RESUMO
Transcutaneous pO2 on thorax and the volar part of the forearm was measured in six healthy volunteers during heavy hyperventilation, and the values compared with simultaneously measured arterial blood pO2. We found a significant rise in arterial pO2 during hyperventilation with a lesser increase in thoracic transcutaneous pO2. When measured on arm the transcutaneous pO2 did not even rise significantly. After hyperventilation pO2 fell to values below the resting level. The transcutaneous/arterial pO2 index, fell significantly during hyperventilation with the greatest reduction in the arm index. After hyperventilation the arm index returned to the control values, whereas the thoracic index remained low. We suggest, that the significant fall in transcutaneous/arterial blood pO2 index during hyperventilation is caused primarily by skin vasoconstriction, whereas the fall in pO2 after hyperventilation is caused by hypoxia. When measured on areas with increased muscular activity transcutaneous pO2 might depend on the local blood flow and skin oxygen consumption also, causing problems in interpretation with certain patient groups.
