Abstract 4: Small-Volume 7.5% NaCl Adenocaine/Mg2+ Preserves Cardiac Function During Hypotensive Resuscitation in the Pig Following Severe Hemorrhagic Shock
Background: Cardiac rescue is critical for successful resuscitation. Previously, we reported that ~1 ml/kg 7.5% NaCl with Adenocaine (adenosine and lidocaine) and Mg2+ (ALM) successfully resuscitated rats following severe hemorrhagic shock, and that in pigs ALM significantly reduced the volume of Ringers acetate required to raise MAP to a target of 50 mmHg following 74% blood loss. The present study examines the effect of small volume 7.5% NaCl ALM on cardiac function during 60 min hypotensive resuscitation following 90 min shock in the porcine model.
Methods: Pigs (35-40kg) were subjected to pressure-controlled hemorrhage at a mean arterial pressure (MAP) of 35-40mmHg for 90 min (~75% blood loss). Pigs were randomly assigned to receive either 4 ml/kg 7.5% NaCl ALM (ALM n=8) or 4 ml/kg 7.5% NaCl (Control n=8). Cardiac output (CO), stroke volume, left-ventricular pressures and hemodynamics were collected continuously. Significance *p<0.05.
Results: MAP, end-systolic pressure and CO were significantly higher in the ALM pigs at the end of hypotensive resuscitation (Table). The higher CO was due to a higher stroke volume (SV) maintained at a significantly lower heart rate (HR). Paradoxically dP/dtmax tended to be higher in the Control group during the first 45min of hypotensive resuscitation (p=0.066) with no difference at 60min. Systolic ejection times were significantly increased in the ALM group and inversely related to HR. There was no difference in LV end-diastolic pressure between the two groups indicating that preload was similar during hypotensive resuscitation. LV blood flow at 30min resuscitation was comparable in the two groups (Control: 2.86±0.6 vs. ALM: 4.1±1.4 ml/min/g; p=0.7)
Conclusion: Superior cardiac rescue was achieved in ALM by a higher SV and CO, lower HR and longer ejection times vs Controls. Longer isovolumic contraction and ejection times may be due to suppression of SA nodal activity or rebalancing of sympathetic/parasympathetic control.
- © 2012 by American Heart Association, Inc.