Shock hemorrhagic

Hemorrhagic shock is a type of hypovolemic shock. The latter also occurs with burns and dehydration. Classification

• • Mild degree (loss of 20% of BCC)
  • Moderate (loss of 20-40% of BCC)
  • Severe (loss of more than 40% of BCC).

Compensatory mechanisms

• • Secretion of ADH
  • secretion of aldosterone and renin
  • secretion of catecholamines. Physiological reactions
  • Decreased diuresis
  • Vasoconstriction
  • Tachycardia.

Pathogenesis. The adaptation of the patient to blood loss is largely determined by changes in the capacity of the venous system (containing up to 75% of blood volume in a healthy person). However, the probabilities for mobilizing blood from the depot are limited: with a loss of more than 10% of the BCC, the CVP begins to fall and the venous return to the heart decreases. There is a syndrome of small ejection, leading to a decrease in perfusion of tissues and organs. In response, nonspecific compensatory endocrine changes are found. The release of ACTH, aldosterone and ADH leads to the retention of sodium, chlorides and water by the kidneys, while increasing potassium loss and reducing diuresis. The result of the release of adrenaline and norepinephrine is peripheral vasoconstriction. Less important organs (skin, muscles, intestines) are switched off from the blood flow, and the blood supply to vital organs (brain, heart, lungs) is saved, i.e. circulation is centralized. Vasoconstriction leads to deep tissue hypoxia and the development of acidosis. Under these conditions, proteolytic enzymes of the pancreas enter the bloodstream and stimulate the formation of kinins. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of shock. Clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of shock. Clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished. The latter increase the permeability of the vascular wall, which contributes to the transition of water and electrolytes into the interstitial space. As a result, aggregation of red blood cells occurs in the capillaries, creating a springboard for the formation of blood clots. This process immediately precedes the irreversibility of shock. Clinical picture. With the development of hemorrhagic shock, 3 stages are distinguished.

• • Compensated reversible shock. The volume of blood loss does not exceed 25% (700-1300 ml). Moderate tachycardia, blood pressure is either not changed or slightly lowered. The saphenous veins become empty, the CVP decreases. There is a sign of peripheral vasoconstriction: cold extremities. The amount of urine excreted is reduced by half (at a rate of 1-1.2 ml / min).
  • Decompensated reversible shock. The volume of blood loss is 25-45% (1300-1800 ml). The pulse rate reaches 120-140 per minute. Systolic blood pressure falls below 100 mm Hg, the value of pulse pressure decreases. Severe shortness of breath occurs, partly compensating for metabolic acidosis by respiratory alkalosis, but can also be a sign of a shock lung. Increased cold extremities, acrocyanosis. Cold sweat appears. The rate of urine output is below 20 ml/h.
  • Irreversible hemorrhagic shock. Its occurrence depends on the duration of circulatory decompensation (traditionally, with arterial hypotension over 12 hours). The volume of blood loss exceeds 50% (2000-2500 ml). The pulse exceeds 140 per minute, systolic blood pressure falls below 60 mm Hg. or not defined. Consciousness is absent. oligoanuria develops.

Treatment:. In hemorrhagic shock, vasopressor products (adrenaline, norepinephrine) are strictly contraindicated, since they aggravate peripheral vasoconstriction. For the treatment of arterial hypotension, which has developed as a result of blood loss, the following procedures are subsequently performed.

• • Catheterization of the main vein (most often the subclavian or internal jugular according to Seldinger).
  • Jet or drip intravenous administration of blood substitutes (polyglucin, gelatinol, rheopolyglucin, etc.). The patient’s blood type and its compatibility with the donor’s blood are determined. Carry out blood transfusion. Transfuse fresh frozen plasma, and if possible, albumin or protein. The total volume of fluid for intensive care can be calculated as follows.
  • With blood loss of 10-12% of the BCC (500-700 ml), the total volume of fluid should be 100-200% of the volume of blood loss at a ratio of saline and plasma-substituting solutions – 1: 1.
  • With an average blood loss (up to 15-20% of the BCC, 1000-1400 ml), compensation is made in the amount of 200-250% of blood loss. The transfusion medium consists of blood (in the amount of 40% of blood loss) and saline and colloid solutions in a ratio of 1:1.
  • With a large blood loss (20-40% of the BCC, 1500-2000 ml), the total volume of the transfused fluid is at least 300% of the blood loss. Blood is transfused in the amount of 70% of the lost. The ratio of salt and colloid solutions – 1:2.
  • With massive blood loss, constituting 50-60% of the BCC (2500-3000 ml), the total volume of infusion should be 300% higher than the blood loss, and the volume of transfused blood should be at least 100% of the blood loss. Salt and colloid solutions are used in a ratio of 1:3.
  • Fight against metabolic acidosis: infusion of 150-300 ml of 4% solution of sodium bicarbonate.
  • Glucocorticoids simultaneously with the beginning of blood replacement (up to 0.7-1.5 g of hydrocortisone IV). Contraindicated in case of suspected gastric bleeding.
  • Removal of spasm of peripheral vessels. Some surgeons recommend simultaneously with blood transfusions to administer ganglion blockers, neuroleptics. However, when they are used, the development of collapse is likely.
  • Trasilol or contrical 30,000-60,000 IU in 300-500 ml of 0.9% NaCl solution intravenously.
  • Humidified oxygen inhalation.
  • With hyperthermia – physical cooling (wrapping with ice packs), analgin (2 ml of 50% solution) or reopyrin (5 ml) deep intravenously.
  • Broad spectrum antibiotics.
  • Maintenance of diuresis (50-60 ml/h)
  • Adequate infusion therapy (until CVP reaches 120-150 mm of water column)
  • If the infusion is ineffective – osmotic diuretics (mannitol [mannitol] 1-1.5 g / kg in 5% glucose solution in / in the stream), if there is no effect – furosemide 40-160 mg

in/M OR in/in.

• Cardiac glycosides (contraindicated in conduction disorders [complete or partial AV block] and myocardial excitability [occurrence of ectopic foci of excitation]). With the development of bradycardia – stimulants of B-adrenergic receptors (izadrin 0.005 g sublingually). In the event of ventricular arrhythmias – lidocaine 0.1-0.2 g IV.