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Is There Still a Place for Dopamine in the Modern Intensive Care Unit?

Is There Still a Place for Dopamine in the Modern Intensive Care Unit?. R1 劉志中. Anesth Analg 2004;98:461-8. What we thought Dopamine Before…. Cardiovascular effect 2 to 5 µg · kg-1 · min-1: dopaminergic (80% to 100%), [beta]-adrenergic effects (5% to 20%).

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Is There Still a Place for Dopamine in the Modern Intensive Care Unit?

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  1. Is There Still a Place for Dopamine in the Modern Intensive Care Unit? R1 劉志中 Anesth Analg 2004;98:461-8

  2. What we thought Dopamine Before… • Cardiovascular effect • 2 to 5 µg · kg-1 · min-1: dopaminergic (80% to 100%), [beta]-adrenergic effects (5% to 20%). • 5 to 10 µg · kg-1 · min-1: [beta]-adrenergic effects predominate, and [alpha]-adrenergic actions gradually become important. • 10 to 20 µg · kg-1 · min-1 : primarily [alpha]- and [beta]-adrenergic effects

  3. What we thought Low Dose Dopamine Before… • Prevention and treatment of acute renal failure • Protection of the gut • Relatively free of side effect

  4. Introduction • Goldberg : a protective effect of low dose dopamine(<5µg · kg-1 · min-1) on renal function • The presumed protective effects on renal and splachnic perfusion have been repeatedly questioned.

  5. Renal effects • Augment renal blood flow • DA-1 recepter: renal vasodilation • DA-2 recepter on presynaptic nerve endings: inhibition of NE release • Large doses: βeffect to increase C.O. • Trigger natriuresis and diuresis through a direct effect on the tubular cell function

  6. Renal effects • Trigger natriuresis and diuresis through a direct effect on the tubular cell function • DA-1, DA-2 recepter on proximal tubule, thick ascending limb of the loop of Henle,cortical collecting tube : inhibit Na/K –ATPase  Natriuresis. • DA-2 recepters in the inner medullary collecting ducts  PGE2 production antagonizes ADH  increase free water clearance

  7. Renal effects • Regional redistribution of blood flow within the kidney (potentially detrimental) • Preferentially increasing cortical blood flow • PGE2:enhance blood flow in inner medulla shunting of blood away from the outer medulla which is very susceptible to ischemic injury in ARF. Dopamine and the kidney: ten years on. Clin Sci (Lond) 1993; 84: 357–75.

  8. Renal effects • Increasing urine output • renal hypoperfusion is a leading cause of ARF • The risk of inducing renal failure in normovolemic and hypovolemic patients • LDD increases urine output by enhancing cardiac output and thus not primarily by a direct renal effect

  9. …During norepinephrine infusion, increasing doses of dopamine from 2 to 6 μg‧kg-1‧min-1,augments CO,diuresis,and sodium excretion in p’t treated for septic shock,without changes in creatinine clearance… The renal and neurohumoral effects of the addition of low-dose dopamine in septic critically ill patients. Intensive Care Med 2000; 26: 1685–9

  10. Controversy of LDD on Renal function • Beneficial or detrimental ? • Increased urine output = improved renal function? • How strong is the clinical evidence on critically ill patient ?

  11. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial—Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group.Lancet 2000; 356: 2139–43

  12. Background • Multicentre, rendomised , double-blind,placebo-controlled study in ICU patients at the risk of ARF to assess whether dopamine attenuated the rise in serum creatinine Lancet 2000; 356: 2139–43

  13. Methods (patients) • Between March,1996 and April, 1999 • Inclusion criteria: • presence of a central venous catheter • two or more of the pathophysiological changes of the SIRS over a 24 h period • At least one indicator of early renal dysfunction (urine output averaging <0·5 mL/kg hourly over 4 h or longer; serum creatinine concentration of >80 mol/L in less than 24 h in theabsence of creatine kinase >5000 IU/L or myoglobin in the urine) Lancet 2000; 356: 2139–43

  14. Methods (patients) • Exclusion criteria: • age under 18 years • an episode of acute renal failure within the previous 3 months • previous renal transplantation • use of dopamine at anydose during the current hospital stay • baseline serum creatinine concentration above 300 μmol/L • Enrolling physician’s belief that the drug could not be administered for 8 h or longer; • unsuitability for use of renal replacement therapy. Lancet 2000; 356: 2139–43

  15. Methods Lancet 2000; 356: 2139–43

  16. Methods • Continuous infusion of dopamine at 2μg‧kg-1‧min-1 ( or equivalent volume for placebo) until .. • Renal replacement therapy • Patient died • a serious adverse event developed thatwas judged to be related to the trial infusion; • the patient’s SIRS and renal dysfunction had resolved for at least 24 h • the patient was discharged from ICU. Lancet 2000; 356: 2139–43

  17. Results Lancet 2000; 356: 2139–43

  18. Results Lancet 2000; 356: 2139–43

  19. Results • There was no difference in • Peak creatinine concentration • Increase from baseline to highest value during treatment • Who required renal replacement therapy • Duration of ICU stay • Hospital stay • Death Lancet 2000; 356: 2139–43

  20. Interpretation • Administration of low-dose dopamine by continuous intravenous infusion to critically ill patients at risk of renal failure does not confer clinically significant protection from renal dysfunction. Lancet 2000; 356: 2139–43

  21. Controversy of LDD on Renal function • Beneficial or detrimental ? • Increased urine output = improved renal function? • How strong is the clinical evidence on critically ill patient ?

  22. LDD on renal effect • LDD may increase urine output in critically ill patient,but it neither prevents nor improves ARF. • When dopamine does increase diuresis, it may actually increase the risk of ARF in normovolemic and hypovolemic patients.

  23. Effects on Splachnic perfusion • The gut may be particularly susceptible to ischemia in shock • Disruption of the gut mucosal barrier is thought to play a key role in the development of multiple organ failure ~Am J Respir Crit Care Med 1998; 158: 444–51

  24. Effects on Splachnic perfusion • The gut may be particularly susceptible to ischemia in shock • Disruption of the gut mucosal barrier is thought to play a key role in the development of multiple organ failure ~Am J Respir Crit Care Med 1998; 158: 444–51 • Theoratically,LDD may increase splanchnic blood flow by stimulation of the splachnic dopaminergic receptors

  25. Effects on Splachnic perfusion • Controversial for human data • Increasing splanchnic flow is not necessarily accompanied by an improvement of mucosal perfusion. • there is no evidence that LDD has beneficial effects on the splanchnic function or reduces the progression to multiple organ failure in sepsis. • Recent data even suggest a potentially detrimental effect of LDD on splanchnic oxygen uptake ~JAMA 1994; 272: 1354–7

  26. Effect on Gastrointestinal Motility • DA-2 :human enteric nervous system • In healthy volunteers: short-term DA could interrupt the fed gastrointestinal motility pattern • In critically ill pateints: DA (2.5 -5μg‧kg-1‧min-1)was found to be the most significant factor associated with poor gastric emptying • DA may aggravate digestive intolerance to enteral feeding.

  27. Respiratory Effects • Impaired the ventilatory drive in response to hypoxemia and probably hypercapnia by depressing the carotid body. • DA reduced arterial oxygen saturation by impairing V/Q matching in the lung. • Patients receiving LDD may be easier to wean, but with the potential danger of precipitating respiratory failure

  28. Endocrine and immunological effects • initial stress response: all anterior pituitary hormones is stimulated • more prolonged critical illness: a uniform suppression of the hypothalamic-pituitary axes ensues while cortisol secretion remains increased through a peripheral drive. • hypothalamic hypopituitarism : evoke inappropriate & harmful metabolic changes

  29. DA infusion: 5μg‧kg-1‧min-1 NS :not significant ** : significant

  30. As a vasopressor • DA: act largely by increasing cardiac output • NE: more specifically increases vascular resistance • Lethalphed :causing end-organ hypoperfusion and severe ischemia of vital organ.

  31. As a vasopressor • NE: • in effectively volume-resuscitated septic shock patients, the fear of end organ ischemia is unwarrant. • Faster restore MAP and lower serum lactate level than DA • No deleterios effects on splachnic perfusion ,even can increase PHi.

  32. As a vasopressor • Dopamine = Dobutamine+ NE ? • Don’t forget Its side effects ! • Separate titration  more target intervention tailored by the patients conditions.

  33. Conclusion • There is indeed no evidence that low “renal” dose DA has any beneficial effect on renal function or on the outcome of patients with ARF. • There is no evidence that LDD has beneficial effects on hepatosplanchnic circulation • Recent data suggest that DA may even have detrimental effects on splanchnic oxygen uptake

  34. Conclusion • DA suppresses the secretion and function of anterior pituitary hormones, aggravating the impairment of anabolism and cellular immune function. • DA aggravates the digestive tolerance of enteral feeding • suppresses the ventilatory drive.

  35. Time to Wake Up !!

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