Imposed power of breathing associated with use of an impedance threshold device.

OBJECTIVE: To measure the imposed power of breathing (imposed work of breathing per minute) associated with spontaneous breathing through an active impedance threshold device and a sham impedance threshold device. DESIGN: Prospective randomized blinded protocol. SETTING: University medical center. PATIENTS: Nineteen healthy, normotensive volunteers (10 males, 9 females, age range 20-56 y, mean +/- SD weight 54.8 +/- 7.7 kg for females, 84 +/- 8 kg for males). METHODS: The volunteers completed 2 trials of breathing through a face mask fitted with an active impedance threshold device set to open at -7 cm H(2)O pressure, or with a sham impedance threshold device, which was identical to the active device except that it did not contain an inspiratory threshold pressure valve diaphragm. Spontaneous breathing frequency (f), tidal volume (V(T)), exhaled minute ventilation, inspiratory pressure, and inspiratory time were measured with a respiratory monitor, and the data were directed to a laptop computer for real-time calculation of the imposed power of breathing. RESULTS: There were no significant differences in heart rate, respiratory rate, tidal volume, and minute ventilation, with and without inspiratory impedance. For the sham and active impedance threshold device groups, respectively, the mean +/- SD imposed power of breathing values were 0.92 +/- 0.63 J/min and 8.18 +/- 4.52 J/min (p < 0.001), the mean +/- SD inspiratory times were 1.98 +/- 0.86 s and 2.97 +/- 1.1 s (p = 0.001), and the mean +/- SD inspiratory airway/mouth pressures were -1.1 +/- 0.6 cm H(2)O and -11.7 +/- 2.4 cm H(2)O (p < 0.001). CONCLUSIONS: Breathing through an active impedance threshold device requires significantly more power than breathing through a sham device. All subjects tolerated the respiratory work load and were able to complete the study protocol.

Cerebral blood flow response and its association with symptoms during orthostatic hypotension.

INTRODUCTION: The preservation of cerebral blood flow with orthostatic hypotension (e.g., following prolonged bed rest or microgravity exposure) is vital for the attenuation of symptoms and the maintenance of consciousness. We tested the hypothesis that decreasing mean arterial pressure (MAP) by > 30% is associated with compromised cerebral autoregulation and orthostatic symptoms during a squat-stand test (SST). METHODS: There were 19 subjects who performed an SST. MAP and middle cerebral artery blood flow velocity (CBFV) were recorded continuously. Subjects were divided retrospectively into those who reported: (1) at least one orthostatic symptom (Sx; n=9); or (2) no orthostatic symptoms (NSx; n=10). Cerebral autoregulation was assessed via the calculation of time to nadir and time to recovery for MAP and CBFV and linear regression analysis of the dynamic changes in MAP and CBFV (within 10 s of standing). RESULTS: On standing, MAP decreased by 37 +/- 2% (NSx) and 42 +/- 4% (Sx) (p = 0.100). CBFV fell by 6% more in the Sx group than in the NSx group (NSx, -33 +/- 1% vs. Sx, -39 +/- 3%, p = 0.032). Cerebral autoregulation remained intact in both groups as indicated by: (1) a faster time to nadir for CBFV compared with MAP; (2) a faster time to recovery for CBFV compared with MAP; and 3) a poor correlation between CBFV and MAP responses on standing (NSx R2 = 0.43; Sx R2 = 0.60). CONCLUSION: Lower cerebral blood flow during severe hypotension may account for the reporting of orthostatic symptoms, despite the maintenance of cerebral autoregulation.

Inspiratory impedance effects on hemodynamic responses to orthostasis in normal subjects.

BACKGROUND: Breathing through an impedance threshold device (ITD) might prove effective as a countermeasure against post-spaceflight orthostatic hypotension since it increased blood pressure (BP) and cardiac output in supine human subjects. OBJECTIVE: We tested the hypothesis that spontaneous breathing through an ITD would attenuate the reduction in stroke volume and BP during orthostasis in human subjects. METHODS: There were 19 volunteers (10 men, 9 women) who completed two 80 degrees head-up tilt (HUT) protocols with (active) and without (sham control) an ITD set to open at -7 cm H2O pressure. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured non-invasively during transition from supine to HUT. RESULTS: HUT caused significant elevation in HR and reductions in SV, CO, TPR, and MAP. Hemodynamic effects of HUT were similar for sham and active ITD. Further analysis revealed a subset (n = 11) of subjects who demonstrated a > 20% decrease in SV during HUT with the sham ITD. In this subset of subjects, the ITD attenuated (p = 0.004) the %deltaSV (-22.5 +/- 3.0%) during HUT compared with the sham ITD (%deltaSV = -37.4 +/- 2.6%). There was no statistical effect of ITD use in the subgroup who demonstrated < 20% reduction in SV (-16.6 +/- 0.4%). CONCLUSIONS: Use of an ITD may provide significant protection against orthostatic compromise in individuals with greater than 20% reductions in SV, such as astronauts returning from space.

Stroke volume during orthostatic challenge: comparison of two non-invasive methods.

BACKGROUND: Real time non-invasive determination of stroke volume (SV) is important to astronaut orthostatic testing. We compared simultaneous estimates of SV calculated from peripheral pulse waveforms with a more conventional non-invasive technique. METHODS: Ten men and nine women completed 12-min protocols. The relative change (% delta) in beat-to-beat SV was estimated non-invasively from changes in pulse waveforms measured by application of infrared finger photoplethysmography (IFP) and thoracic impedance cardiography (TIC). The % deltaSV values were calculated from continuous measurements in the supine posture and over the first 10 s (T1), second 10 s (T2), and 3 min (T3) of 80 degrees head-up tilt (HUT). RESULTS: Average % deltaSV measured by IFP at T1 (-11.7 +/- 3.7%) was statistically less than the average % deltaSV measured by TIC at T1 (-21.7 +/- 3.1%), while average % deltaSV measured by IFP at T2 (-16.2 +/- 3.9%) and T3 (-19.1 +/- 3.8%) were not statistically distinguishable from the average % deltaSV measured by TIC at T2 (-21.8 +/- 2.5%), and T3 (-22.6 +/- 2.9%). Correlation coefficients (r2) between IFP and TIC were 0.117 (T1), 0.387 (T2), and 0.718 (T3). CONCLUSION: IFP provides beat-to-beat (real-time) assessment of % deltaSV after 20 s of transition to an orthostatic challenge that is comparable to TIC. IFP technology flown during space missions can be used to assess physiological status and countermeasure effectiveness for orthostatic problems that may arise in astronauts after spaceflight. While the peripherally measured IFP response is delayed, the ease of implementing this monitor in the field is advantageous.

Effects of repeated Valsalva maneuver straining on cardiac and vasoconstrictive baroreflex responses.

INTRODUCTION: We hypothesized that repeated respiratory straining maneuvers (repeated SM) designed to elevate arterial BPs (arterial baroreceptor loading) would acutely increase baroreflex responses. METHODS: We tested this hypothesis by measuring cardiac baroreflex responses to carotid baroreceptor stimulation (neck pressures), and changes in heart rate and diastolic BP after reductions in BP induced by a 15-s Valsalva maneuver in 10 female and 10 male subjects at 1, 3, 6, and 24 h after performing repeated SM. Baroreflex responses were also measured in each subject at 1, 3, 6, and 24 h at the same time on a separate day without repeated SM (control) in a randomized, counter-balanced cross-over experimental design. RESULTS: There was no statistical difference in carotid-cardiac and peripheral vascular baroreflex responses measured across time following repeated SM compared with the control condition. Integrated cardiac baroreflex response (deltaHR/ deltaSBP) measured during performance of a Valsalva maneuver was increased by approximately 50% to 1.1 +/- 0.2 bpm x mm Hg(-1) at 1 h and 1.0 +/- 0.1 bpm x mm Hg(-1) at 3 h following repeated SM compared with the control condition (0.7 +/- 0.1 bpm x mm Hg(-1) at both 1 and 3 h, respectively). However, integrated cardiac baroreflex response after repeated SM returned to control levels at 6 and 24 h after training. These responses did not differ between men and women. CONCLUSIONS: Our results are consistent with the notion that arterial baroreceptor loading induced by repeated SM increased aortic, but not carotid, cardiac baroreflex responses for as long as 3 h after repeated SM. We conclude that repeated SM increases cardiac baroreflex responsiveness which may provide patients, astronauts, and high-performance aircraft pilots with protection from development of orthostatic hypotension.

Effects of inspiratory impedance on hemodynamic responses to a squat-stand test in human volunteers: implications for treatment of orthostatic hypotension.

Recent studies in our laboratory demonstrated that spontaneous breathing through an inspiratory impedance threshold device (ITD) increased heart rate (HR), stroke volume (SV), cardiac output (Q), and mean arterial blood pressure (MAP) in supine human subjects. In this study, we tested the effectiveness of an ITD as a countermeasure against development of orthostatic hypotension, provoked using a squat-to-stand test (SST). Using a prospective, randomized blinded protocol, 18 healthy, normotensive volunteers (9 males, 9 females) completed two-counterbalanced 6-min SST protocols with and without (sham) an ITD set to open at 0.7 kPa (7-cm H(2)O) pressure. HR, SV, Q, total peripheral resistance (TPR), and MAP were assessed noninvasively with infrared finger photoplethysmography. Symptoms were recorded on a 5-point scale (1 = normal; 5 = faint) of subject perceived rating (SPR). The reduction in TPR produced by SST (-35 +/- 5 %) was not affected by the ITD. Reduction in MAP with ITD during the transient phase of the SST (-3.6 +/- 0.5 kPa or -27 +/- 4 mmHg) was less (P = 0.03) than that measured while breathing through a sham device (-4.8 +/- 0.4 kPa or -36 +/- 3 mmHg) despite similar (P < 0.926) elevations in HR of 15 +/- 2 bpm. SV (+2 +/- 4 %) and Q (+22 +/- 5 %) with the ITD were higher (P < 0.04) than SV (-8 +/- 4 %) and Q (+10 +/- 6 %) without the ITD. SPR was 1.4 +/- 0.1 with ITD compared to 2.0 +/- 0.2 with the sham device (P < 0.04). This reduction in orthostatic symptoms with application of an ITD during the SST was associated with higher MAP, SV and Q. Our results demonstrate the potential application of an ITD as a countermeasure against orthostatic hypotension.

Hemodynamics associated with breathing through an inspiratory impedance threshold device in human volunteers.

OBJECTIVE: Increased negative intrathoracic pressure during spontaneous inspiration through an impedance threshold device (ITD) causes elevated arterial blood pressure in humans. This study was performed to determine whether the acute increase in blood pressure induced by breathing through an ITD is associated with increased stroke volume and cardiac output. DESIGN: Randomized, blinded, controlled trial. SETTING: Laboratory. SUBJECTS: Ten women and ten men. INTERVENTIONS: We measured hemodynamic and respiratory responses during two separate ITD conditions: 1) breathing through a face mask with an ITD (impedance of 6 cm H2O [0.59 kPa]) and 2) breathing through the same face mask with a sham ITD (control). Stroke volume was measured by thoracic bioimpedance. MEASUREMENTS AND MAIN RESULTS: Compared with the control condition, ITD produced higher stroke volume (124 +/- 3 vs. 137 +/- 3 mL; p = .013), heart rate (63 +/- 3 vs. 68 +/- 3 beats/min; p = .049), cardiac output (7.69 vs. 9.34 L/min; p = .001), and systolic blood pressure (115 +/- 2 to 122 +/- 2 mm Hg [15.33 +/- 0.3 to 16.26 +/- 0.3 kPa]; p = .005) without affecting expired minute ventilation (6.2 +/- 0.4 to 6.5 +/- 0.4 L/min; p = .609). CONCLUSIONS: Breathing with an ITD at relatively low impedance increases systolic blood pressure by increasing stroke volume and cardiac output. The ITD may provide short-term protection against cardiovascular collapse induced by orthostatic stress or hemorrhage.

Effects of inspiratory impedance on the carotid-cardiac baroreflex response in humans.

We were interested in a therapeutic device designed to increase carotid-cardiac baroreflex sensitivity (BRS) since high BRS is associated with a lower risk for development of hypotension in humans with experimentally-induced central hypovolemia. We hypothesized that spontaneous breathing through an impedance threshold device (ITD) designed to increase negative intrathoracic pressure during inspiration and elevate arterial blood pressure would acutely increase BRS in humans. We tested this hypothesis by measuring heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures, and carotid-cardiac BRS in 10 female and 10 male subjects breathing through a face mask at three separate ITD conditions: (a) 6 cm H(2)O; (b) 12 cm H(2)O; and (c) a control (0 cm H(2)O). HR was increased (P = 0. 013) from 64 +/- 3 bpm during control to 68 +/- 3 bpm at 6 cm H(2)O ITD and 71 +/- 4 bpm at 12 cm H(2)O ITD breathing conditions. During ITD breathing, BRS was not altered but responses were shifted to higher arterial pressures. However, SBP and DBP were elevated for both the 6 and 12 cm H(2)O conditions compared to the 0 cm H(2)O condition, but returned to control (sham) levels by 30 minutes after cessation of ITD breathing. There were no gender effects for BRS or any hemodynamic responses to breathing through the ITD. We conclude that breathing with inspiratory impedance at relatively low pressures can increase baseline arterial blood pressure, i. e., reset the operational point for SBP on the baroreflex stimulus-response relationship, in healthy subjects. This resetting of the cardiac baroreflex may represent a mechanism that allows blood pressure to increase without a reflex-mediated reduction in HR.