• Alejandro Vasquez, Karl B Kern, Ronald W Hilwig, Joseph Heidenreich, Robert A Berg, and Gordon A Ewy.
• Section of Cardiology, Department of Medicine, Sarver Heart Center, University of Arizona College of Medicine, 1501 N. Campbell Avenue, Tucson, AZ 85724, USA.
• Resuscitation. 2004 May 1;61(2):199-207.

ObjectivesThis study was designed to determine the optimal dose of dobutamine in the treatment of post-resuscitation left ventricular dysfunction.BackgroundGlobal left ventricular dysfunction following successful resuscitation from prolonged, ventricular fibrillation cardiac arrest, negatively impacts long-term survival. Dobutamine can overcome this global myocardial stunning. Previous data indicate a dose of 10 mcg/kgmin improves systolic and diastolic function, but markedly increases the heart rate.MethodsTwenty swine (24 +/- 0.4 kg) were randomized to one of four doses (0, 2, 5, and 7.5 mcg/kgmin) of dobutamine for the treatment of post-resuscitation myocardial dysfunction following 12.5 min of untreated ventricular fibrillation cardiac arrest. Cardiac function was measured at pre-arrest baseline and serially for 6 h post-resuscitation. Left ventricular function was evaluated by contrast ventriculograms, left ventricular pressures, +dP/dt, Tau, -dP/dt, and cardiac output. Myocardial oxygen consumption and myocardial blood flow were measured to assess the functional significance of any dobutamine-mediated heart rate responses.ResultsLeft ventricular dysfunction was evident at 25 min and peaked 4 h post-resuscitation. Significant (P < 0.05) improvements in ventricular systolic (EF, CO) and diastolic (LVEDP, Tau) function were evident within minutes of dobutamine initiation and persisted at 6h for the 5 and 7.5 mcg/kgmin groups. Tachycardia manifested with all dobutamine doses, but only affected myocardial oxygen consumption significantly (P < 0.05) at the highest dose (7.5 mcg/kgmin).ConclusionsDobutamine at 5 mcg/kgmin appears optimal for restoring systolic and diastolic function post-resuscitation without adversely affecting myocardial oxygen consumption.

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