Abstract 8: Mechanism of Pressure Transfer From the Thorax to the Cranium During Application of Negative Intrathoracic Pressure During Treatment of Hypovolemic Hypotension
Background: Application of negative intrathoracic pressure (nITP) to treat hypovolemic hypotension has been shown to decrease intracranial pressure (ICP) and increase vital organ perfusion in animals. The mechanism of pressure transfer underlying generation of nITP and ICP with this therapy remains unknown. We hypothesize that nITP is transferred to the cranium via the spinal fluid within the thorax. To test this hypothesis we applied IPR therapy in an open and closed chest model of hypovolemic hypotension in pigs.
Methods: 16 intubated propofol anesthetized pigs were bled to 45% of their circulating volume and allowed to equilibrate for 10 min to a hypovolemic baseline. In both groups an nITP device that lowers airway pressures to -10 mmHg between positive pressure ventilations was applied for 10 min. In Group A the chest was intact. In group B, a subcostal incision through the diaphragm and pleural spaces bilaterally, exposed the thoracic cavity to atmospheric pressure, thereby eliminated the ability of the thorax to generate nITP. Ventilations were given at 10 bpm with 10 ml/kg tidal volume and a FiO2 of 1.0 in both groups. ICP, right atrial, airway pressure, central aortic pressures and Doppler carotid flow were recorded continuously.
Results: In Group A, nITP of -10mmHg in the distal trachea resulted in a significant increase in mean arterial pressure (MAP), a significant decrease in RA and ICP, and marked improvement in cerebral perfusion pressure and carotid blood flow. In group B, nITP of -10mmHg generated a significant increase in MAP, ICP and RA pressure and no significant change in carotid blood flow (see TABLE⇓).
Conclusion: The mechanism of pressure transmission from the thorax to the cranium during hypovolemic hypotension and treatment with nITP is mediated primarily by the spinal fluid. Optimizing this newly discovered mechanism may have significant implications for the treatment of hypovolemia hypotension and increased ICP.