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J Appl Physiol (February 15, 2002). doi:10.1152/japplphysiol.00394.2001
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Articles in PresS, published online ahead of print February 15, 2002
J Appl Physiol, 10.1152/jap.00394.2001
Submitted on April 26, 2001
Accepted on February 8, 2002

Cardiorespiratory Effects of Inelastic Chest Wall Restriction

Jordan D Miller1, Kenneth C Beck2, Michael J Joyner3, A. G Brice4, and Bruce D Johnson5*

1 Department of Anesthesia Research and Internal Medicine, Mayo Clinic, Rochester, MN, USA; University of Wiconsin - LaCrosse, LaCrosse, WI, USA
2 Divisions of Cardiovascular Disease, Mayo Clinic, Rochester, MN, USA
3 Department of Anesthesia Research and Internal Medicine, Mayo Clinic, Rochester, MN, USA
4 University of Wiconsin - LaCrosse, LaCrosse, WI, USA
5 Division of Thoracic Disease, Mayo Clinic, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: johnson.bruce{at}mayo.edu.

We examined the effects of chest wall restriction (CWR) on cardiorespiratory function at rest and during exercise in healthy subjects in an attempt to approximate the cardiorespiratory interactions observed in clinical conditions that result in restrictive lung and/or chest wall changes and a reduced intrathoracic space. Canvas straps were applied around the thorax and abdomen so that vital capacity (VC) was reduced by >35%. Data were acquired at rest and during cycle ergometry at 25% and 45% of peak workloads. CWR elicited significant increases in the flow resistive work (WFR) performed on the lung (160%) and the gastric pressure-time integral (>400%) at the higher workload, but resulted in a decrease in the elastic work performed on the lung (WEL) (56%) when compared to control conditions. With CWR, heart rate increased and stroke volume (SV) fell resulting in >10% fall in cardiac output at rest and during exercise at matched workloads (p < 0.05). Blood pressure and catecholamines were significantly elevated during CWR exercise conditions (p < 0.05). We conclude that CWR significantly impairs SV during exercise and that a compensatory increase in heart rate does not prevent a significant reduction in cardiac output. Oxygen consumption appears to be maintained via increased extraction and a redistribution of blood flow via sympathetic activation.




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