SHOCK TO RECOGNISE AND MANAGE

5. MANAGEMENT
HYPOVOLEMIC SHOCK is the common form in practice, we use this form as working model.

The signs and symptoms appear only when the loss from
the circulatory system is above a certain volume usually (750 cc)
The compensatory mechanism fail and tissue perfusion suffers as
a result.
A summary of these volume losses and manifestations
in a seventy kilogram man are given below:


-Thus the first sign may be a rise in pulse rate because of increase in catecholamine.
-As the loss of blood or fluid continues the pulse rises and the systolic BP falls.
-The urine production per hour drops.
-The mental state passes through stages of apprehension, anxiety and lethargy to coma

A clinical staging system of hemorrhagic shock based on the percentage of acute blood volume loss has been described

Typically
-Classes I(Loss of 750cc of blood) and II(loss of 750-1500) are referred to as compensated shock states in which the adrenergic response maintains a normal blood pressure.
-Passing from a compensated state of shock to class IV (uncompensated) shock may occur rapidly in children and young adults.
-De-compensation of homeostatic mechanisms and inability to maintain systolic blood pressure above 90 mmHg after trauma induced hypovolemia are associated with a mortality of more than 50%.
However, rapid and adequate restoration of circulating blood volume simultaneous with control of bleeding can reverse even severe hemorrhagic shock.
It is thus crucial to recognize compensated shock early and intervene with speed for good results.
Laboratory evaluation may provide some diagnostic information.
- Non hemorrhagic forms of hypovolemic shock cause hemoconcentration.
- If there is loss of free water, then hemoconcentration will occur with hyponatremia.
- Following acute hemorrhage there may be no alteration in the hemoglobin or hematocrit values when compensatory fluid shifts occur fluids are administered hemoglobin and hematocrit will drop.
In clinical situations in which the cause of underlying shock state is not clear, the most critical decision is to ensure that cardiogenic shock is not cause.
The findings of jugular venous distension, rates, and the presence of an S3 gallop in cardiogenic shock may assist in diagnosis.
Both forms of shock, however, are associated with a reduction in cardiac output and a compensatory sympathetic mediated response.
Further, both types of shock may be treated with, and respond to, volume resuscitation.
If the diagnosis is in doubt or the clinical situation suggests both as a possibility, then invasive monitoring with a pulmonary artery catheter may required to assess effect of therapy.
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