• Paula Y S Poh, Robert Carter, Carmen Hinojosa-Laborde, Jane Mulligan, Gregory Z Grudic, and Victor A Convertino.
• US Army Institute of Surgical Research, JBSA Fort Sam Houston, TX, 78234, USA.
• Exp. Physiol. 2014 Oct 1;99(10):1421-6.

AbstractIntrathoracic pressure regulation (IPR) represents a therapy for increasing systemic circulation through the creation of negative intrathoracic pressure. We hypothesized that using this 'respiratory pump' effect would slow the diminution of the physiological reserve to compensate during progressive reductions in central blood volume. The compensatory reserve index (CRI) algorithm was used to measure the proportion (from 100 to 0%) of reserve capacity that remained to compensate for central volume loss before the onset of cardiovascular decompensation. Continuous analog recordings of arterial waveforms were extracted from data files of seven healthy volunteers. Subjects had previously participated in experiments designed to induce haemodynamic decompensation (presyncope) by progressive reduction in central blood volume using graded lower-body negative pressure. The lower-body negative pressure protocol was completed while breathing spontaneously through a standard medical face mask without (placebo) and with a resistance (approximately -7 cmH2O; active IPR) applied during inspiration. At the onset of presyncope in the placebo conditions, CRI was smaller than the CRI observed at the same time point in the active IPR conditions. The CRI at the onset of presyncope during active IPR (0.08 ± 0.01) was similar to the CRI at presyncope with placebo. Kaplan-Meier and log rank tests indicated that CRI survival curves were shifted to the right by active IPR. Optimizing the respiratory pump contributed a small but significant effect of increasing tolerance to progressive reductions in central blood volume by extending the compensatory reserve.© 2014 The Authors. Experimental Physiology © 2014 The Physiological Society.

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