Fluids and circulatory support

Apart from the utilization of oxygen, correction of plasma volume deficit is the most critical intervention in shock. Early administration of fluid often corrects features of shock such as hypotension or oliguria. Hypovolemia must be treated urgently to avoid the serious complication of progressive organ failure. Indeed, milder degrees of hypovolemia are associated with the pathophysiological changes leading, ultimately, to organ failure or dysfunction.

An adequate circulating volume must be provided before considering other methods of circulatory support. This remains true in the patient with capillary leak, where some would choose to reduce the circulating volume in an attempt to avoid edema formation while supporting the circulation with inotropes ('dry and drive'). Figure.1 shows the effects of inotropes or colloid solutions on components of the Starling equation. The main effect of both inotropes and colloids is to increase capillary pressure; both therefore increase transcapillary fluid flux. The use of inotropic agents in hypovolemic patients often leads to tachycardia with an associated increase in myocardial oxygen demand. Inotropes also have various effects in different parts of the circulation depending on the balance of a, b, and dopaminergic stimulation. Since the endogenous stimulation of these receptors is not predictable for the critically ill individual, it follows that the balance of vasodilatation versus vasoconstriction is also not predictable for particular tissues, particularly where there is an endogenous response to hypovolemia. The result is an unpredictable maldistribution of flow.

Fig. 1 Effects of colloid or inotropes in the hypovolemic patient. Transcapillary fluid flux Jv is increased by both inotropes and colloid since both mainly increase capillary hydrostatic pressure Pc. Colloids have the advantage of providing better microcirculatory flow, and they may increase intravascular oncotic pressure p c and the reflection coefficient s, thus increasing intravascular retention of fluid. Inotopes increase myocardial oxygen demand by increasing heart rate. Minor effects on interstitial pressures Pi and pi are probably of little significance.

The use of fluid to restore circulating volume overcomes many of the problems associated with inotropes in the hypovolemic patient. Increase in stroke volume is achieved without further increase in sympathetic drive, thus avoiding the problem of tachycardia. Indeed, in those who have a tachycardic response to hypovolemia, restoration of circulating volume would reduce the tachycardia and myocardial oxygen demand. Likewise, a reduction in peripheral vasoconstriction secondarily induced by hypovolemia will improve microcirculatory blood flow. Only after the circulating volume has been restored can the use of additional circulatory support be recommended to minimize problems associated with endogenous sympathetic drive.

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