What is cmro2

For instance, Takeshita et al demonstrated an almost-doubled cerebral blood flow in ten elective surgical outpatients, with CMRO 2 remaining basically unchanged. Opdenakker et al hedge differently: for them, ketamine has "differential regional effects on CMRO 2 : frontal regions, the insula, and the anterior cingulate gyrus show an increase, while a decrease is observed in pons, cerebellum, and temporal lobe".

In short, the CMRO 2 -increasing effect of ketamine may be an old superstition. Where supporting references are offered in textbooks, they point to old work done in the s eg. Evans, , and unfortunately, most textbooks parrot older textbooks , uncritically propagating this canard. This has far-reaching effects, among which is the need for CICM trainees to intentionally write exam answers which they know to be incorrect, in order to score marks.

Oh's Intensive Care manual. Chapter 52 pp. Scheinberg, Peritz, and Eugene A. Stead Jr. Normal values for blood flow, oxygen utilization, glucose utilization, and peripheral resistance, with observations on the effect of tilting and anxiety. McCullough, Jock N. Stecker, Mark M. Effects of cooling on electroencephalogram and evoked potentials. Carlsson, C. Sharma, H. Habash, R. Myers, J. Kassell, Neal F. Pierce Jr, Ellison C. Pinaud, Michel, et al. Doyle, P. Derdeyn, Colin P. Schell, Randall M.

Clarke, D. Sokoloff, Louis. Kety, S. Sloviter, H. Owen, O. Kasischke, Karl. Dienel, Gerald A. Pawlosky, Robert J. Greeley, William J. Lennox, William G. Gibbs, and Erna L. Snopek, Albert M. The results indicate high jugular venous oxygen tension and, in some studies, very low oxygen consumption.

A critical, low CMRO2 was not found, and values of about 0. Flows were summed separately over all arterioles and all venules. The two summed flow values arteriolar and venular were used to estimate the mean CBF and the standard deviation. Aliasing or phase wrapping of velocity axial projections greater in magnitude than 9. Hence, for each vessel, an en face plane with a detectable Doppler shift, but without aliasing, was chosen for the flux measurement, as shown in Fig.

A OCT angiogram showing vasculature and numbered transverse locations of vessels designated for absolute flow measurements. Flux F was determined based on the product of the area in the en face plane A xy and average axial velocity v z over this area for a particular ascending venule numbered 16 white arrow. Absolute flow was calculated from the flux magnitude assuming a cortical thickness of 1. CBF was estimated as the average of the summed arteriolar flow and summed venular flow.

Using the spectroscopic fitting method described in [ 40 ], equivalent concentrations of oxyhemoglobin [HbO 2 ] and deoxyhemoglobin [Hb] in microvasculature were estimated. Briefly, a noise bias-corrected absorbance spectrum was estimated using a short-time Fourier transform STFT of the dynamic scattering signal at each location. The absorbance spectrum was fit at each axial position using a model that incorporated the effects of scattering and hemoglobin absorption, yielding LC HbO2 and LC Hb L is the single-pass optical path length through the vessel [ 40 ].

Importantly, all concentrations [HbT], [HbO 2 ], and [Hb] represent intravascular concentrations per unit blood volume, and not per unit brain volume. Thus, our concentrations are more than one order of magnitude higher than those typically associated with diffuse optical imaging, where concentrations per unit brain volume are used. For these reasons [ 40 ], our [HbT] measurements are more directly related to hematocrit intravascular hemoglobin concentration , rather than cerebral blood volume.

The spectroscopic fitting procedure estimated LC HbT at each intravascular location, forming a three-dimensional data set which could then be displayed as a projection image in two dimensions Fig. The slope at the vessel center was found to provide the most robust estimation of C HbT. In Fig. A Locations for C HbT measurements. B Absolute C HbT values were obtained from the slope of LC HbT versus depth, where LC HbT was obtained by spectroscopic fitting at each depth [ 40 ]; the vertical red dotted-lines represent the approximate vessel boundaries.

Next, sO 2 values in arteries and veins were obtained, from which the arteriovenous oxygen saturation difference was determined. Arteries and veins were readily distinguishable based on their oxygen saturation profiles and morphology. In particular, sO 2 values in arteries and veins 6 ROIs each were averaged separately to obtain the mean arterial sO 2 and the mean venous sO 2 , respectively.

By employing this additional measurement, our method obviates an additional assumption implicit in many CMRO 2 estimation methods. Specifically, we combined 6 sO 2 measurements from arteries, 6 sO 2 measurements from veins, 2 CBF measurements arterioles and venules , and 10 [HbT] measurements, resulting in CMRO 2 values in the histogram.

We used the histogram mean and standard deviation s. The two methods yielded similar estimates for the standard deviation of CMRO 2. Figure 3 shows imaging of oxygen saturation in the mouse brain during modulation of FiO 2. Microvascular oxygen saturation was mapped using visible light spectroscopic OCT and displayed on a false-color scale Fig.

A uniform reduction in both arterial and venous saturations was observed during mild hypoxia caused by reduction of FiO 2 Fig. Since arterial and venous oxygen saturation decreased by equal amounts as FiO 2 was decreased, oxygen extraction remained approximately constant for this experiment.

Figure 4 shows imaging of oxygen saturation in the mouse brain during modulation of FiCO 2. Thus, CMRO 2 did not change appreciably during the hypercapnia experiment. A large increase in oxygen saturation was observed in veins, while the sO 2 in arteries remained unchanged.

The reduced oxygen extraction is a consequence of arterial and arteriolar dilation and subsequently, increased CBF during hypercapnia. Note the heterogeneity of oxygen extraction, as evidenced by regionally varying venous sO 2 values both before and after hypercapnia white and gray arrows.

Due to the fact that manipulations were not severe, CMRO 2 was not expected to change for any of these states. Notably, variability in C HbT Fig. The mean and standard deviation for a given state were determined from this histogram. Based on this procedure, which incorporates biological heterogeneity in the standard deviation estimate, CMRO 2 for the example in Fig. In spite of large variability in OE Fig. Therefore, as expected based on Eq.

The lower coefficient of variation of CMRO 2 across animals and states, in spite of its higher relative error Eq. The OE standard deviation estimate A was determined as the square root of the sum of the arterial and venous sO 2 variance estimates, obtained from measurements at different locations.

The CBF standard deviation estimate B was obtained from the summed arteriolar flow and summed venular flow values. C The C HbT standard deviation estimate was obtained from measurements at multiple locations. E CMRO 2 means and standard deviations were estimated from this histogram and shown across states and mice. Error bars in A-F are standard deviations. However, Fig. We anticipate that a flow-weighting of the saturation in each venule as would be required to calculate the oxygen efflux from cortical tissue might be a more appropriate way to account for this heterogeneity than to merely average the saturations.

We will explore flow-weighting of saturations in future work, using a higher optical resolution to quantify oxygen saturation in every venule where flow is measured. It is well-known that glucose metabolism in gray matter is 3-fold higher than in white matter [ 50 ], and that glucose metabolism varies across different cortical layers [ 51 ]. Since oxygen metabolism is expected to parallel glucose metabolism, some of the heterogeneity in venous saturation Fig.

Verification of this conjecture would require a vascular graph [ 52 ] to ascertain the precise cortical layers drained by each surface venule. A recent study using ultrahigh-field In another study, In this study, the mean CMRO 2 value was 2. Comparisons between studies should be performed with caution since metabolic rate varies across brain regions [ 54 ], with age [ 51, 55 ], and with depth of anesthesia [ 56 ].

Several limitations of our methodology may also contribute to these discrepancies. Dissolved oxygen may be important in calculating OE, which is an arteriovenous difference. On average, fringe washout is more severe at the short wavelength end of the broad spectrum, potentially leading to an artifactually higher absorbance at shorter wavelengths.

Nevertheless, in the present study, spectra were measured at the center of vessels that were almost perpendicular to the probe beam, meaning the axial velocities and Doppler shifts were small.

Third, the scattering coefficient is known to decrease with wavelength, leading to a higher absorbance at shorter wavelengths, particularly at greater depths. The effects of attenuation due to scattering were mitigated in the present study by selecting superficial ROIs for spectroscopic analysis. Other potential solutions to account for wavelength-dependent scattering include a depth-dependent normalization procedure [ 40 ] or employing a model that explicitly includes the wavelength-dependence of scattering [ 42 ].

Fourth, both thermal damage thresholds and the maximum permissible exposure MPE limit are lower at visible wavelengths than at near-infrared wavelengths.

No changes in the brain tissue before were noted during and after the imaging session. While a cortical thickness of 1. The substitution of a smaller cortical thickness, perhaps measured experimentally, would bring our CMRO 2 estimates more in line with literature values [ 20, 53 ].

Lastly, isoflurane is known to cause reduction of cerebral metabolism and suppression of neural activity [ 56 ] at high doses; thus, uncontrolled variability in anesthesia depth may explain some of the variability in our results. Future experiments will therefore employ simultaneous cortical electrophysiology as a more direct correlate of CMRO 2. A method of quantifying brain oxygen consumption using three independent optical measurements of cortical blood flow, arteriovenous oxygen saturation difference, and hematocrit, using a single OCT microscope, was presented.

Physiologically plausible CMRO 2 values were demonstrated, and negative control experiments were performed. While the results of these validation experiments do not prove the accuracy of the CMRO 2 measurements, a different set of results could have invalidated the method.

To provide more complete validation, these methods will be compared against gold standards such as PET in the future.

We thank Harsha Radhakrishnan for general support and advice. Hall, M. Howarth, and D. Engedal, R. Aamand, R. Mikkelsen, N. Iversen, M. Anzabi, E. Drasbek, V. Bay, J. Blicher, A.

Tietze, I. Mikkelsen, B. Hansen, S. Jespersen, N. Juul, J. Blood Flow Metab. Dirnagl, C. Iadecola, and M. Jespersen, T. Engedahl, E. Ashkanian, M. Eskildsen, and K. Antonetti, R. Klein, and T. Mozaffarieh, M. Grieshaber, and J. In addition, given the highly variable blood flow velocity within this age range, it is recommended that the TRUST labeling thickness and position should be determined on a subject-by-subject basis, and an automatic algorithm was developed for this purpose.

Although this method provides a global CMRO2 measure only, the clinical significance of an energy consumption marker and the convenience of this technique may make it a useful tool in the functional assessment of the neonatal population.

Abstract The cerebral metabolic rate of oxygen CMRO2 is the rate of oxygen consumption by the brain, and is thought to be a direct index of energy homeostasis and brain health.