Slaid 18 The compensatory-adaptive mechanisms during acute blood loss

Slaid 1 Bleeding and methods of hemostasis

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Bleeding (haemorragia) Haemorrhage, or bleeding, is the escape of blood from the blood vessels into the tissues and cavities of human body or outside, as the result of an injury or defect in the permeability of the blood vessel wall.

Allocate three concepts – bleeding, hemorrhage and a hematoma.

Speak about bleeding when blood actively comes from a vessel (vessels) to environment, hollow body, an organism cavity.

Diffusion treatment by blood of any fabric is called as hemorrhage (hypodermic cellulose, brain fabric, etc.).

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In other cases when the poured out blood causes stratification of tissues, separation of organs and as a result the dimension cavity arised, which is filled with a blood is formed, - we speak about a hematoma

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Classification of bleedings

1. Anatomic classification – as the damaged vessel:

• Arterial – blood of scarlet color, follows the pulsing stream;

• Venous – release of dark blood is characteristic;

• Capillary – the bleeding of the mixed character caused by damage of capillaries;

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• Parenchymatous – it is observed at damage of parenchymatous bodies (a liver, a spleen, kidneys, etc.). Bleeding usually long that is connected with feature of a structure of bodies. Their vessels are strongly connected with stromy body

Slaid 6. Classification according to mechanism of beginning:

n Mechanical failure, vessel rupture;

n Arrosive hemorrhage. This types of bleeding takes place during suppurative melting of wessel wall;

n Diapedetic hemorrhage;

n The violation of chemical composition of blood. The hemophilia, scarlet fever, sepsis, scurvy and others are causing bleeding sometimes. Toxins or beriberi to produce defect in the permeability of the vascular walls and caused of hemorrhage;

n Increased of arterial and venous blood pressure. The diseases, such as essential hypertension, atherosclerosis sometimes coursed of an injury of the vascular wall and bleeding (stroke, hemorrhoidal bleeding, etc.);

n Violation of fibrillation (haemophilia, Werlgof’s disease, cholemic hemorrhage in patients with jaundice)

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Classification according to environment the bleeding:

• External

• Internal: a) obvious, b) the hidden

Internal call bleeding at which blood streams in a gleam of hollow bodies, in fabric or in internal cavities of an organism. Internal bleedings share on obvious and hidden. Internal obvious are bleedings at which blood streams in a gleam of hollow bodies, thus being allocated even in the changed look through some period (gastric contents like "coffee thick", a liquid chair tar-like black melena color), it is necessary to carry also bleedings from kidneys and urinary tract (haematuria), from bilepassing system here – haemobilia.

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The internal hidden – bleedings at which blood streams in various cavities of a body therefore an eye aren't visible:

• In a cavity of a skull (haemorragia cerebri).

• In a cavity of a joint (haemartrosis).

• In a pleural cavity (haemothorax).

• In an abdominal cavity (haemoperitoneum).

• In a cavity of a pericardium (haemopericardium).

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On time of developing of bleeding are divided on:

a) primary, come at the time of wound and are direct result of a trauma,

b) the early secondary – during the first hours and days (about 3 days) after a stop of primary bleeding (before development of an infection in a wound). They develop owing to expression of blood clot at increase of arterial pressure, disappearance of the angiospasm arising at sharp blood loss, sliding from a vessel of the ligature imposed at primary operation

c) the late secondary develop after 3 days after a stop of primary bleeding, are connected with destruction of a vascular wall as a result of development in a wound of purulent process.

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On a current:

• Acute – the expiration of blood is observed in a short period;

• Chronic – bleeding occurs gradually, small portions.

Loss of considerable volume of blood causes heavy violations in work of vitals therefore the special term is applied to these situations: sharp massive blood loss. Understand the blood loss which is followed by falling systolic А/Д, sharp weakness, sometimes loss of consciousness, short wind, fall of peripheral veins, an oliguriya as sharp massive blood loss.

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Pathogenesis of sharp blood loss. Sharp blood loss causes deep reorganization of blood circulation in an organism and puts into operation the most difficult mechanisms of compensation of the broken homeostasis.

Developments of a syndrome of sharp massive blood loss are the cornerstone three leading pathogenetic factors:

1) decrease in the volume of the circulating blood (VCB);

2) loss of oxygen function of blood;

3) violations in system of a hemostasis (DVS-syndrome).

VCB consists of the volume of the circulating plasma (VCP) and the volume of blood cells – the globulyarny volume (GV). More than 90% of GV are provided with erythrocytes. VCB at adults makes about 7% of body weight or 70 ml/kg of body weight at men and 65 ml/kg – at women.

Sharp blood loss leads to fast reduction of volume of the circulating blood. A sudden gipovolemiya, being a powerful factor of a stress, causes vegetative and endocrine shifts.

The main mechanisms of compensation of loss of VCB at sharp blood loss are activation of simpato-adrenalovy system and a gemodilyution. Serve as the starting moments in activation of simpato-adrenalovy system pressure decline in large vessels, first of all in sleepy where in the field of carotid sine there is a large number of bar recipes, and also damage of an adventitsia cover of vessels where pass sympathetic fibers. In response to blood loss activity hypophysial- adrenal glands systems is stimulated. Secretion of an aldosteron and antidiuretic hormone amplifies, emission of the glucocorticoids influencing a tone and permeability of a vascular wall increases. In response to it certain compensatory and adaptive mechanisms turn on.

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Venospazm – veins are the main capacitor part of the vascular course, in them there are 70% of all VCB, in arteries – 15%, in capillaries of-12%, in heart cameras – 3%. At such ratios narrowing of the venous course easily supports a normal blood-groove, despite a gipovolume as the venomotor reflex offsets loss of 10-15% of VCB, i.e. 500 ml of blood at the adult.

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Interstitial fluid inflow – an autogemodilyution. Owing to a gipovolume, and also a syndrome of small warm emission, hydrostatic pressure in capillaries that leads to transition to them of intercellular liquid decreases. Such mechanism the first 5 minutes after blood loss can provide inflow to vessels to 10-15% of VCB. The main exponents of a gemodilyution are gematokrit, level hemoglobin and quantity of erythrocytes – these indicators are used in clinic of an assessment of volume and weight of blood loss.

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Tachycardia – development of a gipovolume leads to decrease in venous inflow to heart and, respectively, warm emission. The developing tachycardia connected with influence of simpaticoadrenal system certain time allows to support minute warm volume at the normal level.

Slaid 15. Oliguriya – at a gipovolume occurs stimulation of secretion of an antidiuretic hormone of a hypophysis and an aldosteron is leads to increase in a reabsorption of water, a delay of ions of sodium and chlorides.

Slaid 16. Hyperventilation – at the beginning adaptive hyperventilation is directed on increase in suction action of a thorax and compensatory increase in inflow of blood to heart, then its development is in many respects connected with metabolic changes in bodies and fabrics and violation of acid-base balance.

Slaid 17. Peripheral arteriolespasm is a transitional stage between compensatory and pathological reactions at blood loss – the most important mechanism of support of system arterial pressure and blood supply of a brain (a vicious circle at sharp blood loss).

Slaid 18 The compensatory-adaptive mechanisms during acute blood loss

Sympaticoadrenal system’ activation;

Дата добавления: 2015-11-14