preshock

Preshock is a clinical state describing early circulatory failure and inadequate tissue perfusion that has not yet progressed to overt shock. In preshock, blood pressure may be normal or only mildly reduced because the body’s compensatory mechanisms, such as tachycardia and peripheral vasoconstriction, help maintain perfusion. It is often considered equivalent to compensated or early shock in some clinical contexts.

The pathophysiology involves a reduced effective circulating volume or cardiac output that triggers sympathetic activation, vasoconstriction, and changes in microcirculation. Tissue hypoxia can lead to lactic acidosis and metabolic disturbances. If the underlying problem is not addressed, perfusion deteriorates and the patient may rapidly progress to decompensated shock with organ dysfunction.

Clinical features of preshock include tachycardia, tachypnea, cool clammy skin, narrowed pulse pressure, delayed capillary refill, decreased urine output, and possible mild mental status changes. Vital signs may still appear near normal, so careful assessment of perfusion and lactate levels, rather than blood pressure alone, is important. The condition can occur in various settings, including hemorrhage with volume loss, dehydration, and early sepsis, as well as cardiogenic ormaladaptive states.

Diagnosis relies on recognizing signs of impaired perfusion in the context of preserved blood pressure. Laboratory and monitoring data such as elevated lactate, base deficit, urine output, and hemodynamic parameters aid assessment, alongside identification of the underlying cause with history, exam, and imaging as needed.

Management focuses on rapid identification and reversal of the inciting problem, cautious fluid resuscitation for hypovolemia, oxygen therapy, and appropriate support. In sepsis, early antimicrobials and source control are essential; in hemorrhage, timely blood products may be required. Continuous monitoring is critical, as progression to overt shock is possible if untreated.