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Clinical note| Volume 79, ISSUE 7, P873-876, July 1998

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Oxyhemoglobin desaturation and aberrant carbon dioxide homeostasis during electrically stimulated exercise in a ventilator-dependent tetraplegic patient

  • Mark S. Nash
    Correspondence
    Reprint requests to Mark S. Nash, PhD, Division of Physical Therapy, Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, 5915 Ponce de Leon Boulevard, 5th Floor, Coral Gables, FL 33146.
    Affiliations
    Department of Orthopaedics and Rehabilitation, University of Miami School of Medicine, Miami, FL. USA

    Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL. USA
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  • Patrick L. Jacobs
    Affiliations
    Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL. USA
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  • Kathleen M. Klerk
    Affiliations
    Department of Physical Therapy, University of Miami/Jackson Memorial Medical Center, Miami, FL. USA
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  • Barth A. Green
    Affiliations
    Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL. USA

    Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, FL. USA
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      Abstract

      This single-subject case examined oxyhemoglobin saturation and alveolar end-tidal carbon dioxide levels in a ventilator-dependent tetraplegic patient undergoing electrical stimulation cycle ergometry. When exercising with a closed tracheostomy cuff under resting ventilator settings (resting intermittent mandatory ventilation; frequency = 6breaths/min, tidal volume = 83.3m-L, minute ventilation =5L/min), his oxyhemoglobin saturation decreased from 100% to 92%, while alveolar end-tidal carbon dioxide increased linearly to 47mmHg. These undesirable changes were corrected under adjusted intermittent mandatory ventilation conditions (frequency = 12breaths/min, tidal volume = 83.3mL, minute ventilation = 10L/min), during which oxyhemoglobin saturation remained above 98% and the alveolar end-tidal carbon dioxide trend resembled that of ventilator-independent tetraplegic individuals undergoing the same exercise. Because the subject's heart rate was higher under adjusted ventilation conditions, these responses may have been caused by augmented venous return resulting from greater abdominothoracic pumping at the higher breathing frequency. These findings support the need to modify ventilator settings in ventilator-dependent tetraplegic persons while undergoing exercise to maintain oxyhemoglobin saturation and carbon dioxide homeostasis.

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