Response to Valsalva Maneuver in Humans

Introduction

Functional metrics of autonomic control of heart rate, including baroreflex sensitivity, have been shown to be strongly associated with cardiovascular risk. A decrease in baroreflex sensitivity with aging is hypothesized to represent a contributing causal factor in the etiology of primary hypertension. To assess baroreflex function in human subjects, two complementary methods to simulate the response in heart rate elicited by the Valsalva maneuver were developed and applied to data obtained from a cohort of healthy normal volunteers.

Data Collection

Data was obtained from 27 participants excluding individuals with histories positive for inherited cardiomyopathy, valvular disease, aneurism, dissection, vascular surgery, pulmonary hypertension, connective tissue disease, or stroke. For each such normal healthy subject, baseline blood pressures were measured at 200 Hz during normal respiration prior to one or more instances of a forced expiration into a closed glottis (i.e Valsalva maneuver). The airway pressures achieved during expiration were measured at 10 Hz, with subjects instructed to maintain a pressure exceeding 30 mmHg for at least 10 seconds, though review of the data will show variability in each participant's results. Data collection of both blood and airway pressures continues throughout a recovery period subsequent to each Valsalva maneuver.

Files

The data for 27 subjects are presented here where for a given subject (e.g. norm001) two simultaneous recordings have been made. One is for the blood pressure obtained with a Finapres blood pressure monitor (e.g. norm001_BP) and the other is the thoracic pressure during three Valsalva maneuvers (e.g norm001_P). The thoracic pressure is measured by the subject breathing into a small closed chamber instrumented to measure the chamber pressure. The age and gender associated with each subject are found in the text file demographics.csv.

Contributors

This data was contributed by: Samuel A. Kosinski, Brian E. Carlson, Scott L. Hummel, Robert D. Brook and Daniel A. Beard.

Contact

For further information, please contact:

Brian Carlson
Department of Molecular and Integrative Physiology, University of Michigan
bcarl@umich.edu

Daniel Beard
Department of Molecular and Integrative Physiology, University of Michigan
beardda@umich.edu