Evidence that large vessels do affect near infrared spectroscopy.

The influence of large vessels on near infrared spectroscopy (NIRS) measurement is generally considered negligible. Aim of this study is to test the hypothesis that changes in the vessel size, by varying the amount of absorbed NIR light, could profoundly affect NIRS blood volume indexes. Changes in haemoglobin concentration (tHb) and in tissue haemoglobin index (THI) were monitored over the basilic vein (BV) and over the biceps muscle belly, in 11 subjects (7 M - 4 F; age 31 ± 8 year) with simultaneous ultrasound monitoring of BV size. The arm was subjected to venous occlusion, according to two pressure profiles: slow (from 0 to 60 mmHg in 135 s) and rapid (0 to 40 mmHg maintained for 30 s). Both tHb and THI detected a larger blood volume increase (1.7 to 4 fold; p < 0.01) and exhibited a faster increase and a greater convexity on the BV than on the muscle. In addition, NIRS signals from BV exhibited higher correlation with changes in BV size than from muscle (r = 0.91 vs 0.55, p < 0.001 for THI). A collection of individual relevant recordings is also included. These results challenge the long-standing belief that the NIRS measurement is unaffected by large vessels and support the concept that large veins may be a major determinant of blood volume changes in multiple experimental conditions.

The Cardiac Caval Index: Improving Noninvasive Assessment of Cardiac Preload.

OBJECTIVES: Inferior vena cava (IVC) pulsatility quantified by the Caval Index (CI) is characterized by poor reliability, also due to the irregular magnitude of spontaneous respiratory activity generating the major pulsatile component. The aim of this study was to test whether the IVC cardiac oscillatory component could provide a more stable index (Cardiac CI-CCI) compared to CI or respiratory CI (RCI). METHODS: Nine healthy volunteers underwent long-term monitoring in supine position of IVC, followed by 3 minutes passive leg raising (PLR). CI, RCI, and CCI were extracted from video recordings by automated edge-tracking and CCI was averaged over each respiratory cycle (aCCI). Cardiac output (CO), mean arterial pressure (MAP) and heart rate (HR) were also recorded during baseline (1 minutes prior to PLR) and PLR (first minute). RESULTS: In response to PLR, all IVC indices decreased (P < .01), CO increased by 4 ± 4% (P = .055) while HR and MAP did not vary. The Coefficient of Variation (CoV) of aCCI (13 ± 5%) was lower than that of CI (17 ± 5%, P < .01), RCI (26 ± 7%, P < .001) and CCI (25 ± 7%, P < .001). The mutual correlations in time of the indices were 0.81 (CI-RCI), 0.49 (CI-aCCI) and 0.2 (RCI-aCCI). CONCLUSIONS: Long-term IVC monitoring by automated edge-tracking allowed us to evidence that 1) respiratory and averaged cardiac pulsatility components are uncorrelated and thus carry different information and 2) the new index aCCI, exhibiting the lowest CoV while maintaining good sensitivity to blood volume changes, may overcome the poor reliability of CI and RCI.

Assessment of Phasic Changes of Vascular Size by Automated Edge Tracking-State of the Art and Clinical Perspectives.

Assessment of vascular size and of its phasic changes by ultrasound is important for the management of many clinical conditions. For example, a dilated and stiff inferior vena cava reflects increased intravascular volume and identifies patients with heart failure at greater risk of an early death. However, lack of standardization and sub-optimal intra- and inter- operator reproducibility limit the use of these techniques. To overcome these limitations, we developed two image-processing algorithms that quantify phasic vascular deformation by tracking wall movements, either in long or in short axis. Prospective studies will verify the clinical applicability and utility of these methods in different settings, vessels and medical conditions.

Vascular reactivity of cutaneous circulation to brief compressive stimuli, in the human forearm.

PURPOSE: A brief compressive stimulus is known to induce a rapid hyperemia in skeletal muscles, considered to contribute to the initial phase of functional hyperemia. Whether the same mechano-sensitivity characterizes the cutaneous circulation is debated. This study aims to investigate whether a rapid hyperemic response to compressive stimuli is also expressed by skin blood flow in humans. METHODS: In 12 subjects, brief compressive stimuli were delivered to the forearm at varying pressures/durations (50/2, 100/2, 200/2, 200/1, 200/5 mmHg/s); the sequence was randomized and repeated with the arm above and below heart level. Laser Doppler flowmetry technique was used to monitor skin blood flow. The response was described in terms of peak skin blood flow normalized to baseline (nSBFpeak), time-to-peak from the release of compression, and excess blood volume (EBV, expressed in terms of seconds of basal flow, s-bf) received during the response. RESULTS: The results consistently evidenced the occurrence of a compression-induced hyperemic response, with nSBFpeak = 2.9 ± 1.1, EBV = 17.0 ± 6.6 s-bf, time-to-peak = 7.0 ± 0.7 s (200 mmHg, 2 s, below heart level). Both nSBFpeak and EBV were significantly reduced (by about 50%) above compared to below heart level (p < 0.01). In addition, EBV slightly increased with increasing pressure (p < 0.05) and duration (p < 0.01) of the stimulus. CONCLUSIONS: For the first time, the rapid dilatator response to compressive stimuli was demonstrated in human cutaneous circulation. The functional meaning of this response remains to be elucidated.

Hyper-Oxygenation Attenuates the Rapid Vasodilatory Response to Muscle Contraction and Compression.

A single muscle compression (MC) with accompanying hyperemia and hyper-oxygenation results in attenuation of a subsequent MC hyperemia, as long as the subsequent MC takes place when muscle oxygenation is still elevated. Whether this is due to the hyper-oxygenation, or compression-induced de-activation of mechano-sensitive structures is unclear. We hypothesized that increased oxygenation and not de-activation of mechano-sensitive structures was responsible for this attenuation and that both compression and contraction-induced hyperemia attenuate the hyperemic response to a subsequent muscle contraction, and vice-versa. Protocol-1) In eight subjects two MCs separated by a 25 s interval were delivered to the forearm without or with partial occlusion of the axillary artery, aimed at preventing hyperemia and increased oxygenation in response to the first MC. Tissue oxygenation [oxygenated (hemoglobin + myoglobin)/total (hemoglobin + myoglobin)] from forearm muscles and brachial artery blood flow were continuously monitored by means of spatially-resolved near-infrared spectroscopy (NIRS) and Doppler ultrasound, respectively. With unrestrained blood flow, the hyperemic response to the second MC was attenuated, compared to the first (5.7 ± 3.3 vs. 14.8 ± 3.9 ml, P < 0.05). This attenuation was abolished with partial occlusion of the auxillary artery (14.4 ± 3.9 ml). Protocol-2) In 10 healthy subjects, hemodynamic changes were assessed in response to MC and electrically stimulated contraction (ESC, 0.5 s duration, 20 Hz) of calf muscles, as single stimuli or delivered in sequences of two separated by a 25 s interval. When MC or ESC were delivered 25 s following MC or ESC the response to the second stimulus was always attenuated (range: 60-90%). These findings support a role for excess tissue oxygenation in the attenuation of mechanically-stimulated rapid dilation and rule out inactivation of mechano-sensitive structures. Furthermore, both MC and ESC rapid vasodilatation are attenuated by prior transient hyperemia, regardless of whether the hyperemia is due to MC or ESC. Previously, mechanisms responsible for this dilation have not been considered to be oxygen sensitive. This study identifies muscle oxygenation state as relevant blunting factor, and reveals the need to investigate how these feedforward mechanisms might actually be affected by oxygenation.