Introduction

Arterial hypotension associated with circulatory shock, and hence altered tissue perfusion, threatens organ function. In all critically ill patients, a priority must be to restore and maintain an adequate tissue perfusion pressure. Fluids must be administered first, but if hypotension persists despite sufficient fluid loading, vasopressor support is indeed required with the aim of restoring a minimal perfusion pressure. Vasoconstrictors can also help to redistribute blood from non-vital organs such as the skin and muscle, where vasoconstriction effects are maximal, to vital organs such as the heart and brain. However, one must be aware of the risks associated with excessive vasoconstriction.

All vasopressors increase cardiac filling pressures as well as systemic pressure, thus favoring the development of pulmonary edema. Therefore it may be misleading to assume that administration of vasopressor agents instead of further fluids will avoid the risk of pulmonary edema. Before any pharmacological intervention, fluid administration must be optimized to ensure that hypovolemia is corrected.

Particular care must be taken about possible impairments in blood flow associated with excessive vasoconstriction. By increasing peripheral resistance, vasoconstriction increases ventricular afterload and thus can limit cardiac output. Its peripheral effects can also limit capillary blood flow and may increase tissue hypoxia, often already compromised. Thus such vasoconstriction may increase the risk of development of multiple organ failure. Hence the additional use of inotropic agents such as dobutamine may be required to maintain oxygen delivery to the tissues.

The effects of agents in common use today, as well as those of some more experimental vasoconstrictors, on common hemodynamic indices are summarized in Table 1.

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Table 1 Relative effects of current and experimental vasoconstrictors on common hemodynamic indices

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