• J M Kim, K Arakawa, K T Benson, and D K Fox.
• Anesth. Analg. 1986 Dec 1; 65 (12): 1333-9.

AbstractThrough a catheter placed in a superficial vein on the finger, we observed a pulsatile venous pressure. To delineate the relationship between the pulsatile venous pressure and the pulse volume amplitude (PVA) recorded by photoelectric plethysmography (PEPG), both tracings were simultaneously recorded. When the PVA changed acutely or gradually, the venous pulse pressure and mean venous pressure simultaneously followed the same trend. We also found that mean PVO2 (135 mm Hg) was greater when the PVA and venous pulse pressure increased above the level (50 mm Hg) observed when they decreased. These findings suggested that the finger pulse detected by PEPG, as well as by pulse oximetry, is caused by pulsations in veins rather than by pulsations in arterial beds. In experiments to evaluate the validity of this hypothesis, we found that the average value of hemoglobin saturation (%SaO2) measured by the pulse oximeter of the dependent fingertip and finger base when dependent was 1.5% and 7.8% lower than when the fingertip and finger base were elevated. Also, the PVA detected by the pulse oximeter followed the same trend as %SaO2. This finding was explained by venous congestion in the dependent finger. On the basis of the high venous pressure, the behavioral trends between the PVA and venous pressure, the high PVO2, and the low %SaO2 and PVA in the dependent finger, we conclude that the PVA of the PEPG is determined mainly by venous pulse volume generated by shunting of arterial pulse via open arteriovenous (AV) anastomoses in the cutaneous circulation.

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