Vasopressors in shock: are we meeting our target and do we really understand what we are aiming at?

Excerpt

The rationale for the use of vasopressors in shock is twofold. First, in a rescue attempt, when arterial blood pressure drops below a critical threshold under which the heart and brain are hypoperfused, vasopressors are administered to restore arterial blood pressure back to levels that maintain coronary and cerebral perfusion, even if this potentiates peripheral vasoconstriction. Second, vasopressors are infused in the intention to reverse excessive vasodilatation in shock. Clinicians assume that systemic blood flow is then redistributed from the muscular, mesenteric, and cutaneous vascular beds to visceral and vital organs. Both in clinical practice [1, 2] and clinical trials [3, 4], mean arterial blood pressure (MAP) has been the primary parameter to guide resuscitation and titrate vasopressors in shock. However, it is increasingly acknowledged that using MAP as the main resuscitation endpoint in shock implies relevant limitations [5]. As MAP is, in simplified form, the mathematical product of cardiac output and vascular resistance, elevating MAP by increasing vascular resistance carries the detrimental risk of further compromising tissue perfusion in low cardiac output/high vascular resistance states. In addition, no clear relationship between MAP and microcirculatory blood flow has so far been established in patients with shock [6, 7]. Similarly, vasopressor-induced changes in MAP have had variable effects on capillary perfusion and single organ function in clinical studies [7]. Finally, it is unlikely that one specific resuscitation endpoint, instead of a physiology-based approach applying individualized endpoints and hemodynamic interventions, will be adequate for all patients in shock. …