Emergency Medical Services. Группа авторов

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SECTION III Circulation

       Francis X. Guyette, Raymond L. Fowler, and Ronald N. Roth

      Shock is a life‐threatening physiological state characterized by decreased tissue perfusion and end‐organ tissue dysfunction, and is a significant predictor for complications including death [1]. The presence of shock must be recognized and therapeutic interventions must be started early to prevent progression. Unfortunately, identification and treatment of shock in the out‐of‐hospital setting are fraught with many difficulties and potential pitfalls. Patient assessment is often limited by the challenging environment. The tools available for the diagnosis and treatment of shock in the field are limited. Even when shock is properly identified, the most appropriate management is often unknown or the subject of debate.

      In the field, identification of shock relies primarily on recognition of signs and symptoms, including tachycardia, poor skin perfusion, and altered mental status. Note that hypotension, arbitrarily defined at a systolic blood pressure (sBP) of less than 90 mmHg, is not an adequate definition of shock and may not adequately reflect the onset of tissue hypoperfusion [2]. Unfortunately, the early stages of compensated shock, with only subtle alterations in physical findings, are easily overlooked or misinterpreted by clinicians. Physiological changes associated with age, pregnancy, or treatment for medical conditions such as beta‐blockers for hypertension, may also mask or alter the body’s compensatory responses. As a result, the patient with severe shock may present with near‐normal vital signs.

      Shock is a complex physiological process defined as the widespread reduction in tissue perfusion leading to cellular and organ dysfunction and death. In the early stages of shock, a series of complex compensatory mechanisms act to preserve critical organ perfusion [3]. In general, the following relationships drive this process:

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      Any condition that lowers cardiac output or peripheral vascular resistance may decrease blood pressure. Alterations of heart rate (very low or very high) can lower cardiac output, and hence can reduce blood pressure secondary to decreased cardiac filling. Decreasing stroke volume may lower cardiac output with a possible reduction in perfusion as well. Cardiac output may be reduced by lower circulating blood volume (e.g., hemorrhage or dehydration), by damage to the heart (e.g., myocardial infarction or myocarditis), or by conditions obstructing blood flow through the thorax (e.g., tension pneumothorax, cardiac tamponade, or extensive pulmonary embolism).

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Type of shock Disorder Examples Comments
Hypovolemic Decreased intravascular fluid volume A. External fluid loss Hemorrhage Gastrointestinal losses Renal losses Cutaneous loss B. Internal fluid loss Fractures Intestinal obstruction Hemothorax Hemoperitoneum Third spacing