Clinicians vary in the use of high dose dopamine or norepinephrine in septic shock. There are several theoretical reasons why norepinephrine is better and this is supported by some studies. Much of our knowledge of the effects of dopamine comes from healthy humans. Dopamine is a naturally occurring catecholamine. You may recall that dopaminergic receptor stimulation predominates at low doses, causing an increase in renal and mesenteric flow. pi stimulation occurs at moderate doses causing increased myocardial contractility, heart rate, and cardiac output; a stimulation occurs at higher doses, increasing systemic vascular resistance and reducing renal blood flow. In the critically ill, there is wide interpatient variation in plasma clearance of dopamine. In healthy humans, dopamine infusions have theoretical beneficial effects on renal and splanchnic circulations but this has not translated into improved outcomes in studies. In fact, there is some evidence to suggest that dopamine may have detrimental effects on the splanchnic circulation in patients with sepsis.
Septic shock is characterised by a high cardiac output, low systemic vascular resistance, and a normal or low pulmonary arterial occlusion pressure. Norepinephrine is a potent a receptor agonist, that is, it vasoconstricts. It also stimulates pi receptors at higher doses, increasing cardiac output, but has no effect on p2 receptors. If norepinephrine is used in patients with uncorrected hypovolaemia, or in haemorrhagic shock, it has severe detrimental effects on tissue perfusion, particularly in the kidneys. Norepinephrine reduces renal, hepatic, and muscle blood flow but, when used in patients with septic shock who have been adequately fluid resuscitated, norepinephrine improves both urine production and renal function. This is because it improves renal perfusion pressure by raising blood pressure.
One prospective, double-blind, randomised trial compared norepinephrine and dopamine in the treatment of septic shock. Patients with similar characteristics were assigned to receive either norepinephrine 0-5-5 micrograms kg-1 per minute or dopamine 2-5-25 micrograms kg-1 per minute. If the haemodynamic and metabolic abnormalities were not corrected with the maximum dose of one drug then the other was added. The aim of therapy was to achieve for at least 6 hours an SVRI of > 1100 dyn.s cm-5 and/or a MAP of > 80 mmHg, a target cardiac index of >4 litres per minute m-2 and normalisation of oxygen delivery and uptake. Only 31% patients were successfully treated with dopamine compared with 93% with norepinephrine. Ten of the 11 patients who did not respond to dopamine and remained hypotensive and oliguric were successfully treated with norepinephrine. The authors conclude that norepinephrine was more effective and reliable than dopamine in reversing the abnormalities in septic shock (defined by hypotension despite adequate fluid therapy with a low SVR, high cardiac output, oliguria, and lactic acidosis). A decrease in lactate levels was also seen with norepinephrine. The effects of norepinephrine on oxygen transport remain unclear from available data; however, most studies have found clinical parameters of peripheral perfusion to be significantly improved. Increased splanchnic blood flow has been demonstrated in patients with septic shock treated with norepinephrine.
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