Based on meta-analyses (eg, Vasu, J Intens Care Med 2012) and the SOAP II trial (De Backer, NEJM, 2010), we prefer norepinephrine over dopamine in shock.
We also prefer norepinephrine as our first-line vasopressor for septic shock and vasopressin as our second-line vasopressor. I remember when low dose (1 - 5 mcg/Kg/min) dopamine was used for renal perfusion, but in practice I found the individual differences were so vast that the guidelines of that dosage for renal-dose dopamine were difficult to apply.
I do not think that there is any strong evidence to support the use of dopamine. The dose response of dopamine on the vascular beds si difficult to nitrate and unpredictable, especially when we use surrogate measures of perfusion, such as end organ function [rather than microvascular changes or mucosal level changes].
Current recommendations go against the use of "the so-called" Renal Dose of iv Dopamine in Septic Shock. Even though there is indeed a vasodilation effect of low-dose iv perfusion of Dopamine, especially at the Renal level, the use of this medication is NOT supported by the literature. The hypothesis is that Dopamine use could be linked with negative neuroendocrine effects. Concerning Urosepsis, NO difference. Best Regards.
According to 2012 KDIGO guidelines for acute renal failure (http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline.pdf) dopamine is not recommended. The recommendation is classified as 1A (i.e. strong recommendation based on high quality evidence).
As in the previous replies, several studies questioned the benefit of dopamine. Moreover, it is potentially harmful. De Baker et al when compared vasopressors' use in shock (N Engl J Med. 2010 Mar 4;362(9):779-89) demonstrated more adverse effects in association with dopamine. A recent meta-analysis (PLoS One. 2015; 10(8): e0129305.) found many benefits of norepinephrine over dopamine.
In our practice in the ICU, we do not use dopamine renal dose, we control the cause of AKI (Hemodynamic optimization, sepsis control, intra-abdominal pressure, holding nephrotoxic drugs), if we fail, we prefer early initiation of RRT based on recent studies (e.g. ELAIN trial, http://jama.jamanetwork.com/article.aspx?articleid=2522434).
This is a old thought of school. Write now there no literature based evidences that low dose dopamine is use in kidney injury. To achieve hemodynamic optimization nor adrenaline is indicated.
There is no proven role of low dose dopamine as renoprotective agents. A mata-analysis reviewing 21 trials in 970 patients showed no added advantage of low dose dopamine. Instead, higher adverse events were recorded in patients who were give low dose dopamine for renoprotective effect.
Vasopressors (noradrenaline and vasopressin) cause less arrhythmias than dopamine (De Backer et al, Avni et al.)
Those with cardiogenic shock may (probably?) do worse with dopamine as compared to noradrenaline. It might be extrapolated that those with septic shock and concurrent heart disease (ischaemic, cardiomyopathy) may also do worse
Early renal replacement therapy in patients with AKI (KDIGO 2+) is advantageous (Zarbock et al)
The neuro-endocrine effects - predominantly thyroid disfunction, and predominantly in those on dopamine continuously for more than a week.
Dopamine does not have an effect on the rate of development of renal failure i.e. it is not renally protective of its own right (balanced against the first point below).
balanced against:
raising the renal perfusion pressure by any means (pressors/inotropes) is probably renally protective if the renal perfusion pressure has fallen below a critical level, whatever that blood pressure happens to be for the individual patient
dopamine moderately increases urine output in a subset of patients (anecdotally, rarely in those who are completely anuric) (Bellomo et al).
dopamine can be administered more safely than noradrenaline through a peripheral IV, and some (non intensive care) wards allow its administration
Therefore as all the other answers, vasopressors are preferred to dopamine for septic shock (and probably the majority of forms of shock). However, it is important to note that they are not comparing pressors with nothing. there are 2 situations when a clinician might reasonably consider dopamine:
working in non-OECD nations, I have run out of a particular (preferred) inotrope or vasopressor, and in the setting of fluid refractory shock, anything to raise perfusion pressure to vital organs is probably preferable to nothing
There are some patients for whom active interventions are indicated, but admission to ICU, central line insertion and RRT are not. If blood pressure and urine output are almost but not quite acceptable , a short run of low dose dopamine on the ward might get them through (from a perfusion pressure and urine output point of view) for long enough for the other treatments (antibiotics, nephrostomy etc) to treat the underlying condition.
Dopamine does not have a specific role in increasing renal function. The side effects of large studies are related to high doses (DeBacker, NEJM,2010). It can be safe in some scenarios, although you may prefer specific vasopressors.