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doi: 10.1097/01.anes.0000296306.22254.79

Surprises in Plethysmography

Sondergaard, Soren M.D., Ph.D.

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To the Editor:—

In a recent editorial,1 Pinsky elaborated on the use of the plethysmographic recording obtained from a pulse oximeter in assessing volume responsiveness before instituting volume resuscitation. Pinsky noted that the plethysmographic signal is dependent on the density of tissue and pulsatile blood in the pathway of the infrared and red wavelengths and that this “… will be a function of both perfusion pressure and vasomotor tone. As upstream vasomotor tone increases, for example, pulse oximeter plethysmographic changes would decrease for the same pulse pressure, and vice versa with vasodilation.” The question is, however, whether it is the density or the variation in density that defines the plethysmographic variability.
I have for a couple of years routinely monitored pulse oximetry and plethysmography (Datex-GE, Helsinki, Finland) bilaterally in the lower extremities during abdominal aortic aneurysm repair and unilaterally in peripheral vascular reconstructive surgery. The plethysmographic signal is the first and failsafe herald of peripheral perfusion, and the lack of it likewise immediately warns of thromboembolic complications after declamping.
Fig. 1
Fig. 1
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During one such procedure involving popliteal artery reconstruction under general anesthesia and spontaneous ventilation using a laryngeal mask, the plethysmographic signal after declamping is shown in figure 1, with the insert showing highly irregular beat-to-beat variation in amplitude.
Fig. 2
Fig. 2
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The variation corresponds to variation in amplitude seen in the arterial pressure recording of the radial artery. The “silent” period at approximately 150 s represents manual compression of vascular graft. A perivascular Doppler flow probe was attached to the graft measuring a flow of 100 ml/min. The surgeon decided to assess the flow reserve of the receiving vascular bed, and papaverine 40 mg was injected intraarterially proximally to the graft. The Doppler signal instantaneously increased to 200 ml/min, and the ensuing plethysmographic recording is shown in figure 2. The plethysmogram was all but abolished in response to the injection of papaverine. The arterial pressure remained largely unaffected by the peripheral vasodilation.
Initially, the response baffled me as I was expecting an increase with vasodilation, as stated by Pinsky. On second thought, the explanation became evident: the plethysmographic signal in Datex-GE pulse oximeters is highpass filtered, which resets the oscillations to vary between negative and positive values, and the signal is normalized by the direct current value. By vasodilating the vascular bed in the foot and increasing the direct current component (tissue and diastolic blood) of the plethysmographic signal, the oscillations of the arterial wall diminished even though the vessels carried a higher flow, decreasing the alternating current (systolic blood) component of the plethysmographic signal. This observation was later repeated in another patient.
In conclusion, knowledge of the software algorithm of the pulse oximeter is essential to the interpretation of changes. In addition, without proper estimate of flow in and diameter of the vessel, any change in plethysmographic signal after a pharmacological intervention or fluid challenge must be interpreted with utmost caution.
Soren Sondergaard, M.D., Ph.D.
Sahlgrenska University Hospital, Gothenburg, Sweden.
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1. Pinsky MR. At the threshold of noninvasive functional hemodynamic monitoring. Anesthesiology 2007; 106:1084–5

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