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Clinical picture of hemorrhagic shock

In clinical course of hemorrhagic shock three phases are distinguished:

— phase of compensation (erectile phase): continues up to 30 min, in very severe injury is not practically expressed. A patient is conscious, skin is pale and covered with cold clammy sweat, glance is anxious, he complains of pain loudly, verbal excitation, reflexes are reinforced, tachypnea, normal pulse or tachycardia, normal or even high AP, CVP is normal or raised, diuresis is reduced, temperature gradient is >1°C. The sharper is the erectile ph; se expressed, the worse is prognosis;

— phase of decompensation (torpid phase): tachycardia, AP and CVP are reduced, oliguria or anuria, pale skin, cyanosis, temperature gradient > 1°C A suggestion to divide, in addition, a phase of decompensation into 3 degrees of severity, in fact, for a choice of methods of treatment is of no significance;

— phase of irreversibility (terminal phase): AP, CVP and diuresis drop down to a critical level in spite of infusion therapy with the use of dopamin.

Thus, for the present, AP remains a basic criterion of shock severity. There is a notion of "critical level of AP" in shock. This level is 70-80 mm Hg. In the group of patients with AP lower the critical one, a death-rate sharply increases, since profound disorders of blood circulation arise in tissues that lead to development of irreversible shock.

In protracted hypotonia, < 70 mm Hg, for 1-2 hours, a development of necrosis is possible in the tissues of the brain, heart, kidneys and others, a barrier is reduced in the intestine for microorganisms and toxins that passing via the ischemic liver, are a real substrate for aggravation of shock.

Causes of irreversible shock:

— insufficient replenishment of VCB by volume and quality;

— continuing hemorrhage. "The tap must be shut";

— renewed hemorrhage;

— inadequate anesthesia and immobolization;

— bacterial and tissue toxemia;

— application of vasopressors in unreplenished VCB: on the background of generalized vascular spasm an additional pressure is exerted on vessels, tissue hypoxia is aggravated and lysis of cells and destruction of tissues advance.

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