Cardiovascular effects of 6% hetastarch and lactated Ringer's solution during spinal anesthesia

The purpose of this prospective, randomized, double-blinded study was to compare the hemodynamic effects of 6% hetastarch with lactated Ringer's solution and to determine the main reasons for hemodynamic impairment following spinal anesthesia in elderly patients undergoing emergent hip surgery.

After receiving institutional approval and informed consent, we enrolled 24 ASA physical status III patients for this study. Hemodynamics were recorded with pulmonary artery and arterial catheters and an electrocardiogram. Following fluid administration with either 500 mL 6% hetastarch (group H) or 1500 mL lactated Ringer's solution (group R), spinal anesthesia was administered with 3.0 mL 0.5% bupivacaine (isobaric). Hemodynamic measurements were recorded prior to fluid administration, before spinal anesthesia, and 10, 20, and 30 minutes following spinal anesthesia and reported as relative changes relating to baseline.

Although the hemodynamic measurements after spinal anesthesia remained stable in group H throughout the observation period, blood pressure, central venous pressure, pulmonary artery (PA) wedge pressure and systemic vascular resistance decreased significantly in group R (blood pressure: -7 +/- 10 vs - 14 +/- 8% 30 minutes after spinal anesthesia, P < .05 to group R; central venous pressure: 51 +/- 106 vs -26 +/- 27% 10 minutes, 63 +/- 89 vs -36 +/- 30% 20 minutes and 73 +/- 112 vs -33 +/- 29% 30 minutes after spinal anesthesia, P < .01 to group R; PA wedge pressure: 40 +/- 37 vs -5 +/- 40% 10 minutes, 40 +/- 35 vs -23 +/- 32% 20 minutes and 38 +/- 36 vs -23 +/- 32% 30 minutes after spinal anesthesia, P < .01 to group R; systemic vascular resistance: -10 +/- 16 vs -18 +/- 7% 20 minutes and -10 +/- 15 vs - 19 +/- 12% 30 minutes after spinal anesthesia, P < .05 to group R).

Six percent hetastarch minimizes the hemodynamic responses during spinal anesthesia in elderly patients undergoing emergent hip surgery. In this study population, spinal anesthesia-induced hemodynamic impairment is caused by decreases in cardiac filling pressures and systemic vascular resistance.