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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...

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Main Authors: Convertino, Victor A, Ratliff, Duane A, Ryan, Kathy L, Doerr, Donald F, Ludwig, David A, Muniz, Gary W, Britton, Deanna L, Clah, Savran D, Fernald, Kathleen B, Ruiz, Alicia F
Format: Report
Language:English
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Summary: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 H 2 O [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 + or - 3 vs. 137 + or - 3 mL; p = .013), heart rate (63 + or - 3 vs. 68 3 beats/min; p = .049), cardiac output (7.69 vs. 9.34 L/min; p = .001), and systolic blood pressure (115 + or - 2 to 122 + or - 2 mm Hg [15.33 + or - 0.3 to 16.26 + or - 0.3 kPa]; p = .005) without affecting expired minute ventilation (6.2 + or - 0.4 to 6.5 + or - 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. Published in Critical Care Medicine, v32 n9 pS381-S386, 2004.