Systemic and microcirculatory effects of dobutamine in patients with septic shock.

PURPOSE: The aim of this study was to characterize the cardiovascular responses to dobutamine and their predictors. Our hypotheses were that dobutamine mainly produces tachycardia and vasodilation and fails to improve the microcirculation of patients with septic shock. MATERIALS AND METHODS: Systemic hemodynamics and sublingual microcirculation were evaluated with dobutamine (0, 2.5, 5.0, and 10.0 µg kg(-1) min(-1)) in 23 patients with septic shock. RESULTS: Dobutamine increased heart rate, cardiac index, and stroke volume index (SVI). Mean blood pressure was unchanged, and systemic vascular resistance decreased. Individual responses were heterogeneous. Stroke volume index increased in 52% of the patients. These patients showed lower changes in mean blood pressure (3 ± 16 mm Hg vs -10 ± 6 mm Hg, P < .05) and higher increases in cardiac index (1.47 ± 0.93 L m(-1) m(-2) vs 0.20 ± 0.5 L m(-1) m(-2)) than did nonresponders. Changes in SVI significantly correlated with echocardiographic left ventricular ejection fraction (r = 0.55). In the whole group, perfused capillary density remained unchanged (14.0 ± 4.3 mm/mm(2) vs 14.8 ± 3.7 mm/mm(2)), but improved if basal values were 12 mm/mm(2) or less (9.1 ± 4.3 mm/mm(2) vs 12.5 ± 4.8 mm/mm(2)). CONCLUSIONS: Dobutamine produced variable hemodynamic effects. Systolic dysfunction was the only variable associated with increases in SVI. Finally, dobutamine only improved sublingual microcirculation when severe alterations were found at baseline.

Alterations in urinary strong ion difference in critically ill patients with metabolic acidosis: a prospective observational study.

BACKGROUND AND OBJECTIVE: The correct renal response to metabolic acidosis should be a negative shift in the urinary strong ion difference ([SID](urinary) = [Na(+)](urinary) + [K(+)](urinary) - [Cl(-)](urinary)). Our hypothesis was that the failure to decrease the [SID](urinary) is frequently present and leads to a more severe metabolic acidosis. DESIGN, SETTING AND PARTICIPANTS: Prospective observational study conducted in the medical/surgical intensive care unit of a teaching hospital between 1 January 2006 and 30 April 2007. Participants were 98 patients with metabolic acidosis on ICU admission and 10 healthy volunteers. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Severity of metabolic acidosis; behaviour of acid-base variables according to positive or negative [SID](urinary). RESULTS: Twelve patients (12%) had negative [SID](urinary) and 86 (88%) had positive [SID](urinary). Compared with patients with positive [SID](urinary), those with negative [SID](urinary) had higher [HCO(3) (-)] (20 ±2 v 18 ±3 mmol/L), base excess ([BE]) (-5 ±2 v -7 ±2 mmol/L), anion gap ([AG]) (21 ±5 v 17 ±4 mmol/L), Δ[AG] - Δ[HCO(3)(-)] (1 ±5 v -3 ±3 mmol/L) and lower [Cl(-)] (105 ±5 v 111 ±3 mmol/L). CONCLUSIONS: Most of the critically ill patients with metabolic acidosis showed inappropriate renal compensation, as evidenced by positive [SID](urinary) and higher plasma [Cl(-)]. These patients had more severe metabolic acidosis. On the other hand, patients with adequate renal response and negative [SID](urinary) had positive Δ[AG] - Δ[HCO(3)(-)]. These findings, usually considered as a diagnosis of associated metabolic alkalosis, might be interpreted as the proper renal response to metabolic acidosis.