Noradrenaline: friend or foe?

Septic shock, systemic inflammation and pharmacological vasodilatation are often complicated by systemic hypotension despite aggressive fluid resuscitation and an increased cardiac output. If the physician wishes to restore arterial pressure to higher levels (> 80-85 mmHg), with the aim of sustaining cerebral and coronary perfusion pressure, the administration of systemic vasopressor agents, such as norepinephrine (noradrenaline), becomes necessary. However, because norepinephrine (NE) induces vasoconstriction in many vascular beds (visibly in the skin), it may decrease renal and visceral blood flow, impairing visceral organ function. This unproven fear deters clinicians from using NE more consistently. Vasodilated states, however, are often associated with impaired peripheral vascular responsiveness. In such states, unlike under normal circulatory conditions, NE may actually improve visceral organ blood flow by selectively increasing organ perfusion pressure. Data available from animal studies show that the increased organ perfusion pressures achieved with NE results in improved GFR and renal blood flow. In fact, recent sophisticated physiological analysis of its effects on the kidney shows that, even after controlling for the pressure effect, NE therapy is associated with an increase in renal blood flow after endotoxin administration. In particular, the renal Pzf (pressure at which there is no further blood flow) is decreased such that, at a constant pressure, renal blood flow increases after NE. There are no controlled human data to define the effects of NE on the kidney in the clinical context. However, many patient series have now been reported. They show a seemingly positive effect of NE administration on GFR and urine output. Our clinical experience in septic patients and cardiac patients with inflammatory or pharmacological vasodilatation is also positive. We have demonstrated a positive effect on coronary blood flow. There is no reason to fear the effect of NE. If it is used to support a vasodilated circulation after adequate intravascular filling has occurred and after a normal or increased cardiac output has been established, it is likely to be a friend not a foe.