October 19, 2009
2:00 PM - 4:00 PM
Room Area O
Non-Invasive Treatment of Hypotension with a Novel Intrathoracic Pressure Regulator
  *  Keith G. Lurie, M.D., Scott H. McKnite, B.S., Martin Birch, M.D., Michael Loushin, M.D., Younghoon Kwon, M.D.
Emergency and Internal Medicine, University of Minnesota, Minneapolis, Minnesota
Background: Intrathoracic pressure regulation (IPR) devices have been recently developed to generate a negative intrathoracic pressure to increase circulation to the heart and brain during CPR, in spontaneously breathing hypotensive patients, and inintubated hypotensive apneic patients. By lowering intrathoracic pressures during the chest recoil phase of CPR, with each spontaneous breath, or during the expiratory phase of positive pressure ventilation (PPV), this family of IPR technologies enhance cardiac preload, increase cardiac stroke volume and cardiac output, and reverse clinically significant hypotension in spontaneously breathing and apneic patients intra-operatively without fluid resuscitation or vasopressors. Mechanistic studies have shown that inspiration through a low level of resistance (-7 cm H2O) increases blood pressure and modulates sympathetic nerve activity in humans subjected to hypotension in a lower body negative pressure chamber.

Hypothesis: Generation of a continuous negative intrathoracic pressure to -10 cm H2O during the expiration after each PPV in apneic hypotensive pigs will result in an increase in mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) and modulate the autonomic nervous system.

Methods and Results: 8 Female farm pigs (28-30 kg) were anesthetized with isoflurane (1.0%). Central aortic, intracranial (ICP) and right atrial pressures were measured invasively. Heart rate (HR) variability was determined with Fast Fourier transformation. Pigs were bled to 50% of the total blood volume, after recovering for 10 minutes were paralyzed with succinylcholine (90mcg/kg/min) to assure apnea, and then ventilated with PPV. After 10 min they were treated with an IPR device named the CirQLator TM (Advanced Circulatory Systems, Inc., Minnesota) that delivered PPV (10ml/kg) at a rate of 12/min with FiO2=1.0 followed by generating -10 cm H2O intrathoracic pressure during the expiratory phase. When compared with post-bleed values, the MAP and CPP with the CirQLator increased from 49.5±2.8 to 74.5±1.8 (p<0.01) and 43.4±2.7 to 68.5±3.2 (p<0.01). HR remained similar before (185±12) and during CirQLator treatment (188±14) p=0.47). By contrast, low (LF) and high (HF) frequency power spectra indicative of sympathetic and parasympathetic activity, respectively, were 47.5±3.2 and 42.0±3.9 post bleed and 28.9±5.3 and 59.9±6.5 after the CirQLator (P<0.01 for LF and HF post bleed vs during CirQLator treatment). Conclusions: IPR therapy improves circulation to the heart and brain in apneic pigs by multiple mechanisms including increasing venous cardiac preload, stroke volume, and MAP, lowering ICP, increasing CPP, and by shifting the autonomic nervous system balance away from the sympathetic limb. These mechanistic studies help explain the clinical benefit of IPR in hypotensive patients.

From Proceedings of the 2009 Annual Meeting of the American Society Anesthesiologists.