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Continuous Use of Intrathoracic Pressure Regulation Device Improved Cardiac Output in Porcine Peritonitis
Author(s) -
Goldfarb Roy David,
Jaffe J. Douglas,
Torjman Marc C,
Mitrev Ludmil,
Jasti Purnachandra,
Knob Christopher,
Metzger Anja,
Lurie Keith,
Parrillo Joseph E.,
Dellinger R. Phillip
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1132.3
Subject(s) - medicine , cardiac output , cardiac index , pulmonary artery catheter , central venous pressure , septic shock , resuscitation , anesthesia , peritonitis , pulmonary artery , shock (circulatory) , catheter , circulatory system , cardiology , mean arterial pressure , blood pressure , hemodynamics , sepsis , surgery , heart rate
Septic shock initiates multiple pathophysiologic pathways manifesting characterized by reduced cardiac output. We tested an Intrathoracic Pressure Regulator (IPR) a device which decreases intrathoracic pressure during passive exhalation creating more negative intrathoracic pressure enhancing venous return and cardiac output. We hypothesized that continuous IPR therapy would improve cardiac output without fluid resuscitation during porcine peritonitis. Six 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 a treatment or control group. After a basal period, peritonitis was induced by implanting a fibrin clot containing 4×10 9 cfu·kg −1 E. coli O11.B4. At 2 hours IPR was applied for 4 hrs or until the animal met euthanasia criteria. The primary outcome measurement was cardiac index. Continuous IPR augmented cardiac index and mean arterial blood pressure for duration therapy, becoming larger as time increased while pulmonary vascular resistance declined. This study demonstrated that IPR treatment for peritonitis caused significant cardiovascular support in this model. Further studies are needed to determine the potential clinical benefit of this non‐invasive circulatory enhancement technology.