 70%.

2. Nursing process

2.1 Manipulations performed by a nurse.

Intravenous drip infusion

Equipment: an additional disposable needle, sterile trays, a tray for used material, sterile tweezers, 70 ° C alcohol or other skin antiseptic, sterile cotton balls (napkins), tweezers (in a stem eye with disinfectant), containers with a disinfectant, for soaking waste material, gloves, drug ampoules, tourniquet, oilcloth pad, bandage, IV drip system, drug bottle.

Preparation for the procedure

Clarify the patient's awareness of the drug and his consent to the injection.

Check Availability allergic reaction for a medicinal product. ask the patient to go to the toilet.

Wash and dry hands.

Prepare equipment.

Remove sterile trays, tweezers from the package..

Prepare 5-6 cotton balls, moisten them with skin antiseptic in a tray.

Using non-sterile tweezers, open the cap covering the rubber stopper on the vial.

Wipe the cap of the bottle with one cotton ball with an antiseptic.

Discard the used cotton ball in the waste tray.

Check the expiration date of the IV drip system.

Open the package with scissors, remove the system from the package, close the system clamp, remove the cap from the needle inserted into the vial, insert the needle into the vial stopper until it stops, fix the vial on the tripod.

Fill the system for intravenous drip infusion (until the air is completely expelled).

Check the patency of the needle.

3 pieces of plaster up to 10 cm long should be fixed on a tripod.

Performing a procedure

Place an oilcloth pad under the patient's elbow (for maximum extension of the limb in elbow joint.

Put on gloves.

Treat the inner surface of the elbow twice (in the direction from the periphery to the center), determining the direction of the vein, successively with two cotton balls (napkins) with a skin antiseptic; the patient at the same time compresses and unclenches the brush.

Remove the cap from the needle and puncture the vein as usual (while the patient's hand is clenched into a fist).

When blood appears from the cannula of the needle, remove the tourniquet.

Open the clamp, attach the system to the needle cannula.

Adjust the screw clamp the rate of drops according to the doctor's prescription.

Secure the needle with adhesive tape and cover it with a sterile napkin.

Remove gloves, wash hands.

Monitor the condition and well-being of the patient throughout the drip infusion procedure.

End of procedure

Wash and dry hands.

Put on gloves.

Intravenous technique

Equipment: a disposable syringe with a needle, an additional disposable needle, sterile trays, a tray for used material, sterile tweezers, 70 ° C alcohol or other skin antiseptic, sterile cotton balls (napkins), tweezers (in a stem eye with a disinfectant), containers with a disinfectant, for soaking waste material, gloves, drug ampoules, tourniquet, oilcloth pad, bandage.

intravenous injection

I. Preparation for the procedure

Clarify the patient's awareness of the drug and his consent to the injection. If you are not informed, check with your doctor for further tactics.

Explain the purpose and course of the forthcoming procedure.

Find out if you have an allergic reaction to a drug.

Wash the hands.

Prepare equipment.

Check the name, expiration date of the medicinal product.

Remove sterile trays, tweezers from the packaging.

Collect a disposable syringe.

Prepare 4 cotton balls (napkins), moisten them with skin antiseptic in a tray.

File the ampoule with the drug with a special nail file.

Wipe the ampoule with one cotton ball and open it.

Discard the used cotton ball with the end of the ampoule into the waste tray.

Draw up the drug from the ampoule into the syringe, change the needle.

Put the syringe in the tray and transport it to the ward.

Help the patient to take a comfortable position for this injection.

II. Performing a procedure

Place an oilcloth pad under the patient's elbow (for maximum extension of the limb in the elbow joint).

Apply a rubber tourniquet (on a shirt or napkin) in the middle third of the shoulder, while the pulse on the radial artery should not change. Tie the tourniquet so that its free ends point up and the loop down.

Ask the patient to squeeze and unclench the brush several times.

Put on gloves.

Treat the inner surface of the elbow bend twice (in the direction from the periphery to the center), determining the direction of the vein.

Take the syringe: fix the cannula of the needle with the index finger, cover the cylinder from above with the rest.

Check the absence of air in the syringe (if there are a lot of bubbles in the syringe, shake it, and small bubbles will merge into one large one, which is easy to force out through the needle into the cap, but not into the air). Remove the cap from the needle.

Pull the skin with your left hand in the area of ​​the elbow, slightly shifting it in the periphery to fix the vein.

Without changing the position of the syringe in your hand, hold the needle with the cut up (almost parallel to the skin), pierce the skin, carefully insert the needle 1/3 of the length parallel to the vein.

Continuing to fix the vein with the left hand, slightly change the direction of the needle and carefully puncture the vein until “hitting in the void” is felt.

Make sure that the needle is in the vein: pull the plunger towards you - blood should appear in the syringe.

Untie the tourniquet with the left hand, pulling on one of the free ends, ask the patient to unclench the hand.

Without changing the position of the syringe, press the plunger with your left hand and slowly inject the drug solution, leaving 1-2 ml in the syringe.

III. End of procedure

Press a cotton ball (napkin) with a skin antiseptic to the injection site, remove the needle; ask the patient to bend the arm at the elbow joint (you can fix the ball with a bandage).

Put the syringe in the tray without putting a cap on the needle.

Take from the patient (after 5-7 minutes) a cotton ball, with which he pressed the injection site. Do not leave a cotton ball contaminated with blood with the patient. Place the ball in the waste tray.

Clarify the patient's condition.

Disinfect used equipment in separate containers for the duration of the exposure.

Remove gloves, soak them in a disinfectant solution for the duration of the exposure.

Wash and dry hands.

Oxygen Therapy Technique

Equipment: sterile catheter, humidifier, distilled water, oxygen source with flow meter, sterile glycerin, adhesive plaster.

Preparation for the procedure.

Clarify with the patient or his relatives the understanding of the purpose of oxygen therapy, the consequences of the procedure and obtain their consent.

Wash the hands.

Execution of a procedure.

Open the package, remove the catheter and moisten it with sterile glycerin.

Insert the catheter into the lower nasal passage to a depth equal to the distance from the earlobe to the wings of the nose.

Secure the catheter with adhesive tape so that it does not fall out and cause discomfort.

Attach the catheter to a source of humidified oxygen at a given concentration and delivery rate.

Allow sufficient freedom of movement for the catheter and oxygen tubes and secure them to clothing with a safety pin.

Check the condition of the catheter every 8 hours.

Ensure that the humidifying vessel is constantly full.

Examine the patient's nasal mucosa for possible irritation.

End of procedure.

Every 8 hours Check oxygen flow rate, concentration.

Note the method, concentration, rate of oxygen delivery, patient response, and the results of the final assessment of meeting the patient's need for normal breathing.

Technique for determining the water balance

Equipment: medical scales, a graduated glass container for collecting urine, a sheet of water balance.

Preparation for the procedure.

Make sure the patient is able to take fluid counts. It is necessary to realize participation in joint work.

Explain to the patient the need to comply with the usual water-food and motor regimen. Special training is not required.

Ensure that the patient has not taken diuretics for 3 days prior to the study.

Give detailed information about the order of entries in the water balance sheet. Make sure you can complete the sheet.

Explain the approximate percentage of water in food to facilitate the accounting of the injected fluid (not only the water content of the food is taken into account, but also the injected parenteral solutions).

Execution of a procedure.

Explain that at 6 p.m. urine must be emptied into the toilet.

Collect urine after each urination in a graduated container, measure diuresis.

Fix the amount of allocated metering fluid.

Record the amount of fluid that has entered the body on a record sheet.

At 6 o'clock hand over the registration sheet to the nurse the next day.

End of procedure.

The nurse should determine how much fluid should be excreted in the urine (normal); tell the patient.

Compare the amount of excreted fluid with the amount of calculated fluid (normal).

Make entries in the water balance sheet.

Artificial lung ventilation

Algorithm of measures for hypotension, shock and pulmonary edema

* 1 Inject bolus 250-500 ml of isotonic sodium chloride solution, if blood pressure does not rise, adrenomimetics are prescribed.

*2 Norepinephrine is discontinued when blood pressure returns to normal.

*3 Dobutamine should not be given if Adsyst.< 100 мм рт.ст.

*4 If 1st line therapy fails, move on to 2nd line therapy. Stage 3 therapy is a reserve for patients who are refractory to previous therapy, with specific complications that exacerbate acute heart failure.

*5 Nitroglycerin is used if acute myocardial ischemia and BP remain elevated.

SPECIAL SECTION

The algorithm for carrying out an event to restore adequate cardiac activity in case of sudden circulatory arrest is presented in the diagrams and comments below. It should be borne in mind that it is permissible to make changes to the specialized resuscitation program in accordance with the clinical situation.

In this section, the problem of resuscitation of patients in whom circulatory arrest is caused by VF is described in most detail, since the latter is the most common cause of sudden cardiac death, and other aspects of emergency cardiology are also covered.

CPR for ventricular fibrillation

VF is characterized by disparate and multidirectional contractions of myocardial fibers, leading to complete disorganization of the work of the heart as a pump and almost immediate cessation of effective hemodynamics. VF can occur in acute coronary insufficiency, drowning in fresh water, electric shock and lightning, hypothermia. Some medications, especially adrenomimetics (adrenaline, norepinephrine, orciprenaline, isadrin), antiarrhythmic drugs (quinidine, amiodarone, ethacizine, mexiletine, etc.), can cause life-threatening arrhythmias. VF can occur during intoxication with cardiac glycosides and develop against the background of electrolyte disturbances and acid-base imbalance (hypo- and hyperkalemia, hypomagnesemia, hypercalcemia, acidosis and alkalosis), hypoxia, during anesthesia, operations, endoscopic studies, etc. VF can be manifestation of terminal disorders in serious illnesses heart and other organs.

Diagnosis of VF and its stages is based on the ECG method. The precursors of VF, which in some cases can play the role of a trigger mechanism, include early, paired, polytopic ventricular extrasystoles, jogging ventricular tachycardia. Special prefibrillatory forms of ventricular tachycardia include: alternating and bidirectional, polymorphic ventricular tachycardia in congenital and acquired interval lengthening syndrome Q-T and at its normal duration.

FJ stages. Stage I VF is characterized by a relatively regular rhythm of the main fibrillar oscillations (amplitude of about 1 mV), which form characteristic “spindle” figures. The frequency of oscillations is more than 300 per 1 min, but can exceed 400 per 1 min. The duration of stage I is 20-40 s. Stage II is determined by the gradual disappearance of "spindles" and a decrease in the amplitude and frequency of the main rhythm of oscillations. The duration of stage II is 20-40 s. Stage III is characterized by a further decrease in the amplitude and frequency of oscillations, often resembling a frequent idioventricular rhythm (amplitude more than 0.3 mV, but less than 0.7 mV). The frequency of oscillations is about 250-300 per 1 min. The duration of the stage is 2-3 minutes. IV stage - ordered fluctuations disappear. Duration 2-3 min. Stage V is a low-amplitude arrhythmic oscillation (amplitude more than 0.1 mV, but less than 0.3 mV). It is important to note that VF amplitude correlates with defibrillation efficiency.

Often, when registering an ECG from the electrodes of a defibrillator, VF may look like asystole. Therefore, in order to avoid a possible error, it is necessary to verify this by changing the location of the electrodes, moving them 90 ° relative to the original location. An important point for successful defibrillation is the correct location of the electrodes: one electrode is placed in the region of the right edge of the sternum under the clavicle, the second - the lateral left nipple along the mid-axillary line. During defibrillation, a special electrically conductive gel or gauze moistened with a saline solution is used to reduce the electrical resistance of the chest. It is necessary to ensure a strong pressing of the electrodes to the surface of the chest (pressure force should be about 10 kg). Defibrillation must be carried out in the expiratory phase (in the presence of respiratory excursions of the chest), since transthoracic resistance in these conditions decreases by 10-15%. During defibrillation, none of the resuscitation participants should touch the bed and the patient.

by the most effective way termination of VF is electrical defibrillation. Conducted indirect heart massage and mechanical ventilation are temporary, but necessary support, providing a minimum perfusion pressure in the vital organs.

The electrical discharge leads to a short-term asystole, during which the myocardium becomes electrophysiologically homogeneous, i.e. capable of responding to its own pacemaker impulses with correct electrical activity and coordinated mechanical contractions. The effectiveness of defibrillation depends on the duration of VF, the initial functional state of the myocardium, previous antiarrhythmic therapy, and the shape of the electrical impulse (Table 2). For effective defibrillation of the ventricles by defibrillators with a bipolar pulse shape (DKI-N-02, DKI-A-06, DIS-04, Definar-01, VR-5011CA), approximately 2 times less energy is required than in cases of using monopolar discharge (all models of defibrillators manufactured by firms in the USA, Europe and Japan). In table. 2a shows the energy values ​​for fixed dose defibrillators with a bipolar pulse shape.

In patients with extensive myocardial infarction and a complicated course in the form of cardiogenic shock or pulmonary edema, as well as in patients with severe chronic heart failure, the elimination of VF is often accompanied by its recurrence or the development of EMD, severe bradycardia, asystole. This is especially often observed in cases of using defibrillators that generate monopolar pulses. In table. 3-6 shows the algorithms for the treatment of EMD, asystole, brady- and tachycardia, in table. 7 - cardioversion (in patients without cardiac arrest), in table. 8 - treatment of hypotension, shock and pulmonary edema.

The sequence of measures to restore cardiac activity in VF is now quite well known. The algorithm for carrying out diagnostic and therapeutic measures is given in Table. 1 and 2. The main criterion for potentially successful resuscitation and full recovery of patients is early defibrillation, i.e. during the first 8 minutes of VF, provided that mechanical ventilation and heart massage are started no later than the 4th minute. In the absence of severe myocardial hypoxia in the case of primary VF, defibrillation alone, carried out within 30–90 s from the onset of VF, can lead to recovery effective work hearts. In this regard, the technique of blind defibrillation is justified.

After the restoration of cardiac activity, monitoring is necessary for subsequent timely and adequate therapy. In some cases, so-called post-conversion rhythm and conduction disturbances can be observed (migration of the pacemaker through the atria, junctional rhythm or lower atrial, dissociation with interference, incomplete and complete atrioventricular blockade, atrial, nodal and frequent ventricular extrasystoles). In case of occurrence paroxysmal tachycardias urgent measures are taken, as set out in Table. 6 and 7. The algorithm of measures for concomitant phenomena of hypotension and shock is presented in Table. eight.

Recurrent VF. In the event of VF recurrence, defibrillation should begin with a shock energy that was previously successful.

Prevention of the recurrence of VF in acute diseases or lesions of the heart is one of the priorities after the restoration of effective cardiac activity. Preventive therapy for recurrent VF should be differentiated as far as possible. Most common causes recurrent. and refractory VF:

respiratory and metabolic acidosis due to inadequate CPR, respiratory alkalosis, unreasonable or excessive administration of sodium bicarbonate, excessive exogenous and endogenous sympathetic or, conversely, parasympathetic stimulation of the heart, leading, respectively, to the development of prefibrillatory tachycardia or bradycardia; initial hypo- or hyperkalemia, hypomagnesemia; toxic effect of antiarrhythmic drugs; frequent repeated discharges of the defibrillator with a monopolar maximum energy pulse shape.

The use of antiarrhythmic drugs for the prevention and treatment of VF. When determining the tactics of preventive therapy, special importance should be given to the effectiveness of the drug, the duration of its action and the assessment possible complications. In cases where VF is preceded by frequent ventricular extrasystole, the choice of drug should be based on its antiarrhythmic effect.

1. Lidocaine (Xycaine) has been considered the drug of choice for VF prevention over the past 20 years. However, at present, significant prospective studies have not revealed unambiguous data on its sufficiently high efficacy specifically for the prevention of VF. A number of large studies indicate frequent complications and increased mortality in acute myocardial infarction from asystole. Currently, lidocaine is recommended for: a) frequent early, paired and polymorphic extrasystoles, in the first 6 hours of acute myocardial infarction; b) frequent ventricular extrasystoles, leading to hemodynamic disturbances; c) ventricular tachycardia or their jogging (over 3 in 1 hour); d) refractory VF; e) for the prevention of recurrent VF. Scheme of administration: bolus 1 mg/kg for 2 minutes, then 0.5 mg/kg every 5-10 minutes up to 3 mg/kg; simultaneously administered lidocaine intravenously drip 2-4 mg / min (2 g of lidocaine + 250 ml of 5% glucose solution). During refractory fibrillation, large doses are recommended: bolus 1.5 mg / kg 2 times with an interval of 3-5 minutes.
2. Novocainamide (procainamide) is effective in the treatment and prevention of sustained ventricular tachycardia or VF. Saturating dose up to 1500 mg (17 mg/kg), diluted in isotonic sodium chloride solution, injected intravenously at a rate of 20-30 mg/min, maintenance dose 2-4 mg/min.
3. Ornid (bretilium) is recommended for VF when lidocaine and/or novocainamide are ineffective. It is administered intravenously at a dose of 5 mg/kg. If VF persists, after 5 minutes, a dose of 10 mg/kg is administered, then after 10-15 minutes another 10 mg/kg. The maximum total dose is 30 mg/kg.
4. Amiodarone (Cordarone) serves as a backup for the treatment of severe arrhythmias refractory to standard antiarrhythmic therapy and in cases where other antiarrhythmic drugs have side effect. Assign intravenously at 150-300 mg for 5-15 minutes and then, if necessary, up to 600 mg for 1 hour under the control of blood pressure.
5. Mexiletine (mexitil; similar in chemical structure to lidocaine) is used to treat ventricular arrhythmias 200 mg intravenously over 10 to 15 minutes followed by 250 mg over 1 hour (up to 1200 mg over 24 hours).

In the complex of therapeutic measures, along with antiarrhythmic drugs, it is necessary to include drugs that improve myocardial contractility, coronary blood flow and systemic hemodynamics; great importance is attached to the means that eliminate the acid-base and electrolyte imbalance. Currently, in everyday practice, the use of potassium and magnesium preparations has proven itself well.

First aid for pulmonary edema is a necessary measure to maintain human life.

First aid is a set of measures aimed at eliminating acute symptoms and providing life support.

If pulmonary edema occurs, then first aid consists in calling an ambulance, since out-of-hospital conditions rarely have all the necessary medicines and devices. While waiting for qualified doctors, people around the patient must take the necessary measures.

Pulmonary edema: clinic and emergency care

Pulmonary edema is a condition where too much fluid builds up in the lungs. This is due to the large difference in the indicators of colloid osmotic and hydrostatic pressure in the capillaries of the lungs.

There are two types of pulmonary edema:

Membraneogenic- occurs if the permeability of capillaries has increased sharply. This type of pulmonary edema often occurs as an accompaniment to other syndromes.

Hydrostatic- develops due to diseases in which the hydrostatic capillary pressure rises sharply, and the liquid part of the blood finds an outlet in such an amount that it cannot be removed through the lymphatic pathways.

Clinical manifestations

Patients with pulmonary edema complain of lack of air, have frequent shortness of breath and sometimes attacks of cardiac asthma that occur during sleep.

The skin is pale, and from the side nervous system there may be inadequate reactions in the form of confusion or its oppression.

With pulmonary edema, the patient has a cold sweat, and when listening to the lungs, wet rales are found in the lungs.

First aid

At this time, it is very important to act quickly and accurately, because in the absence of support, the situation can deteriorate dramatically.

When the ambulance arrives, all the actions of the specialists will be aimed at three goals:

• reduce the excitability of the respiratory center;
• relieve the load of the pulmonary circulation;
• remove foam.

In order to reduce the excitability of the respiratory center, the patient is injected with morphine, which relieves not only pulmonary edema, but also an asthma attack. This substance is not safe, but here it is a necessary measure - morphine selectively affects the brain centers responsible for breathing. Also, this medication makes the blood flow to the heart not so intense and due to this, stagnation in the lung tissue is reduced. The patient becomes much calmer.

This substance is administered either intravenously or subcutaneously, and after 10 minutes its effect occurs. If the pressure is lowered, promedol is administered instead of morphine, which has a less pronounced, but similar effect.

Strong diuretics (such as furosemide) are also used to relieve pressure.

To unload the circle of small blood circulation, they resort to a dropper with nitroglycerin.

If there are symptoms of impaired consciousness, then the patient is given a weak antipsychotic.

Together with these methods, oxygen therapy is indicated.

If the patient has developed persistent foam, then this treatment will not give the desired effect, as it can block Airways. To avoid this, doctors give inhalation with 70% ethyl alcohol, which is passed through oxygen. Then the specialists suck out excess fluid through the catheter.

Causes of pulmonary edema

Hydrostatic edema can occur due to:

1. Heart dysfunctions.
2. Entry into the vessels of air, blood clots, fat.
3. Bronchial asthma.
4. Tumors of the lungs.

Membrane pulmonary edema can occur for the following reasons:

1. Renal failure.
2. Chest injury.
3. Ingress of toxic fumes, gases, smoke, mercury vapor, etc.
4. Reflux of gastric contents into the respiratory tract or water.

Pulmonary edema is a pathophysiological process in which the liquid part of the blood, as a result of stagnation in the vessels of the small (pulmonary) circulation, begins to flow into the interstitial tissue or directly into the respiratory alveoli.

The occurrence of pulmonary edema means the development of acute left ventricular failure, in which the left ventricle of the heart is not able to provide an adequate ejection of blood into the vessels great circle blood circulation, and the blood "stagnates" in the pulmonary vessels under increasing pressure.

Pulmonary edema can occur in any person, so it is important to know everything about his clinic (symptoms), causes and emergency tactics for this condition - you can save someone's life.

With stagnation of blood in the capillaries of the lungs, special changes begin to occur, leading to an increase in the permeability of the membrane created by the cells of the alveolar and vascular walls. Due to the accumulation of a large amount of fluid in the capillaries, the hydrostatic pressure of the blood increases, while the oncotic pressure falls.

Both pathophysiological factors, combined, contribute to the “leakage” of plasma (the liquid part of the blood) through the membrane that has become permeable either into the interstitium of the lung tissue (interstitial edema) or into the alveoli (alveolar edema). Thus, in the tissues there is a liquid that sharply disrupts normal gas exchange.

Pathogenesis: what happens

More often the reasons are acute and chronic decompensated diseases of the heart muscle. These include:

• Myocardial infarction, accompanied by a significant area of ​​tissue damage or complete rupture of the heart wall.
• Various kinds of cardiac arrhythmias (extrasystole supraventricular or ventricular, blockade of the sinoatrial or atrioventricular nodes of the conduction system).
• Heart defects (and stenosis - narrowing - or insufficiency).
• An increase in the size of the right chambers of the heart - "cor pulmonale".
• Cardiomyopathy with hypertrophy of the heart muscle.
• Hypertensive crisis with a sharp increase in blood pressure.
• cardiac tamponade.
• Mechanical injury to the heart.
• Pulmonary embolism ().

Also, the causes of edema can be conditions such as anemia, symptomatic arterial hypertension as a manifestation of glomerulonephritis, thyrotoxicosis with an increased release of thyroid hormones into the blood, and a toxic effect on the alveolar membrane. Edema can lead to chest trauma, pneumothorax, pneumonia, pleurisy, cirrhosis of the liver.

Classification: types and stages

As mentioned above, swelling may be either interstitial or alveolar. In fact, these two types are successively alternating stages of a common pathophysiological process.

It is quite possible that the liquid part of the blood will remain only in the interstitium (intercellular substance) of the lung tissue, then the course of pulmonary edema will be much easier than if the liquid enters the alveoli. This is the main difference between these types of pulmonary edema.

Along with the above pathophysiological, there is etiological classification:

1. against the background of low or high blood output by the heart muscle, that is, developing due to changes in the heart.
2. , whose cause lies in the disruption of the work of other organs and systems (toxic, inflammatory, allergic, as a result of the introduction of significant volumes of parenteral solutions into the body).

How dangerous

Pulmonary edema is a deadly pathophysiological process that complicates the course of a number of diseases of other human organs and requires urgent medical care.

His high risk due to lack of oxygen in the body due to a violation of the normal transport of gases through the alveolar-capillary membrane.

Thereby all organs and tissues do not receive sufficient amounts of oxygen and cannot remove carbon dioxide, entering into a state of ischemia. The first target organs are vital: the brain, heart, kidneys, adrenal glands, liver.

Due to ischemia, their functions can be so impaired that death becomes inevitable without timely assistance.

Besides, pulmonary edema can lead to changes in the respiratory system itself, which include:

• Atelectasis of the lung (lung tissue collapses due to partial or complete replacement of air masses in it with liquid);
• Emphysema (an increase in the volume of the terminal bronchioles and alveoli with ruptures of the wall of the latter);
• Sclerotic changes in the lung parenchyma (replacement of normal lung tissue with connective tissue incapable of gas exchange with blood);
• Pneumonia due to stagnant fluid.

Main symptoms

Patients with developed edema visually cyanotic ("bluish").

Their breathing is noisy with blistering rales distinguishable at a distance, the skin is moist and cold, position - orthopnea(a person is forced to sit, often rests his hands on the seat of a chair to facilitate attempts to inhale).

In breathing, not only those muscles that usually produce this act are involved, but also auxiliary muscles. This is manifested by a visually noticeable retraction of the intercostal spaces, supraclavicular and subclavian fossae, increased work of the abdominal muscles in accordance with the rapid rhythm of breathing.

There is inspiratory (with difficulty inhaling air) shortness of breath accompanied by the patient's panic and fear of death.

Speaking of interstitial edema, it is worth noting the presence of predominantly wheezing with other symptoms, rarely auscultated finely bubbling. With alveolar edema, wheezing is medium and large bubbling, loud, the patient coughs intensively with a large amount of frothy pink (or blood-streaked) sputum.

Which doctor will help

Most often, when edema occurs, emergency medical care is provided by therapists, cardiologists, doctors who are part of the ambulance team, and anesthesiologists-resuscitators.

If symptoms occur, an ambulance should be called immediately.

However a doctor of any specialty must know how to provide adequate care to a patient with pulmonary edema, because such a situation can occur not only at home or in hospital departments of the corresponding profile.

How to treat before and after the arrival of the ambulance

Even before the arrival of the medical team, the people around the patient should help him accept this. a sitting position in which his legs would be lowered down. This action will reduce venous return to the right side of the heart, which will "unload" the pulmonary circulation, reducing the preload on the heart muscle.

If the patient's mouth contains copious amount of foamy sputum, remove it freeing the airways. To do this, you can use your own fingers wrapped in cloth or a handkerchief. Be sure to open the window and unfasten the clothes that are restricting the human body in order to maximize the oxygen supply at this point in time.

With the arrival of doctors, it is they who take over the provision of first aid. To stop pulmonary edema, the following measures are taken:

1. The supply of oxygen mixture (100%) through the mask at a speed of 6 to 8 liters per minute. Often, with pulmonary edema, so-called defoamers are introduced along with the mixture, which can eliminate foamy sputum (ethyl alcohol vapor with a usual concentration of 70%).
2. Intravenous administration of morphine (2 to 5 mg), which selectively affects the respiratory center in medulla oblongata and reduces the flow of venous blood to the heart muscle, reducing pressure in the pulmonary circulation.
3. The use of diuretics (diuretics), which will reduce the volume of circulating blood in the body and also reduce the venous load. The drugs are administered intravenously, usually the drug "Lasix" (furosemide) is used in a dose of 40 to 100 mg.
4. Intravenous jet administration of prednisolone at a dose of 60-90 mg to relieve bronchospasm and reduce fluid extravasation through the alveolar-capillary membrane.
5. To increase blood pressure, cardiotonic drugs (heart muscle stimulants), such as dopamine or dobutamine, are used.
6. If systolic blood pressure is more than 100 mm Hg. Art., then intravenous infusion of sodium nitroprusside (or nitroglycerin solution) is performed to reduce afterload on the heart.
7. Venous tourniquets are applied to three limbs (the fourth limb without a tourniquet is intended for intravenous infusion medicines) to ensure less venous return.

Further treatment

The following therapeutic measures are carried out in intensive care units under strict control of hemodynamic parameters (blood pressure, heart rate), saturation of blood gases, the usefulness of the act of breathing.

If necessary, continue the introduction cardiac and diuretic drugs taking into account the presence of concomitant pathology in the patient. In cases where edema has developed against the background of an infectious process, antibacterial agents according to their spectrum of activity.

Pulmonary edema, being a serious and even fatal in some cases complication of other equally serious diseases, requires high professionalism from doctors of all specialties and care from the patient's relatives.

For the most part, it develops against the background of acute or decompensated cardiac pathology. Call an ambulance at the first sign of symptoms and start taking immediate action.