Intensive care medicine · 1998
The effects of low-dose dopamine infusions on haemodynamic and renal parameters in patients with septic shock requiring treatment with noradrenaline.
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Juste R N, Panikkar K, Soni N
Аннотация
OBJECTIVE: To investigate whether low-dose dopamine (LDD) has a significant effect on systemic haemodynamic variables and renal function when used in conjunction with high-dose noradrenaline in optimally volume-resuscitated patients with septic shock.
DESIGN: A prospective clinical study in which each patient acted as his/her own control.
SETTING: Teaching hospital Intensive Care Unit.
PATIENTS: Twenty-one patients with septic shock treated with high-dose noradrenaline were studied, 17 patients completed the study.
INTERVENTIONS: Fluid loading to an optimal left ventricular stroke work index (LVSWI) whilst on more noradrenaline than 10 mcg/min and dopamine of 2.5 mcg/kg per min. Three study periods each of 2 h with LDD present, withdrawn and restarted. During each period a complete haemodynamic profile and measurement of urine flow rate, creatinine clearance and sodium excretion was performed.
MEASUREMENT AND RESULTS: Removing and restarting LDD caused marked changes in cardiac index (CI, 17% fall, p < 0.01: 23% rise, p < 0.01), stroke volume (SV, 11% fall, p < 0.05: 14% rise, p < 0.05) and systolic blood pressure (SBP, 11% fall, p < 0.05: 14% rise, p < 0.05). Urine volume fell by 40% (p < 0.05) when dopamine was withdrawn. Significant reductions in sodium excretion (p < 0.05) and fractional sodium excretion (p < 0.05) also occurred on stopping LLD. Changes in creatinine clearance were not statistically significant.
CONCLUSION: Low-dose dopamine causes significant increases in SBP SV, cardiac output and urine flow during treatment with noradrenaline.
DESIGN: A prospective clinical study in which each patient acted as his/her own control.
SETTING: Teaching hospital Intensive Care Unit.
PATIENTS: Twenty-one patients with septic shock treated with high-dose noradrenaline were studied, 17 patients completed the study.
INTERVENTIONS: Fluid loading to an optimal left ventricular stroke work index (LVSWI) whilst on more noradrenaline than 10 mcg/min and dopamine of 2.5 mcg/kg per min. Three study periods each of 2 h with LDD present, withdrawn and restarted. During each period a complete haemodynamic profile and measurement of urine flow rate, creatinine clearance and sodium excretion was performed.
MEASUREMENT AND RESULTS: Removing and restarting LDD caused marked changes in cardiac index (CI, 17% fall, p < 0.01: 23% rise, p < 0.01), stroke volume (SV, 11% fall, p < 0.05: 14% rise, p < 0.05) and systolic blood pressure (SBP, 11% fall, p < 0.05: 14% rise, p < 0.05). Urine volume fell by 40% (p < 0.05) when dopamine was withdrawn. Significant reductions in sodium excretion (p < 0.05) and fractional sodium excretion (p < 0.05) also occurred on stopping LLD. Changes in creatinine clearance were not statistically significant.
CONCLUSION: Low-dose dopamine causes significant increases in SBP SV, cardiac output and urine flow during treatment with noradrenaline.