a condition characterized by an increase in total blood volume and, most often, a violation of the ratio of formed elements and plasma.

Simple (normocythemic) hypervolemia- increase in total blood volume while maintaining the normal percentage of plasma and formed elements. It occurs for a short time during the transfusion of large quantities of donor blood, during heavy physical activity, during acute hypoxia, at the beginning of high ambient temperatures, when deposited blood enters the bloodstream from the depot, and intercellular fluid from the tissues. This condition can lead to a decrease in vascular tone, overload of the heart, and the development of heart failure.

Oligocythemic hypervolemia (hydremia)- an increase in blood volume due to a predominant increase in its liquid part, while the hematocrit indicator is below 36%. Occurs when the excretory function of the kidneys is impaired and fluid retention in the bloodstream, pathological thirst, excessive administration of saline or blood substitutes, and overproduction of antidiuretic hormone. As a result, circulatory disorders may occur due to overstretching of blood vessels, heart cavities and microcirculation disorders.

Polycythemic hypervolemia- a condition in which the volume of circulating blood increases mainly due to formed elements (erythrocytes), and therefore the hematocrit exceeds 48%. Occurs with heart defects, chronic circulatory failure, alveolar hypoventilation, a decrease in the oxygen capacity of the blood and the efficiency of biological oxidation, exogenous (hypo- and normobaric) hypoxia, as well as erythremia (Vaquez disease) - leukemia with a predominant lesion of the red sprout of the bone marrow. The disease is accompanied by an increase in blood viscosity, blood pressure, an increase in the load on the heart with subsequent hypertrophy of the left ventricle, etc.

Hypovolemia

a condition characterized by a decrease in total blood volume and a violation of the ratio of formed elements and plasma.

Simple (normocythemic) hypovolemia characterized by a decrease in blood volume with a normal hematocrit. The causes are acute bleeding, shock, and vasodilation collapse. In the last two cases, a significant amount of blood is deposited in the venous (capacitive) vessels and a significant decrease in blood volume occurs; the hematocrit indicator has not yet changed. The danger of the condition is a decrease in blood pressure, disruption of peripheral blood flow, leading to hypoxia and metabolic disorders in tissues.

Oligocythaemic hypovolemia characterized by a decrease in total blood volume with a predominant decrease in the number of formed elements and a decrease in hematocrit below 36%. It is observed immediately after blood loss, when its supply from the depot and tissue fluid does not yet eliminate hypovolemia, and the release of blood cells from the hematopoietic organs is a deficiency of erythrocytes. It manifests itself as a circulatory disorder in various vessels, an excess of the need of organs and tissues for blood supply above its level, and a decrease in the oxygen capacity of the blood due to erythropenia.

Polycythaemic hypovolemia(anhydremia) is observed when the total blood volume decreases due to a predominant decrease in plasma volume, while the hematocrit level exceeds normal. The most common causes of this condition are various forms of dehydration: uncontrollable vomiting, profuse diarrhea, polyuria, increased sweating, extensive burns, water fasting, hyperthermia, diabetes insipidus, etc. Disorders of central, organ-tissue and microhemocirculation are observed.

The materials are published for informational purposes only and are not a prescription for treatment! We recommend that you consult a hematologist at your medical institution!

Hypervolemia is a pathological increase in circulating blood volume. What are the causes of hypervolemia, how does the disease develop? Let's take a closer look at the stages of hypervolemia, diagnostic methods and treatment of a pathological increase in circulating blood volume.

An abnormal increase in the volume of circulating blood in hematology is called hypervolemia, which has a pronounced clinical picture and is diagnosed in 3% of the population of different age categories. The normal volume of circulating blood and circulating plasma is 69 and 39 ml/kg of body weight in men, 65 and 40 ml/kg in women. With a pathological change, the amount of blood increases, which significantly affects a person’s well-being. There are many reasons and predisposing factors for the development of hypervolemia, but in any case, such a disease requires proper treatment under the supervision of specialists.

Causes of hypervolemia

With the development of hypervolemia, there is an excessive release of blood volume from the depot, which leads to the fact that the human body cannot cope with the load and, as a result, fails. The causes of hypervolemia can be very different, but they are mainly associated with other pathologies occurring in the body, as well as overhydration, in which the balance of water and salt in the body is disturbed, subsequently causing tissues and organs to contain an excess amount of water. The following conditions can provoke the development of hypervolemia:

• excessive fluid intake during the day;
• swelling of the upper and lower extremities;
• sodium retention in the body;
• physical exercise;
• heart and vascular diseases;
• pathologies of the respiratory system;
• kidney diseases.

Kinds

There are several types of hypervolemia, each of which has its own characteristics and signs:

Normocythemic hypervolemia (simple)— the increase in the equivalent of formed elements is increased, but remains within normal limits. This condition can be provoked by acute hypoxia or transfusion of large amounts of blood.

Oligocythemic- characterized by an increase in blood volume as a result of an increased amount of fluid in the body. Ht indicators are below normal. This condition is observed in diabetes mellitus, renal failure and other conditions associated with the excretory function of the kidneys.

Polycythemic hypervolemia is an increase in total blood volume with an increased number of formed elements. Ht indicators exceed the normal limit. This stage of the disease is a whole group of pathological conditions in which the number of red blood cells, leukocytes and platelets in the blood is significantly increased.

Important! Only a doctor can determine the stages of hypervolemia after the results of laboratory blood tests.

Symptoms

Clinical signs of hypervolemia are quite pronounced and may be accompanied by the following conditions and ailments:

1. Heart rhythm disturbance.
2. Shortness of breath, which may be present during exercise or at rest.
3. General weakness.
4. Labored breathing.
5. Frequent headaches.
6. Increased fatigue.
7. Pain in the lumbar region.
8. Feeling of heaviness in the stomach.

Diagnosis and treatment

The initial patient appointment consists of collecting anamnesis, examination, and ordering laboratory tests of blood and urine, which will help determine the number of red blood cells in the blood plasma and urine. The research results will allow you to create a complete picture of the disease, determine the stage, cause, and prescribe the necessary treatment.

• What is Hypervolemia
• What causes hypervolemia?
• Symptoms of Hypervolemia
• Treatment of Hypervolemia

What is Hypervolemia

Hypervolemia- conditions characterized by an increase in total blood volume and usually a change in Ht. There are normocythemic, oligocythemic and polycythemic hypervolemia.

What causes hypervolemia?

Normocythemic hypervolemia(simple) - a state manifested by an equivalent increase in the volume of formed elements and the liquid part of the bcc. Ht remains within normal limits.

Main reasons for downtime hypervolemia: transfusion of a large volume of blood, acute hypoxic conditions, accompanied by the release of blood from its depot, as well as significant physical activity leading to hypoxia.

Oligocythaemic hypervolemia

Oligocythaemic hypervolemia(hydremia, hemodilution) is a condition characterized by an increase in the total volume of blood due to an increase in its liquid part. The Ht indicator is below normal.

The main causes of oligocythemic hypervolemia.

• Excessive intake of fluid into the body due to pathological thirst (for example, in patients with diabetes) and the introduction of a large amount of plasma substitutes or blood plasma into the vascular bed.
• Decreased excretion of fluid from the body as a result of insufficiency of excretory function of the kidneys (for example, in renal failure), overproduction of ADH, hyperosmolality of blood plasma.

Polycythemic hypervolemia- a condition manifested by an increase in the total volume of blood due to a predominant increase in the number of its formed elements. In this regard, Ht exceeds the upper limit of normal.

The main causes of polycythaemic hypervolemia.

• Polycythemia (erythrocytosis) is a group of pathological conditions characterized by an increase in the number of erythrocytes (regardless of the number of leukocytes and platelets).
• Polycythemia vera (polycythemia vera, Vaquez's disease) is a chronic leukemia with damage at the level of the myelopoiesis precursor cell with the unlimited proliferation of this cell characteristic of the tumor, which retains the ability to differentiate along four lineages, mainly red. Erythremia is accompanied by significant erythrocytosis and, as a consequence, increased Ht.
• Chronic hypoxia of any type (hemic, respiratory, circulatory, tissue, etc.).

Polycythemia at the same time, it reflects the hyperregenerative state of the bone marrow, which is accompanied by increased proliferation of blood cells, mainly erythrocytes, and their release into the vascular bed. Polycythemic hypervolemia is detected in chronic circulatory failure, alveolar hypoventilation, a decrease in the oxygen capacity of the blood and the efficiency of biological oxidation, and in exogenous (normo- and hypobaric) hypoxia.

Symptoms of Hypervolemia

For hypervolemia characterized by an increase in cardiac output and an increase in blood pressure.

• The increase in cardiac output is the result of compensatory hyperfunction of the heart due to increased blood volume. However, with cardiac decompensation and the development of cardiac failure, cardiac output usually decreases.
• The increase in blood pressure is caused mainly by an increase in cardiac output, as well as volumetric blood volume and the tone of resistive vessels.
• Polycythemia vera is also characterized by a significant increase in blood viscosity, aggregation and agglutination of blood cells, disseminated thrombus formation, and microcirculatory disorders.

Treatment of Hypervolemia

Treatment symptomatic

Which doctors should you contact if you have Hypervolemia?

Anesthesiologist

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TREATMENT OF HYPERVOLEMIA OF THE SMALL CIRCULAR AFTER RASTELLI OPERATION IN A PATIENT WITH TETHROD OF FALLOT AND PULMONARY ARTERY ATRESIA

R. A. Ibadov, Kh. K. Abralov, L. A. Nazyrova, A. Sh. Arifzhanov, N. A. Strizhkov, D. I. Zhulamanova, S. Kh. Ibragimov

Republican Specialized Center for Surgery named after. V. Vakhidova, Republic of Uzbekistan, 100115, Tashkent, Chilanzar district, st. Farhad, 10

Intensive Care of Hypervolemia of Lesser Circulation after Rastelli Procedure Carried out for the Patient with a Pulmonary Atresia

R. A. Ibadov, H. K. Abrolov, L. A. Nazirova, D. I. Julamanova, A. Sh. Arifjanov, N. A. Strijkov, S. Kh. Ibragimov

V. Vakhidov Republican Specialized Center of Surgery, 10, Farhad Str., Chilanzar district, Tashkent 100115, Republic of Uzbekistan

The patient, 17 years old, was operated on for tetralogy of Fallot with pulmonary atresia. In the early postoperative period, clinical hypervolemia of the pulmonary circulation was observed. After intensive therapy using non-invasive pulmonary ventilation methods, the patient was transferred from the ICU in satisfactory condition on the 5th day.

Key words: tetralogy of Fallot; pulmonary atresia; Rastelli operation; hypervolemia of the pulmonary circulation; non-invasive artificial ventilation

17-year-old patient with hypervolemia of lesser (pulmonary) circulation was operated for tetralogy of Fallout with pulmonary atresia. She was successfully treated by intensive therapy using techniques of noninvasive ventilation with regard to clinical status of hypovolemia of the lesser (pulmonary) circulatory system in the early postoperative period.

Key words: tetralogy of Fallot; pulmonary atresia; Rastelli procedure; hypervolemia of pulmonary circulation; non-invasive ventilation

DOI:10.15360/1813-9779-2016-3-78-83

Introduction

Respiratory support is an essential element of intensive treatment. Tetralogy of Fallot (TF) is a congenital heart defect that includes: high (subaortic) ventricular septal defect (VSD); stenosis of the right ventricular outflow tract (RVOT) (valvular, subvalvular, stenosis of the pulmonary trunk and (or) branches of the pulmonary artery or combined); dextral position of the aorta; right ventricular (RV) hypertrophy, as a result of obstructed blood outflow from the ventricle. There are several forms of this defect: with the absence of the pulmonary valve One of the main elements of intensive care is respiratory support. Tetralogy of Fallot (TOF) is a congenital heart defect that includes four components: pulmonary infundibular stenosis, overriding aorta, ventricular septal defect (VSD), and right ventricular hypertrophy. Several forms of this defect include the one with a lack of a pulmonary valve, another one associated with stenosis and pulmonary atresia (PA) and the forms with or without major aorto-pulmonary collateral arteries (MAPCA). There are two types of PA: with Intact Ventricular Septum (PA-IVS) and PA with VSD (PA-VSD).

Correspondence to:

Nikolay Strizhkov E-mail: [email protected] Mr. Nikolai Strijkov E-mail: [email protected]

Classification of pulmonary atresia with ventricular septal defect by Sommervile J., 1970. The classification of pulmonary atresia with ventricular septal defect by Sommervile J., 1970.

Type Characteristic and pathology features

1 Atresia at the level of pulmonary valve. The pulmonary trunk, right and left pulmonary arteries are fully formed and passable

2 Atresia of pulmonary valve and truct. Both pulmonary arteries exist and could be in a joint or separated

3 Atresia of valve, tract and one of the two pulmonary artery branches. Other pulmonary artery is formed and passable

4 Atresia of valve, tract and both of pulmonary artery branches. Blood flow in the lungs employs a collateral vessels system

Note. Type - type; Characteristic and pathology features - characteristics and description of pathology; Atresia at the level of pulmonary valve. The pulmonary trunk, right and left pulmonary arteries are fully formed and passable - Atresia at the level of the pulmonary valve. The pulmonary trunk, right and left pulmonary arteries are fully formed and patent; Atresia of pulmonary valve and truct. Both pulmonary arteries exist and could be in a joint or separated - Atresia of the valve and trunk of the pulmonary artery. Both pulmonary arteries are preserved and can be fused or severed; Atresia of valve, tract and one of the two pulmonary artery branches. Other pulmonary artery is formed and passable - Atresia of the valve, trunk and one of the branches of the pulmonary artery. The other pulmonary artery is formed and patent; Atresia of valve, tract and both of pulmonary artery branches. Blood flow in the lungs employs a collateral vessels system - Atresia, valve, trunk, both branches of the pulmonary artery. Blood flow in the lungs is carried out by a network of collateral vessels.

(PA), with stenosis and atresia of the pulmonary artery (PA) with or without large aortopulmonary collateral arteries (PACC).

Pulmonary atresia with ventricular septal defect is characterized by a congenital lack of direct communication between the RV and PA at the level of the infundibular portion of the RV, pulmonary valve ring, pulmonary trunk, right and/or left branches (Table 1).

For APA with VSD, the most characteristic feature is the presence of large aortopulmonary collaterals (PACC), which are the main type of compensatory pulmonary circulation.

In APA, there may be a well-developed pulmonary artery behind the atretic valve, which requires surgical intervention using a heterograft pulmonary valve - the Rastelli method (Rastelli).

The main complications of the early postoperative period are: hypervolemia of the pulmonary circulation, bleeding, acute heart failure. Hemodynamic disturbances associated with hypervolemia of the pulmonary circulation in patients after Rastelli surgery can lead to severe complications and cause death.

Description of a clinical case

Patient B. 17 years old. Diagnosis: congenital heart disease, TF, blue form. PA atresia type II according to 8-step X BALK. SPO overlay of MAA on the left (2012).

Multislice computed tomography (MSCT) data are presented in Fig. 1. Before surgery, oxygen saturation in the gas composition of arterial blood is 8aO2 - 80%.

The operation was performed: intraventricular, left ventricular-aortic tunneling with a xenopericardial patch with simultaneous VSD repair, formation of the RVOT with a biovalve-containing synthetic conduit according to the Rastelli method under combined general anesthesia, under conditions of artificial circulation (166 min) and cardioplegia (135 min). ).

Pulmonary atresia with ventricular septal defect is characterized by congenital absence of direct communication between the RV and pulmonary artery at the level of infundibular department of RV, pulmonary valve ring, or pulmonary trunk (Table 1).

The presence of MAPCA is most typical for the PA-VSD. It comprises the main type of compensatory pulmonary circulation.

Pulmonary artery located behind the inperfo-rate valve in PA could be satisfactory developed that requires surgical intervention using a xenograft of a pulmonary artery valve - the Rastelli procedure.

The major postoperative complications after Rastelli procedure are hypervolemia of pulmonary circulation, bleeding and acute heart failure. Hemodynamic disturbances associated with heperv-olemia of pulmonary circulation in patients after Rastelli procedure can lead to serious complications and even cause death.

Case Presentation

A 17-year-old girl with a documented history of TOF, PA-VSD type II on Somerville J was operated in our clinic.

The data of CT scan (Fig. 1). Saturation of arterial blood oxygen (SO2) was 80%.

Surgery: intraventricular, left ventriculo-aortic tunneling with xenopericardial patch and simultaneous VSD surgery, forming of right ventricle output tract with synthetic conduit containing biological valve (Rastelli's method) under combined general anesthesia, cardiopulmonary bypass (166 min) and cardioplegia (135 min).

After surgery the patient was added to the intensive care unit (ICU) in a state of sleep medication on the ventilator. Hemodynamics (following dopamine administration at a dose of 5 mg/kg/min): blood pressure 105/55 mm Hg, pulse 90 beats/min, central venous pressure (CVP) 100 mm H2O.

General and biochemical blood test parameters were within the normal ranges. The gas composition of arterial blood: p02 - 211 mm Hg.; pC02 - 39.6 mm Hg., SaO2 - 99.7%; FiO2 - 50%. Echocardiography data: end-diastolic volume - 59 ml, end-systolic volume - 26 ml, ejection

Rice. 1. Multislice computed tomography of patient B. before surgery. Fig. 1. Patient" CT scan before surgery.

After the operation, the patient was taken to the ICU in a state of drug-induced sleep, receiving mechanical ventilation. Hemodynamics against the background of dopamine at a dose of 5 mcg/kg/min, while blood pressure is 105/55 mm. rt. art., pulse - 90 / min., central venous pressure (CVP) - 100 mm water column.

Indicators of general and biochemical blood tests are within normal limits. Arterial blood gas composition: pO2 - 211 mm Hg. Art.; рСО2 - 39.6 mm Hg. Art., SaO2 - 99.7% with FiO2 - 50%. During echocardiography: EDV - 59 ml, ESV - 26 ml, EF -56%, systolic pressure gradient (SPG) at RVOT - 9.8 mm Hg. Art. On a chest x-ray, the lung fields are straightened, the sinuses and domes of the diaphragm are free (Fig. 2).

Postoperative mechanical ventilation was carried out until complete awakening, followed by tracheal extubation according to the high-risk algorithm according to the British DAS Society protocol, 2012.

4 hours after weaning from mechanical ventilation and extubation of the trachea, the patient’s condition worsened, symptoms of respiratory failure progressed (respiratory rate 30 per minute, decrease in SaO2 to 90%, decrease in paO2 to 90 mm Hg, increase in paCO2 to 50 mm Hg. ). A chest x-ray shows a picture of pulmonary edema, increased vascular pattern, signs of increased blood flow in the pulmonary circle, the roots of the lungs are stagnant (Fig. 3).

On the 5th day of treatment in the ICU, after relief of pulmonary edema, reduction of signs of pulmonary hypervolemia, stabilization of hemodynamics and general condition (Fig. 5), the patient was transferred to the ward of the congenital heart disease surgery department for further treatment and postoperative rehabilitation.

Discussion

Many works have been devoted to the study of the state of hemodynamics during the development of hypervolemia of the pulmonary circulation in patients with heart defects and the treatment of these conditions.

Rice. 2. Chest X-ray upon admission to the ICU.

Fig. 2. Chest X-ray at admission to ICU.

fraction - 56%, systolic pressure gradient on RVOT - 9.8 mm Hg. Chest X-ray showed straightened lung fields and free sinuses and the cupula of diaphragm (Fig. 2).

Postoperative mechanical lung ventilation (MLV) was performed until full awakening, followed by tracheal extubation according to the high-risk algorithm of the DAS-protocol, 2012.

After 4 hours the patient condition worsened, features of respiratory failure were progressing (respiratory rate - 30 per minute, SaO2 values ​​reduced to 90%, reduced values ​​of paO2 to 90 mm Hg, increased paCO2 vacuums to 50 mm Hg). Chest X-rays revealed a picture of pulmonary edema, signs of increased blood flow and congested lung roots (Fig. 3).

There were progression of hypovolemia, events of cardiac small output, metabolic acidosis (pH - 7.33; paCO2 - 52 mm Hg; BE - -7.2; paO2 - 84 mm Hg; SaO2

Rice. 3. X-ray of the chest with pulmonary hypervolemia.

Fig. 3. Chest X-ray: data of hypervolemia of pulmonary circulation.

The presented clinical observation examines the possibility of modulating the pulmonary circulation after cardiac surgical correction using non-invasive ventilation.

One of the common complications of the early postoperative period in patients with TF with APA is pulmonary hypervolemia. A sharply increased blood flow after radical correction may cause the development of such

90%). It was decided to carry out of non-invasive respiratory support with the help of an oxygen mask-PEEP and a subsequent transfer to a non-invasive CPAP (NiCPAP) in SIMV mode. To improve alveolar ventilation, therapy was supplemented by stimulation of diuresis and administration of glucocorticosteroids (60 mg prednisolone administered intravenously as a bolus).

Respiratory support in a NiCPAP mode was performed with the aid of the VELLA respirator (Viasys Healthcare Inc.) and a sealed oxygen-mask and standard sterile breathing circuit: f - 12 per minute, pressure support - 20 cm H2O, PEEP - 7 cm H2O, Flow - 12 l/min, FiO2 - 50%. FiO2 values ​​were reduced to 30% during an hour, whereas a pressure support and PEEP values ​​were reduced to 5 cm H2O during 4 hours.

As a result of the use of noninvasive methods of respiratory support, there was clinical improvement in the patient's condition in 5 hours, which was reflected in the reduction of tachycardia and dyspnea, improving the peripheral blood flow (the color, temperature and moisture of the skin were changed in a positive sense), while the wet stagnant wheezing in the lungs was significantly decreased. Positive clinical dynamics was accompanied by a decrease in preload and afterload of the left ventricle on the background of reduced heart rate and increased pumping function of the left ventricle (echocardiography). The positive dynamics of arterial blood gas and acid-base balance (Figure 4) were as follows: pH - 7.47; pCO2 - 38 mm Hg. Art, BE - +3.6.; pO2 - 176 mm Hg. Art, SaO2 - 99.5%. On the control chest X-ray, the lung fields were straight, with no signs of infiltration, sinuses looked empty (Fig. 5).

On the 5th day on admission to the ICU, after the relief of pulmonary edema, reduced signs of hypervolemia of pulmonary circulation and stabilization of hemodynamics, the patient was transferred to the Congenital Heart Surgery Department for further treatment and postoperative rehabilitation.

Nasal catheter Nasal Nasal catheter catheter PEEP mask PEEP mask PEEP mask NiCPAP NiCPAP NiCPAP

88 94 90 95 95 97 99.1 99.5 99.8

90 84 82 90 93 95 132 176 196

Rice. 4. Changes in blood gas parameters in the dynamics of respiratory therapy for a crisis of hypervolemia in the pulmonary circulation after the Rastelli operation. Fig. 4. Changes of blood gases in the dynamics of respiratory care for the hypervolemia of pulmonary circulation after the Rastelli procedure.

Note: Nasal catheter - nasal cannulas; PEEP mask - PEEP mask.

Various studies were dedicated to clarification of hemodynamic dysfunctions in patients with a hypervolemia of pulmonary circulation associated with heart defects, as soon as treatment of these conditions and complications.

Reported clinical case dealt with the possibility of adaptation of the pulmonary circulation after cardiac surgery corrected by a non-invasive ventilation.

Hypervolemia of pulmonary circulation is one of the most frequent complications of the early postoperative period in patients with TF and PA. The sharp increase in blood flow after TOF repair

Rice. 5. Chest X-ray on day 5, upon transfer from the ICU.

Fig. 5. Chest X-ray on the 5th day.

vital complications such as pulmonary edema and acute left ventricular failure.

However, the rate of development of the alveolar stage of pulmonary edema is sometimes so rapid that it often does not leave time for the implementation of therapeutic measures, especially if this is the early postoperative period. Increasing asphyxia rapidly leads to fatal hypoxemia (30-50%), and performing artificial invasive ventilation of the lungs is an additional stress.

Predictors of the development of pulmonary hypervolemia are hemodynamic parameters, increased blood pressure, heart rate and central venous pressure, and respiratory status.

When pulmonary edema occurs in patients after the Rastelli operation, complicated by pulmonary hypervolemia, standardization and rational pharmaco- and respiratory therapy allows a qualified assessment of the current situation, competently and consistently solving a number of treatment and tactical problems. In the postoperative period, maintaining stable hemodynamics and negative water balance are necessary conditions for preventing pulmonary hypervolemia.

NiCPAP during spontaneous breathing of the patient, along with a decrease in the work of breathing, promotes the sweating of the liquid part of the blood from the alveoli and interstitium of the lung tissue into the bloodstream, which contributes to the rapid optimization of gas exchange.

Thus, the response of altered hemodynamics in the early period after cardiac surgery is largely unpredictable, and monitoring and timely use of the necessary technologies, including non-invasive respiratory support, is the main art of a cardiac resuscitator.

can cause the development of such vital complications, such as pulmonary edema and acute left ventricular failure.

However, the pace of development of the alveolar stage of pulmonary edema is sometimes so increased that often leaves no time for implementation of remedial measures, especially if it occurs at the early postoperative period. Increasing asphyxia rapidly leads to fatal hypoxemia (30-50%), and conducting invasive ventilation of the lungs results an additional stress.

Hemodynamic parameters, increased blood pressure, heart rate, central venous pressure and respiratory status represent predictors of hypervolemia of pulmonary circulation.

In the event of pulmonary edema in patients after Rastelli surgery complicated by a hypervolemia of pulmonary circulation, standardization and rational pharmacological and respiratory therapy allow to professionally manage the condition to correctly and consistently solve a number of therapeutic and tactical objectives. Postoperatively, the maintenance of stable hemodynamics and a negative balance are main essentials for preventing the hypervolemia of pulmonary circulation.

NiCPAP during patient's spontaneous breathing, while reducing the work of breathing, contributes to “squeeze out” the liquid portion of blood from the alveoli and interstitium of lung tissue into the bloodstream that optimizes gas exchange.

Therefore, the reaction of the altered hemodynamics in the early period after cardiosurgical interventions are largely unpredictable, and monitoring and timely application of necessary technologies and methods of correction is a sort of a chief art in car-dioreumatology.

Non-invasive respiratory support in a CPAP mode (NiCPAP) in complex and intensive adequate pharmacotherapy is an effective method, which allows to quickly stabilize the clinical condition associated with an altered respiratory status and hemo-dynamics of patients to relieve crises of hyperv-olemia of pulmonary circulation occurring after the Rastelli procedure.

Conclusion

Non-invasive respiratory support in the CPAP mode (NiCPAP) is an effective method that, in combination with adequate intensive and pharmacotherapy, allows the clinical condition, respiratory status and hemodynamics of patients to be stabilized in the shortest possible time when relieving crises of hypervolemia of the pulmonary circulation after the Rastelli operation.

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Received 02/17/16

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2. Rozenberg O.A.Preparaty legochnogo surfaktanta pri ostrykh i khronicheskikh zabolevaniyakh legkikh (chast II). Obshchaya Reanimatologiya. . 2014; 10 (5): 69-86. http://dx.doi.org/10.15360/1813-9779-2014-5-69-86.

3. Hundley W.G., Bluemke D.A., Finn J.P., Flamm S.D., Fogel M.A., Friedrich M.G., Ho V.B., Jerosch-HeroldM., Kramer C.M., Manning W.J., Patel M., Pohost G.M., Stillman A.E., White R.D., Woodard P.K., Harrington R.A., Anderson J.L., Bates E.R., Bridges C.R., Eisenberg MJ, Ferrari V.A., Grines C.L., Hlatky M.A., Jacobs A.K., Kaul S., Lichtenberg R.C., Lindner J.R., Moliterno DJ, Mukherjee D, Rosenson R.S., Schofield R.S., Shubrooks S.J., Stein J.H., Tracy C.M., Weitz H.H., Wesley D.J. ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. Circulation. 2010; 121(22):2462-2508. http://dx.doi.org/ 10.1161/CIR.0b013e3181d44a8f. PMID: 20479157

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5. Marathe S.P., Talwar S. Surgery for transposition of great arteries: a historical perspective. Ann. Pediatr. Cardiol. 2015; 8 (2): 122-128. http://dx.doi.org/10.4103/0974-2069.157025. PMID: 26085763

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Submitted 02/17/16

Dissertations for the degree of Doctor of Science without publication of the main scientific results in leading journals and publications, the list of which is approved by the Higher Attestation Commission, will be rejected due to a violation of clause 10 of the Regulations on the procedure for awarding academic degrees.

List of journals of the Higher Attestation Commission published in the Russian Federation in the specialty 01/14/20 “Anesthesiology and Reanimatology”, in which it is recommended to publish the main results of dissertations for the scientific degree of Doctor and Candidate of Medical Sciences:

Anesthesiology and resuscitation;

General resuscitation.

Vadim Korzhik

Head of the clinic. Doctor of Medical Sciences, Professor. Cardiologist

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Patent ductus arteriosus (PDA) is the presence of a communication between the aorta and the pulmonary artery, which is considered an anomaly in the postnatal period.

The frequency of this defect ranges from 5 to 34%, more often in females (2-4:1).

As a rule, PDA is combined with other congenital heart defects - coarctation of the aorta, VSD.

In case of ductus-dependent heart defects (TMA, extreme form of tetralogy of Fallot, critical stenosis of the aorta and pulmonary artery, interruption of the aortic arch, left ventricular hypoplasia syndrome), this cardiac anomaly is vital.

The PDA, unlike vessels of the main type of blood circulation, is a muscular type vessel with powerful vagal innervation, which ensures its ability to contract in the early neonatal period.

Hemodynamics.

Does your heart often hurt?

YesNo

In the prenatal period, the patent ductus arteriosus and patent foramen ovale are physiological fetal communications.

Due to the fact that the pulmonary circulation does not function, about 2/3 of the volume of oxygenated blood enters the descending aorta through the patent ductus arteriosus. Normally, soon after birth, a spasm of smooth muscle fibers occurs in the patent ductus arteriosus, which leads to functional closure of the duct. Anatomical closure or obliteration occurs during the first 2 weeks of postnatal life.

Such pathological conditions of the newborn period as respiratory distress syndrome, congenital pneumonia, and asphyxia during childbirth prevent the closure of the PDA. Physiological closure of the duct is delayed in premature infants, and the lower the gestational age of the child, the longer the time required for closure of the PDA. Thus, with a body weight of less than 1000 g, in 80% of children the ductus arteriosus functions within several months.

For the development of hemodynamic disorders, the size of the duct, the angle of its origin from the aorta, and the pressure difference in the systemic and pulmonary circulation are important. With a thin, long and tortuous duct extending from the aorta at an acute angle, resistance to blood flow is created and pronounced hemodynamic disturbances do not occur; Over time, the duct may become obliterated.

The short and wide ductus arteriosus is accompanied by a significant discharge of blood from the aorta into the pulmonary artery. Such ducts are not capable of obliteration. The additional volume of blood discharged from the aorta into the pulmonary artery will lead to the development of diastolic overload and dilatation of the left chambers of the heart, especially the left atrium, hypervolemia in the lungs with the formation of pulmonary hypertension.

Clinical picture will depend on the size of the duct.

In the neonatal period, the child has a systolic murmur with r. swing - in the 2nd intercostal space to the left of the sternum. The diastolic component of the murmur is absent due to neonatal pulmonary hypertension characteristic of this period of life. For the same reason, in the neonatal period, cross-discharge of blood may occur through the PDA, which will be clinically expressed in the appearance of cyanotic coloration of the skin during the child’s screaming, sucking, and straining. As the pressure in the pulmonary circulation decreases, left-to-right shunting of blood occurs both in systole and diastole, which leads to the phenomenon of systole-diastolic noise with a “machine” component. In older age, as pulmonary hypertension progresses, the diastolic component of the noise weakens again until it disappears completely. Auscultatory features of the PDA also include intensification and splitting of the second sound above the pulmonary artery. At the final stage of the natural course of the defect, one can note the appearance of a diastolic murmur of pulmonary artery insufficiency - a Graham-Still murmur.

X-ray There is an increase in the size of the cardiothoracic index (from minimal to cardiomegaly), signs of diastolic overload of the left sections (smoothness of the waist, immersion of the apex of the heart in the diaphragm, bulging of the ascending aorta). Enlargement of the left chambers of the heart is clearly visible in lateral and oblique projections with simultaneous contrasting of the esophagus with barium. In the lungs there is an increase in the pulmonary pattern.

At electrocardiography in the initial stages of PDA. signs of left atrium overload and left ventricular hypertrophy are recorded. Later they are joined by signs of overload and hypertrophy of the right sections.

EchoCG allows you to determine indirect signs of the presence of a PDA and visualize it directly, measure the size of the duct, and determine the degree of pulmonary hypertension.

In its natural course, the life expectancy of patients is 20-25 years. After 12 months of age, spontaneous closure of the ductus arteriosus rarely occurs. Main complications of PDA are heart failure, pulmonary hypertension, infective endocarditis, aortic and/or pulmonary artery aneurysm.

Surgical treatment involves ligation or intersection with suturing of the aortic and pulmonary ends of the duct, but recently catheter endovascular occlusion of the duct has also been used. The therapeutic method of treatment involves the use of prostaglandin inhibitors in the neonatal period. Indomethacin can be administered either enterally or intravenously. In the latter case, the effectiveness of treatment is 88-90%. The drug is administered at a rate of 0.1-0.2 mg/kg body weight in 1-2 doses over 1-3 days. The course dose should not exceed 0.6 mg/kg. This method is not widely used, as it has significant limitations and contraindications. Indomethacin has antiaggregation properties, which can lead to intracranial hemorrhage, gastrointestinal bleeding, and transient renal dysfunction.

Ventricular septal defect (VSD) is the most common, both in isolated form and as part of many other heart defects. Among congenital heart diseases, the frequency of this defect varies from 27.7 to 42%. It is equally common in both boys and girls.

The interventricular septum is divided into 3 sections:

the upper part is membranous, adjacent to the central fibrous body,

middle part - muscular,

and the lower one is trabecular.

Accordingly, these sections are also called ventricular septal defects, but most of them have perimembranous localization (up to 80%). Per share muscular VSD accounts for 20%. Based on size, defects are divided into large, medium and small. To correctly assess the size of the defect, its size must be compared with the diameter of the aorta. Small defects measuring 1-2 mm located in the muscular part of the IVS are called Tolochinov–Roger disease. Due to the good auscultatory picture and the absence of hemodynamic disturbances, the expression “much ado about nothing” is appropriate to characterize them. Separately, there are multiple large defects of the IVS, of the “Swiss cheese” type, which have an unfavorable prognostic value.

Intracardiac hemodynamic disturbances with VSD begin to form some time after birth, usually on days 3-5 of life. In the early neonatal period, a heart murmur may be absent due to equal pressure in the right and left ventricles due to the so-called neonatal pulmonary hypertension. A gradual drop in pressure in the pulmonary artery system and in the right ventricle creates a pressure difference (gradient) between the ventricles, resulting in a left-to-right discharge of blood (from an area of ​​high pressure to an area of ​​low pressure). The additional volume of blood entering the right ventricle and pulmonary artery leads to overflow of the vessels of the pulmonary circulation, where pulmonary hypertension develops.

There are three stages of pulmonary hypertension according to V.I. Burakovsky. Stagnation of blood ( hypervolemic stage of pulmonary hypertension) can lead to pulmonary edema, frequent infection, and the development of pneumonia that manifests in early life, has a severe course and is difficult to treat. If hypervolemia cannot be managed with conservative methods, in such cases a palliative operation is performed - narrowing of the pulmonary artery according to Muller. The essence of the operation is to create a temporary artificial stenosis of the pulmonary artery, which prevents excess blood from entering the ICC. However, the increased load that falls on the right ventricle dictates in the future (after 3-6 months) the need for radical surgery.

During the natural course of the defect, over time, the Kitaev reflex (spasm in response to overstretching) is triggered in the vessels of the pulmonary circulation, which leads to the development transitional stage of pulmonary hypertension. During this period, the child stops getting sick, becomes more active, and begins to gain weight. The stable condition of the patient in this phase is the best period for radical surgery. The pressure in the pulmonary artery (and accordingly in the right ventricle) during this phase ranges from 30 to 70 mmHg. The auscultatory picture is characterized by a decrease in noise intensity with the appearance of an accent of the second tone above the pulmonary artery.

Subsequently, if surgical correction of congenital heart disease is not performed, processes of hardening of the pulmonary vessels begin to form ( high pulmonary hypertension - Eisenmenger syndrome). This pathological process does not develop back and leads to a significant increase in pressure in the pulmonary artery (sometimes up to 100-120 mmHg). On auscultation, you can hear a pronounced accent of the second tone over the pulmonary artery (“metallic” tint). Systolic murmur becomes weakly intense, and in some cases may be completely absent. Against this background, it is possible to record the appearance of a new diastolic murmur caused by insufficiency of the pulmonary valves (Graham-Still murmur). The clinical picture of the disease shows many pathological signs: cardiac “hump”, expansion of the boundaries of relative cardiac dullness, more to the right. Areas of weakened and harsh breathing can be heard over the lungs, and wheezing may occur. The most characteristic sign of Eisenmenger syndrome is a gradual increase in cyanosis, first peripheral, and later diffuse. This occurs due to cross-discharge of blood in the area of ​​the ventricular septal defect, which, when the pressure in the right ventricle exceeds, becomes right-left, i.e. changes its direction. The presence of stage 3 pulmonary hypertension in a patient may be the main reason for cardiac surgeons to refuse to perform an operation.

Clinical picture with VSD consists of a symptom complex of heart failure, which usually develops at 1-3 months of life (depending on the size of the defect). In addition to signs of heart failure, VSD can manifest with early and severe pneumonia. When examining a child, you can identify tachycardia and shortness of breath, expansion of the boundaries of relative cardiac dullness, and a displacement of the apex impulse down and to the left. In some cases, the symptom of “cat purring” is identified. Systolic murmur, as a rule, is intense, dries over the entire area of ​​the heart, is well carried out on the right side of the chest and on the back with a punctum maximum in the 4th intercostal space to the left of the sternum. Palpation of the abdomen reveals an enlarged liver and spleen. Changes in peripheral pulsation are not typical. Children with VSD and NK usually quickly develop malnutrition.

Diagnostics any heart defect consists of an X-ray examination of the chest organs, electrocardiography and two-dimensional Doppler echocardiography.

At X-ray examination of the chest cavity organs describes the shape of the heart and the state of the pulmonary pattern, and determines the size of the cardiothoracic index (CTI). All these indicators have their own characteristics for different degrees of pulmonary hypertension. In the first (hypervolemic) stage, a flattened waist and immersion of the apex into the diaphragm and an increase in the CTI are revealed. From the side of the pulmonary pattern, its intensification, indistinctness, and blurriness are noted. The extreme degree of hypervolemia in the lungs is pulmonary edema. In the transitional stage of pulmonary hypertension, normalization of the pulmonary pattern and some stabilization of the size of the CTI are noted. The sclerotic stage of pulmonary hypertension is characterized by a significant increase in the size of the heart, mainly due to the right sections, enlargement of the right atrium (formation of a right atrio-vasal angle), bulging of the pulmonary artery arch (Moore index more than 50%), elevation of the apex of the heart, which forms a aperture acute angle. In terms of the pulmonary pattern, the symptom of a “cut tree” is often described: bright, clear, enlarged roots, against the background of which the pulmonary pattern can be traced only to a certain level. On the periphery there are signs of emphysema. The chest has a swollen shape, the course of the ribs is horizontal, the diaphragm is flattened and stands low.

ECG has its own patterns, closely related to the phase of the course of congenital heart disease and the degree of pulmonary hypertension. First, signs of left ventricular overload are revealed - an increase in its activity, then the development of its hypertrophy. Over time, signs of overload and hypertrophy of the right parts of the heart - both the atrium and the ventricle - appear - this indicates high pulmonary hypertension. The electrical axis of the heart is always deviated to the right. Conduction disturbances may occur, ranging from signs of incomplete right bundle branch block to complete atrioventricular block.

At Doppler EchoCG The location of the defect and its size are specified, and the pressure in the right ventricle and pulmonary artery is determined. In the first stage of pulmonary hypertension, the pressure in the pancreas does not exceed 30 mmHg, in the second stage - from 30 to 70 mmHg, in the third - more than 70 mmHg.

Treatment of this defect involves conservative treatment of heart failure and surgical correction of the heart defect. Conservative treatment consists of inotropic support drugs (sympathomimetics, cardiac glycosides), diuretics, cardiotrophics. In cases of high pulmonary hypertension, angiotensin-converting enzyme inhibitors - capoten or captopril - are prescribed. Surgical interventions are divided into palliative operations (in the case of VSD - the operation of narrowing of the pulmonary artery according to Muller) and radical correction of the defect - plastic surgery of the ventricular septal defect with a patch of pericardial leaves under conditions of artificial circulation, cardioplegia and hypothermia.

Hypervolemia– a condition in which the volume of blood circulating in the vascular bed increases. There are simple, oligocythemic and polycythemic hypervolemia, which differ in hematocrit.

Isolated hypervolemia pulmonary circulation is called pulmonary hypertension.

The experience accumulated over the entire period of development of medicine has established certain limits for various laboratory indicators, exceeding the limits of which is regarded as a disease. The same framework defines the amount of blood simultaneously located inside our vessels.

The norm for an adult is a condition when a total amount of blood circulates inside the vessels of the whole body, equal in weight to 6 to 8 percent of body weight or 1/13. That is, a person weighing 75 kilograms simultaneously contains about 5 liters of blood inside the vessels.

Causes and types of hypervolemia

An increase in the volume of blood simultaneously circulating in the vascular bed is called hypervolemia. This condition is not an independent disease and is regarded as a syndrome - a complex of manifestations (symptoms) of any disease. Blood is represented by two main components: plasma (the liquid part) and formed elements (the totality of all blood cells). The ratio of the total volume of blood cells to the total volume of blood is called hematocrit and normally it is 36% - 48%, that is, in one liter of blood there are from 360 to 480 milliliters of cells, and the rest is plasma.

Depending on the change in hematocrit number, hypervolemia is divided into three types:

• Simple hypervolemia;
• Oligocythemic hypervolemia;
• Polycythemic hypervolemia.

blood from polycythemic hypervolemia

Each of the listed types of hypervolemia has its own separate cause, which determines the different approaches to treatment and diagnosis.

Simple hypervolemia

Simple hypervolemia - a condition when there is a proportional increase in the amount of circulating blood, that is, the ratio of all cells and the liquid part per unit volume of blood remains within normal values. This condition is observed quite rarely, its causes are:

1. Transfusion (transfusion) of excessive amounts of blood;
2. High ambient temperature;
3. Acute lack of oxygen (hypoxia).

In the first case, hypervolemia develops as a result of the intake of an excessive amount of normal blood in terms of hematocrit from the outside; in the rest, the same blood corresponding to the norm enters the vascular bed from the depot (reserves) of one’s own body.

In a situation oligocythemic hypervolemia an increase in the amount of circulating blood is associated with an increase in the amount of the liquid component of the blood, while the hematocrit becomes lower than normal. This condition is called hydremia and is caused by:

• Pregnancy - hydremia when carrying a child is the norm and promotes adequate metabolism between the body of mother and child;
• Increasing the flow of fluid into the vascular bed (excessive drinking, transfusion of plasma and plasma substitutes, transfer of fluid during edema from tissues to blood vessels);
• Decreased fluid excretion from the body (acute and chronic renal failure, increased formation of antidiuretic hormone, sodium retention).

Polycythemic hypervolemia – develops in cases where an increase in blood volume in the vascular bed is achieved due to the cellular component, which is accompanied by an increase in hematocrit. This condition is caused by:

1. Chronic hypoxia: heart defects, chronic lung diseases with insufficient lung function, prolonged stay in high altitude conditions, etc.;
2. Blood diseases - malignant and benign tumors, hereditary anomalies, accompanied by increased formation of blood cells.

Clinical manifestations, diagnosis and treatment of hypervolemia

Signs of hypervolemia and treatment tactics largely depend on its type and the reasons that caused this condition.

In the case of physiological and functional reasons that do not go beyond the adaptive abilities of our body, the manifestations are short-term and without any special medical manipulations the body will independently restore its normal state.

If hypervolemia is caused by any chronic or acute disease, treatment tactics are aimed primarily at the disease itself, which causes an increase in the amount of intravascular blood, and also, if necessary, at relieving the immediate symptoms of hypervolemia, which manifests itself in a variety of ways and nonspecifically:

• Increased blood pressure;
• An increase in the load on the heart can lead to manifestations of heart failure and angina pectoris;
• unexplained weight gain;
• Edema;
• Dyspnea;
• Feeling of dry skin and dry mouth;
• Urinary disorders;
• Increased breathing rate and feeling of heaviness when breathing;
• General weakness;
• Headache;
• Pain in the lumbar region;
• Increased fatigue.

Diagnosis of a hypervolemic state in practical medicine is difficult, which is due to the lack in clinical practice of objective, reliable, and most importantly safe methods for determining the volume of circulating blood. In other words, the methods that are used have proven themselves well in experimental science, explained this pathological process and laid the scientific foundations for the treatment of hypervolemia. Only the hematocrit indicator remains available for practical use, which is of great importance in determining the type of hypervolemia and the reasons that caused it.

Treatment tactics are based on two directions:

Etiotropic (directed at the cause of the pathology) treatment:

1. Fighting kidney diseases;
2. Surgical treatment of heart defects as early as possible;
3. Treatment of endocrine diseases;
4. Fighting tumors and congenital diseases of the blood system;
5. Treatment of acute and chronic lung diseases;
6. Carefully monitor the volume of intravenous infusions.

Symptomatic (aimed at combating the manifestations of pathology) treatment:

1. High blood pressure is treated with the use of antihypertensive drugs with an emphasis on diuretics;
2. Angina caused by hypervolemia requires, first of all, a reduction in the load on the heart and only then the use of antianginal drugs;
3. One of the leading elements of help with hypervolemia is placing the patient in comfortable conditions with normal ambient temperature and a sufficient amount of oxygen in the inhaled air.

Traditional medicine can also be considered effective and gentle treatment methods:

• Hirudotherapy (use of leeches) has a direct effect on blood volume, reducing it, and also reduces blood viscosity and slightly reduces the number of formed elements, which can normalize hematocrit in polycythemic hypervolemia;
• Herbal diuretics: fennel, dill, viburnum, bearberry, horsetail and others.

Treatment and especially diagnosis of hypervolemia requires a careful, comprehensive approach on the part of a qualified doctor, since the apparent simplicity and harmlessness of this condition may hide the initial manifestations of a serious disease, the early and timely diagnosis of which can save a person’s health and even life.

The blood inside the vascular bed is distributed unevenly: approximately 70% of all blood is constantly in the veins, about 15% in the arteries, 12% is in the thinnest vessels that perform the direct function of metabolism - capillaries, 3% inside the heart. The entire circulatory system is divided into large (includes vessels of all organs and tissues with the exception of the vessels of the lungs) and small (includes only the vessels of the lungs) circulatory circles.

About 75-80% of the total volume of circulating blood is simultaneously in the systemic circulation, and only 20-25% in the pulmonary circulation.

Isolated hypervolemia of the pulmonary circulation, or hypervolemia of the lungs, is called pulmonary hypertension in medicine, since signs of high pressure in the vessels of the lungs come to the fore in the clinic.

Causes of pulmonary hypervolemia

Pulmonary hypervolemia has a fairly large number of different factors in its causes, and not all of them have been well studied, and some have not yet been established. Known causes include:

1. Long-term insufficient oxygen content (hypoxia) inside the end sections of the respiratory tract - the alveoli. It is caused by chronic bronchitis (including smoker's bronchitis), emphysema, bronchiolitis, bronchiectasis, chronic obstructive pulmonary disease, silicosis, anthracosis and other diseases of the lungs and respiratory tract.
2. Acute reflexogenic narrowing of the small arteries of the lungs. Develops with severe emotional shock, embolism of pulmonary vessels (even small branches), mitral valve stenosis.
3. Increased pressure inside the respiratory tract. Occurs with intense coughing, increased external barometric pressure, and errors in artificial ventilation.
4. Insufficiency of left ventricular function, which occurs with heart attack, arrhythmia, myocarditis.

Also, one should not discount idiopathic – unknown causes that lead to primary pulmonary hypervolemia.

Signs of pulmonary hypervolemia

At the initial stages of its course, pulmonary hypervolemia does not have any pronounced manifestations, which is its danger - being undiagnosed, it slowly progresses and manifests itself only at the stages of an advanced and, alas, already irreversible pathological process:

• Asthenization – increased fatigue, mood lability, weight loss, sleep disturbances, etc.;
• Shortness of breath, even suffocation, worsening with physical activity;
• Frequent attacks of dizziness;
• Unexplained fainting, especially during exercise;
• Severe, unproductive cough, sometimes, in advanced cases, mixed with streaks of blood;
• Pain in the heart area;
• Cyanosis (blueness) of the skin at the beginning of the disease is barely noticeable, but as the disease progresses it becomes more pronounced;
• Edema, in severe cases ascites (fluid in the abdominal cavity);
• Pain in the right hypochondrium (in the liver area);
• Heart rhythm disturbances.

Diagnosis of pulmonary hypervolemia

Establishing a diagnosis of pulmonary hypervolemia is based on the above clinical manifestations and a number of laboratory and instrumental methods:

1. ECG - can indicate an increase in the size of the right chambers of the heart, identify a heart attack, arrhythmia and pulmonary embolism;
2. X-ray examination of the chest organs diagnoses an increase in the size of the heart, an increase in the vascular pattern of the pulmonary fields (effective in the later stages of the disease);

PH on x-ray

Treatment of pulmonary hypervolemia

Medical tactics for pulmonary hypervolemia are primarily aimed at treating the pathology that caused it, since pulmonary hypertension itself is only a manifestation of the underlying disease. The greatest difficulty, or rather the almost complete ineffectiveness of treatment measures, is primary (with an unknown cause) pulmonary hypertension, since the original source of the disease is unknown.

For the treatment of hypervolemia of the pulmonary circulation, all drugs and methods that are used to treat ordinary arterial hypertension are effective. A special feature is the more pronounced effectiveness of aminophylline and oxygen therapy against the background of a slightly reduced effectiveness of antihypertensive therapy.

Hypervolemia is an increase in the volume of circulating blood and plasma.

This condition can develop for the following reasons:

• Excessive water consumption
• Edema
• Water retention in the vascular bed
• Large volume blood transfusion
• Acute hypoxic conditions accompanied by the release of blood from the depot
• Sodium retention in the body
• Diseases of the cardiovascular system, respiratory system or kidneys
• Polycythemia, polycythemia vera
• Significant physical activity

Characteristic clinical manifestations of hypervolemia: weight gain, impaired urination and sweating, edema syndrome, hypertensive syndrome, dry skin, dry mouth, shortness of breath, weakness, headaches, difficulty breathing.

Normocythemic hypervolemia is manifested by an equivalent increase in the volume of formed elements and the liquid part of the circulating blood volume. Hematocrit (Ht) is within normal limits.

Oligocythemic hypervolemia is characterized by an increase in total blood volume. The Ht indicator is below normal.
Polycythemic hypervolemia is also manifested by an increase in the total volume of blood and an increase in the number of its formed elements. Ht is higher than normal.

Diagnosis of hypervolemia is based on the results of a patient interview, laboratory blood tests (to determine the number of red blood cells and plasma), and urine analysis.

The following types of hypervolemia are distinguished:

• normocythemic (simple)
• oligocythemic (hydremia, hemodilution)
• polycythemic

If symptoms characteristic of hypervolemia appear, you should consult a hematologist or anesthesiologist.

Treatment is determined by the cause of hypervolemia. If the condition is caused by sodium retention in the body, it is necessary to limit sodium intake from food. As prescribed by your doctor, use diuretics, hormones to improve kidney condition, and drugs to maintain cardiac function.

An increase in hypervolemia threatens pulmonary edema. Hypervolemia is especially dangerous against the background of massive intravenous administration of drugs, parenteral or tube nutrition.

There is evidence that hypervolemia has toxic effects on organ function and increases mortality in critically ill patients.

Prevention of hypervolemia is based on timely treatment of diseases of the cardiovascular system. To reduce the risk of hypervolemia, avoid excessive fluid intake and limit your intake of foods containing sodium (salty foods, fast food, baked goods (containing baking soda), hard cheese, etc.).

Hypervolemia is an increase in blood volume in the vascular bed. Depending on the characteristics of the hematocrit, hypervolemia is distinguished between oligocythemic, simple and polycythemic.

If we are talking about hypervolemia of the pulmonary circulation, then this condition is called pulmonary hypertension. Hypervolemia is not just a physiological deviation from the norm, but a pathological syndrome that accompanies various disorders. Inside the vessels of a healthy person, an amount of blood that corresponds to 6-8% of his weight should constantly circulate. Thus, if an individual weighs 75 kg, then there should be about 5 liters of blood in his body. Exceeding these values ​​is a deviation from the norm.

Why does hypervolemia develop?

An increase in the volume of blood circulating in the body does not occur by itself. Hypervolemia is always accompanied by a certain disorder in the body. Therefore, hypervolemia is not an independent pathology. It has a direct relationship with such a concept as hematocrit. Hematocrit characterizes the volume of red blood cells in the blood relative to the total volume of blood. Normally, a liter of blood should contain 360-480 ml of cells, and the rest of its composition will be plasma. Therefore, normal hematocrit values ​​in percentage terms look like 36-48%.

Hypervolemia, depending on the cause of its development, can be of 3 types:

Approaches to diagnosing and treating each type of hypervolemia will vary.

The photo below shows blood from polycythemic hypervolemia:

Simple hypervolemia

Simple hypervolemia develops when not only the volume of red blood cells increases in parallel, but also the level of blood plasma increases. The relationship between them is not violated.

Simple hypervolemia is not often diagnosed. The following reasons may lead to its development:

Large volume blood transfusions.

Excessive physical activity.

Exposure of a person to high temperatures.

If a person is transfused with a lot of blood, this naturally provokes an increase in its volume in the body. With increased physical activity, exposure to heat, and hypoxia, blood volumes increase due to the body’s own reserves.

Oligocythaemic hypervolemia

Oligocythemic hypervolemia is called hydremia. In this case, the volume of the liquid component of the blood increases, while the level of red blood cells remains unchanged.

The following conditions can lead to oligocythemic hypervolemia:

Conceiving a child. In this case, an increase in the liquid component of blood with a normal hematocrit is a variant of the norm. The body independently launches similar mechanisms in order to stabilize a woman’s metabolism in accordance with her new position.

Drinking plenty of fluids, transfusion of plasma and plasma analogues, release of fluid from edema into the vascular bed.

Acute or chronic renal failure, increased synthesis of antidiuretic hormone, sodium retention are situations that contribute to the retention of large volumes of fluid in the body.

Polycythemic hypervolemia

Polycythemic hypervolemia is characterized by an increase in blood volume due to an increase in the number of red blood cells.

Reasons that can provoke this violation:

Oxygen starvation of a chronic course, which is caused by heart defects, pathologies of the respiratory system with chronic respiratory failure, and a person being at significant altitudes.

Blood diseases: cancerous tumors (malignant and benign), increased formation of blood cells due to hereditary pathologies.

Symptoms of hypervolemia

If hypervolemia was provoked by physiological reasons, then after a short time the blood volumes will return to normal without any consequences for human health. No specialized treatment is required.

When hypervolemia was caused by chronic or acute pathologies, it is necessary to direct efforts to eliminate the root cause that led to an increase in blood volumes. Symptomatic therapy is also provided.

As for the symptoms of hypervolemia, they can be as follows:

Jumps in blood pressure in the direction of its increase.

The development of heart failure or angina pectoris, as the heart works under high stress.

The appearance of shortness of breath. In general, it becomes difficult for a person to breathe, despite the fact that the breathing rate increases.

The patient gets tired faster.

The skin becomes dry and a dry mouth appears.

Dysuric disorders develop.

Diagnosis of hypervolemia

Detecting hypervolemia is a rather difficult task that doctors face. There are no specific symptoms of the disorder, and it is quite difficult to calculate the total volume of blood in the body. Therefore, the diagnosis of hypervolemia comes down to determining hematocrit values. This study makes it possible not only to detect hypervolemia itself, but also to determine its type, as well as to clarify the cause of the development of this condition.

Treatment of hypervolemia

Therapy for hypervolemia should be aimed at the cause that provoked this disorder:

Treatment of kidney pathology.

Treatment of heart defects.

Therapy for disorders of the endocrine glands.

Surgical and drug treatment of tumor neoplasms.

Treatment of blood diseases.

Therapy of diseases of the respiratory system.

Performing blood transfusions in accordance with existing medical protocols, without violating the rules of the procedure.

To get rid of the symptoms of hypervolemia and alleviate the patient’s condition, the following measures may be recommended:

Taking medications to lower blood pressure. Diuretics are prescribed for this purpose.

Reducing the load on the heart muscle.

Controlling the ambient temperature, ensuring sufficient oxygen supply to the tissues, which is aimed at eliminating hypoxia.

Alternative medicine methods can also be used in the treatment of hypervolemia:

Treatment with leeches, which helps to reduce the volume of circulating blood in the body, reduce its viscosity, and normalize the qualitative composition.

Taking herbal diuretics. Bearberry, horsetail, viburnum, dill, and fennel have such properties.

Hypervolemia should be treated by a doctor. Self-therapy can lead to serious health problems and even be life-threatening.

Hypervolemia of the pulmonary circulation

If we consider the distribution of blood in the vascular bed, then about 70% of its volume will always be present in the veins, about 15% in the arteries and about 12% in the capillaries. The remaining 3% falls on the heart cavity.

The circulatory system consists of a large and small circle. The systemic circulation includes vessels of all organs and tissues, with the exception of the vessels of the lungs. The pulmonary circulation includes vessels that supply blood to the lungs.

About 25% of the total blood volume circulates in the pulmonary circulation, and the systemic circulation accounts for the remaining 75%.

With the development of hypervolemia of the pulmonary circulation, the lungs are included in the pathological process, so the main symptoms will appear precisely from these organs.

Why does hypervolemia of the pulmonary circulation develop?

The development of hypervolemia of the pulmonary circulation can occur for the following reasons:

Hypoxia of the alveoli to which oxygen will not reach. The cause of this disorder is chronic bronchitis, chronic pulmonary obstruction, silicosis, anthracosis, bronchiectasis, etc.

Spasm of the small arteries of the lungs. Stress, pulmonary embolism, and mitral valve stenosis can lead to the development of such a disorder.

High pressure in the respiratory tract leads to a strong cough, a jump in barometric pressure, and violations of technology when performing mechanical ventilation.

Malfunction of the left ventricle of the heart, which is observed during myocardial infarction, against the background of arrhythmia and myocarditis.

Excessive ejection of blood from the right ventricle of the heart.

Tumors, aneurysms, adhesions and other disorders that interfere with the blood vessels that carry blood from the lungs.

Chronic poisoning of the body with narcotic substances.

Genetic disorders leading to enzymatic failures.

Increased pressure in the portal vein system, which can occur due to cirrhosis, syndrome and Budd-Chiari disease.

AIDS virus.

Short-term pauses in breathing during night rest.

In addition, there is a type of hypervolemia of the pulmonary circulation, which develops for unknown reasons.

Symptoms of pulmonary hypervolemia

When the disorder first begins to develop, the person will not experience any symptoms.

As hypervolemia of the pulmonary circulation progresses, the following health problems are possible:

A person gets tired quickly, has mood swings, loses weight, and suffers from insomnia.

The patient often experiences dizziness.

Shortness of breath increases, it will be very difficult to breathe during severe physical exertion.

In severe cases, fainting is possible.

A person begins to suffer from paroxysmal coughing, accompanied by sputum and blood.

Periodically there are attacks of heart pain.

The skin is pale, and as the disease progresses, cyanosis increases.

Painful sensations begin to disturb the liver area.

The heart works intermittently.

How to detect hypervolemia of the pulmonary circulation?

A preliminary diagnosis is made based on symptoms of hypervolemia. To confirm it, the doctor refers the patient to the following examinations:

An electrocardiogram can detect abnormalities in the heart.

A chest x-ray provides information about the condition of the lungs; with hypervolemia, their vascular pattern increases. The heart increases in size.

Ultrasound of the heart allows you to assess its size, clarify the speed of blood flow and the volume of pumped blood.

The level of pressure in the pulmonary system can be determined using the pulmonary trunk catheterization method. This is an invasive procedure during which special sensors are inserted into the lumen of the lung vessels. This study makes it possible to detect hypervolemia with a high degree of probability, even at the earliest stages of its development.

How to treat?

To eliminate hypervolemia of the pulmonary circulation, you will need to direct efforts to the cause that provoked such a disorder. It makes no sense to treat hypervolemia without identifying the etiological factor.

Most often, drugs that are effective in correcting high blood pressure are used in therapy. A drug such as Eufillin has proven itself well. It is also necessary to take measures aimed at eliminating tissue hypoxia (oxygen therapy).

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