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Abstract
Background
The 'Surviving Sepsis' Campaign guidelines recommend the use of dopamine or noradrenaline as the first vasopressor in septic shock. However, information that guides clinicians in choosing between dopamine and noradrenaline as the first vasopressor in patients with septic shock is limited.
Objective
This article presents a review of the literature regarding the use of dopamine versus noradrenaline in patients with septic shock.
Results
Two randomised controlled trials (RCT) and two large prospective cohort studies were analysed. RCT data showed dopamine was associated with increased arrhythmic events. One cohort study found dopamine was associated with higher 30-day mortality. The other cohort study found noradrenaline was associated with higher 28-day mortality.
Discussion
Data on the use of dopamine versus noradrenaline in patients with septic shock is limited. Following the recent SOAP II study, there is now strong evidence that the use of dopamine in septic shock is associated with significantly more cardiovascular adverse events, compared to noradrenaline.
Conclusion
Noradrenaline should be used as the initial vasopressor in septic shock to avoid the arrhythmic events associated with dopamine.
Key Words
Dopamine, noradrenaline, norepinephrine, sepsis, septic shock, vasopressor
Background
The 2008 'Surviving Sepsis Campaign International Guidelines' define severe sepsis as acute organ dysfunction (e.g. hypotension, decreased urine output and elevated creatinine) secondary to infection.1 Septic shock is defined as severe sepsis with hypotension that is refractory to fluid resuscitation.1 Septic shock needs to be recognised and treated immediately as it carries high mortality. To maintain adequate organ perfusion, the administration of a vasopressor is required. The Surviving Sepsis Campaign recommends either noradrenaline or dopamine as the first choice vasopressor agent to correct hypotension in septic shock.1
Dopamine is the precursor for noradrenaline in the sympathetic nervous system.2 At doses of 1- 2µg/kilogram/minute, it mainly acts on vascular dopamine-1 receptors causing selective vasodilatation. At doses between 5 and 10 µg/kilogram/minute, dopamine also acts on beta-1 adrenergic receptors in the heart to increase cardiac output by increasing stroke volume and heart rate; at doses above 10 µg/kilogram/minute, it mainly acts on vascular alpha-1 adrenoceptors to cause vasoconstriction, increasing the systemic vascular resistance.3 The adverse effects of dopamine include the suppression of prolactin, thyroid stimulating hormone and luteinising hormone.4 It was previously believed that low dose dopamine in...