Abstract 58: An Intrathoracic Pressure Regulation Device Improved Cardiac Output in Porcine Peritonitis
Background: Septic shock initiates multiple pathophysiologic pathways manifesting as microvascular hypoperfusion, cellular dysfunction and ultimately tissue death. Septic shock is characterized by reduced cardiac output. To improve cardiac output in septic shock, we tested an Intrathoracic Pressure Regulator (IPR), a novel, non-invasive therapy which decreases intrathoracic pressure during passive exhalation in mechanically ventilated patients. By creating a more negative intrathoracic pressure during exhalation, IPR enhances venous return and thereby increases cardiac output. We hypothesized that intermittent IPR therapy will transiently improve cardiac output without fluid resuscitation in porcine peritonitis.
Materials and Methods: 9 female Yorkshire pigs (30-40kg) were anesthetized with isofluorane, intubated, mechanically ventilated, instrumented with a Swan-Ganz and a femoral artery catheter. Animals were assigned to either a treatment group (n=4) or a control group (n=5). Following a one hour period of hemodynamic monitoring, a fibrin clot containing 4x109 cfu.kg-1 E. coli O11.B4 was implanted into the peritoneum. Two hours after implantation, IPR was applied for cycles of 30 minutes on and 15 minutes off. This treatment regimen was performed for six hours in total or until the animal met euthanasia criteria. The control group was monitored without the IPR for 6 hours or until meeting euthanasia criteria. The primary outcome measurement was maximum change in cardiac index during IPR.
Results: During ITP therapy, cardiac index rose 0.125 L/minute/m2 in treated animals whereas in time matched controls, cardiac index rose 0.011L/minute/m2 (P<0.05). In treated animals, ITP therapy caused pulmonary vascular resistance (PVR) to drop significantly when compared to before therapy or after therapy; whereas in time matched control animals, PVR increased over time.
Conclusions: This study demonstrated that IPR treatment for septic shock caused significant increases in cardiac output and decreases in pulmonary vascular resistance. Further studies are needed to determine the potential clinical benefit of this non-invasive circulatory enhancement technology.
- © 2011 by American Heart Association, Inc.