Submitted on April 23, 2007
Accepted on February 22, 2008
Breathing through an inspiratory threshold device improves stroke volume during central hypovolemia in humans
Kathy L. Ryan1*, William H. Cooke2, Caroline A. Rickards3, Keith G. Lurie4, and Victor A. Convertino5
1 Laboratory Division, U.S. Army Institute of Surgical Research, Fort Sam Houston, Texas, United States
2 Health and Kinesiology, The University of Texas at San Antonio, San Antonio, Texas, United States
3 Laboratory Divison, U.S. Army Institue of Surgical Research, Fort Sam Houston, Texas, United States
4 Advanced Circulatory Systems, Inc., Minneapolis, Minnesota, United States; Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota, United States
5 Combat Casualty Care, US Army Inst Sugical Research, Fort Sam Houston, Texas, United States
* To whom correspondence should be addressed. E-mail: kathy.ryan{at}amedd.army.mil.
Inspiratory resistance induced by breathing through an impedance threshold device (ITD) reduces intrathoracic pressure and increases stroke volume (SV) in supine normovolemic humans. We hypothesized that breathing through an ITD would also be associated with a protection of SV and a subsequent increase in the tolerance to progressive central hypovolemia. Eight volunteers (5 men, 3 women) were instrumented to record ECG and beat-by-beat arterial pressure and SV (Finometer®). Tolerance to progressive lower body negative pressure (LBNP) was assessed while subjects breathed against either 0 (sham ITD) or -7 cmH2O inspiratory resistance (active ITD); experiments were performed on separate days. Because the active ITD increased LBNP tolerance time from 2,014 ± 106 to 2,259 ± 138 s (p = 0.006), data were analyzed (time and frequency domains) under both conditions at the time at which cardiovascular collapse occurred during the sham experiment to determine the mechanisms underlying this protective effect. At this time point, arterial blood pressure, SV and cardiac output were higher (p 
0.005) when breathing on the active ITD rather than the sham ITD, while indirect indicators of autonomic activity (low and high frequency oscillations of the R-to-R interval) were not altered. ITD breathing did not alter the transfer function between systolic arterial pressure and R-to-R interval, indicating that integrated baroreflex sensitivity was similar between the conditions. These data show that breathing against inspiratory resistance increases tolerance to progressive central hypovolemia by better maintaining SV, cardiac output and arterial blood pressures via primarily mechanical rather than neural mechanisms.
