Simultaneous multi-depth assessment of tissue oxygen saturation in thenar and forearm using near-infrared spectroscopy during a simple cardiovascular challenge

Hypovolemia and hypovolemic shock are life-threatening conditions that occur in numerous clinical scenarios such as in the emergency room, during surgery, and in intensive care patients [1‐4]. Compensatory mechanisms that protect against alterations in blood pressure make standard hemodynamic measurements poor indicators for early assessment of hypovolemia and shock. One of these compensatory mechanisms is extreme peripheral vasoconstriction, and therefore measurement of alterations in the peripheral circulation could aid in the early detection of hypovolemia.

To this end, near-infrared spectroscopy (NIRS) - an optical technique for measuring tissue oxygen saturation - has been widely explored, successfully and unsuccessfully, in attempts to identify the severity of hypovolemia [5‐8], to monitor blood loss [9‐11] and guide resuscitation [12‐14], and to predict patient outcome [15‐17]. The main problem with the interpretation of tissue oxygen saturation (StO₂) data from these studies, however, is the diversity of methodologies used for assessing StO₂. Two major aspects regarding the inconsistent methodology are the application site and the probing depth. The application site is important because differences may exist in the sensitivity of underlying muscle groups and other anatomical structures to cardiovascular challenges such as central hypovolemia. The probing depth, additionally, determines the relative contribution of muscular and (sub)dermal tissue to the StO₂ measurement.

Although it is often discussed that these aspects affect the assessment of StO₂, no studies have simultaneously measured StO₂ in the thenar and forearm at multiple depths. In order to investigate the actual measurement site dependence and probe dependence of NIRS in response to hemodynamic changes, such as hypovolemia, we applied a simple cardiovascular challenge: a posture change from supine to upright, causing a decrease in stroke volume (as in hypovolemia) and a heart rate increase in combination with peripheral vasoconstriction to maintain adequate blood pressure [18‐22]. Multi-depth NIRS was used to assess changes in StO₂ in the thenar and forearm in response to the hemodynamic changes associated with the described cardiovascular challenge.

Subjects started the experiment in a supine position. After stable baseline traces were obtained for the heart rate and NIRS measurements, the subjects changed posture to an upright position. Fifteen minutes later, the subjects changed posture back to supine. The heart rate and StO₂ data were obtained during the supine position, then upright for 5 and 15 minutes, and again in the supine position. The hand and forearm were kept at heart level during the entire experimental protocol using a sling.

Statistical analysis was performed in GraphPad Prism software (GraphPad Software, San Diego, CA, USA). Normal distribution of the data was confirmed for each StO₂ parameter (15 mm, 25 mm, and 25 - 15 mm) using the D'Agostino and Pearson omnibus normality test. Comparative analysis between groups was performed using analysis of variance (ANOVA) with a Bonferroni post-hoc test. All data are presented as the mean ± standard deviation. Differences between groups with P < 0.05 were considered statistically significant.

The present study investigated the application site dependence and probing depth dependence of NIRS measurements for the detection of changes in StO₂ following a simple cardiovascular challenge. The main findings were that forearm StO₂ is a more sensitive parameter to hemodynamic changes than thenar StO₂ and that the depth at which StO₂ is measured is of minor influence. In addition, our data indicated that the change in StO₂ during a cardiovascular challenge is more important than the absolute StO₂ values for monitoring the effects of hemodynamic changes on peripheral tissue oxygenation.

In the present study, a simple cardiovascular challenge was created by a posture change from supine to upright. This challenge is associated with a decrease in stroke volume, an increase in heart rate, and an increase in peripheral vascular tone in order to maintain adequate blood pressure. Since we did not measure the stroke volume and cardiac output we could not assess the extent of this cardiovascular challenge further than its effect on the heart rate. The observed increases in heart rate, however, indicate that the applied posture change did induce significant alterations at the macrocirculatory level. This is supported by several studies investigating hemodynamic responses in healthy subjects undergoing passive upright tilt [18‐22]. Furthermore, the focus of the present study was to investigate the capability of NIRS to detect alterations in StO₂ following macrocirculatory changes and, especially, the role of NIRS application site and probing depth. This capability we have evidently shown.

We have shown that forearm StO₂ is more responsive to hemodynamic changes than thenar StO₂. This is surprising given that the employed NIRS device is promoted for use on the thenar and not the forearm. Many researchers using NIRS technology claim that the contribution of (sub)dermal tissue to the NIRS signal is deleterious for its interpretation, and many optical and algorithmic solutions are explored to minimize this effect. Indeed, the present study shows that the standard deviation in distribution of StO₂ values obtained in the forearm is much larger compared with that in the thenar and, in addition, StO₂ values in the forearm tended to be lower in females than in males. Both these observations could be attributed to interindividual variability in the contribution of subdermal adipose tissue to the NIRS signal. The variance in forearm StO₂ appeared to be independent of probing depth, however, as the 15 mm, 25 mm, and 25 - 15 mm signals all provided very similar StO₂ values. Furthermore, the StO₂ change in response to the posture change was of similar extent for all probing depths. Taken together, these results suggest that the (micro)vascular response to a cardiovascular challenge might be similar in (sub)dermal tissue and in the muscle, and it is the forearm tissue as a whole that is more sensitive to hemodynamic changes compared to the thenar.

In a recent study by Soller and colleagues, where central hypovolemia was induced by lower body negative pressure (LBNP) [6], forearm StO₂ was measured using a device developed by the authors (equipped with a 30 mm probe) and was shown to be a sensitive parameter to the stroke volume decrease associated with application of LBNP. The stroke volume and forearm StO₂ decreased immediately at onset of simulated hypovolemia (LBNP = -15 mmHg), while the heart rate remained unresponsive until an LBNP of -45 mmHg and increased significantly at an LBNP of -60 mmHg. These data support our finding that forearm is a sensitive measure to detect alterations in StO₂ cardiovascular autonomic tone associated with central hypovolemia.

In a subsequent LBNP study by the same group [7], thenar StO₂ was measured with a device similar to the device used in the present study (HT device, 15 mm probe) and forearm StO₂ was measured using the device developed by the authors (30 mm probe). The authors found that their device on the forearm was more sensitive to hypovolemia than the HT device on the thenar, and concluded that their device had superior sensitivity to detect acute hypovolemia. The authors furthermore hypothesize that the 15 mm probe spacing of the HT device is probably too small to collect light from a sufficiently deep layer of muscular tissue to detect hypovolemia and, additionally, it was suggested that the relatively large contribution of (sub)dermal tissue (due to the smaller probing depth) might affect the StO₂ measurements. The present study, however, where thenar and forearm StO₂ were measured at multiple depths simultaneously, clearly shows that forearm StO₂ is a more sensitive parameter to detect changes in cardiovascular autonomic tone than thenar StO₂ (both measured with the HT device), and that the sensitivity of these measurements was independent of probing depth.

Crookes and colleagues showed in a study in trauma patients that thenar StO₂ could be used to identify severe hypovolemic shock, but that it was unable to detect mild and moderate hypovolemic shock [5]. The patient population in that study was categorized into mild, moderate, and severe hypovolemic shock, where maximum heart rates were 108 ± 26 beats/minute, 118 ± 23 beats/minute, and 130 ± 35 beats/minute, respectively. Their finding that thenar StO₂ is insensitive to mild and moderate hypovolemic shock is supported by our data and, in addition, our data support the use of forearm StO₂ as a more sensitive parameter for the detection of central hypovolemia and hypovolemic shock in (trauma) patients.

In conclusion, the present study has shown that forearm StO₂ is more responsive to hemodynamic changes compared with thenar StO₂ and that the response is similar for the applied probing depths. In addition, our results indicate that the change in StO₂ during a cardiovascular challenge is more important than the absolute StO₂ values for monitoring the effects of hemodynamic changes on peripheral tissue oxygenation. Our data furthermore suggest that the (micro)vascular response to a cardiovascular challenge might be similar in (sub)dermal tissue and in the muscle, and that it is the forearm tissue as a whole that is more sensitive to hemodynamic changes compared to the thenar tissue. This hypothesis, however, warrants further investigation.