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Editorial
This letter to the editor argues that plethysmographic waveform variation can indicate hypovolemia before the onset of hypotension, challenging a previous study's methodology involving sodium nitroprusside.
To the Editor: I read with interest the article by Golparvar et al. (1). The authors state that the applicability of plethysmographic indices changes at normotensive hypovolemic conditions (as Shamir et al. (2) found) is limited since hypovolemia is associated with hypotension. We believe that the contrary is the true. Systolic blood pressure decreases only when the patient is in grade 3 hypovolemic shock (30–40% blood volume loss) (3). Hypovolemia needs to be unmasked before arterial blood pressure decreases (grade 1–2 hypovolemic shock). Perhaps Golparvar et al.’s results are the consequence of using an arterial vasodilator (sodium nitroprusside) that interferes with the increase in diastolic pressure that is characteristic of hypovolemic shock grade 2 (3). Otherwise, the authors believe that their patients were euvolemic. Actually, the patients might have suffered relative hypovolemia secondary to vasodilatation. In this case, the conclusion of this study supports our previous investigation (2). Unfortunately, the authors did not monitor hemodynamic parameters during the hypotension, and therefore the reader cannot judge the patients’ volume status. Arterial blood pressure was monitored noninvasively. Clinically, it is safer (and recommended practice) to continuously monitor invasive blood pressure while infusing sodium nitroprusside. If an intraarterial catheter was inserted, comparison of the plethysmographic indices and systolic pressure variation parameters could have validated or rejected the hypothesis. Close examination of the scatter plots and error bars include two unaddressed points: In the scatter plot, the ventilatory systolic variation (VSV) intersects the y-axis at a value of about 350%, while the D-Down intersects this axis at a value of about 250%. It is likely that D-Up is the factor that added 100% to VSV (tidal volume is too large). In the error bars figure, there is a plateau in VSV change despite ongoing decrease in blood pressure. The same, though less clear, exists in the D-Down figure. The implication of the plateau is that VSV and D-Down stayed almost constant while blood pressure decreased significantly without absolute hypovolemia (sodium nitroprusside induced hypotension). The authors did not check if these bars differ statistically. If there is no statistical difference then the conclusion of the paper should be the opposite: pharmacological hypotension does not create plethysmographic indices changes while hypovolemia does.
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Shamir et al. (2003) studied this question.
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