Perioperative monitoring of the oxygen reserve: where do we stand?

The Oxygen Reserve Index (ORi) is an advanced plethysmography-derived variable that may help to quantify the degree of hyperoxia in patients receiving supplemental oxygen administration. ORi is a (relative) indicator of the actual partial pressure of oxygen dissolved in arterial blood (PaO2). As such, it may help in the titration of oxygen administration or it may help to warn the clinician of a deterioration of oxygen status of the patient.In this issue of the journal, Fadel et al. provide a 'classical' clinical validation study by assessing the correlation between ORi and PaO2 in patients about to undergo open-heart surgery. Within the moderate hyperoxic range (100-200 mmHg PaO2), there is a sound correlation between ORi and PaO2. This editorial discusses the clinical implications of this validation study and elaborates on the possible role of ORi monitoring in addition to SpO2 (peripheral arterial oxygen saturation) monitoring alone.

Agreement of somatic and renal near-infrared spectroscopy with reference blood samples during a controlled hypoxia sequence: a healthy volunteer study.

PURPOSE: O3® Regional Oximetry (Masimo Corporation, California, USA) is validated for cerebral oximetry. We aimed to assess agreement of somatic and renal near-infrared spectroscopy with reference blood samples. METHODS: O3 sensors were placed bilaterally on the quadriceps and flank of 26 healthy volunteers. A stepped, controlled hypoxia sequence was performed by adding a mixture of nitrogen and room air to the breathing circuit. O3-derived oxygen saturation values were obtained at baseline and at six decremental saturation levels (5% steps). Blood samples (radial artery, iliac vein (somatic reference) and renal vein) were obtained at each step. Reference values were calculated as: 0.7 × venous saturation + 0.3 × arterial saturation. The agreement between O3-derived values with blood reference values was assessed by calculating root-mean-square error accuracy and Bland-Altman plots. RESULTS: The root-mean-square error accuracy was 6.0% between quadriceps oxygen saturation and somatic reference values. The mean bias was 0.8%, with limits of agreement from -7.7 to 9.3%. These were 5.1% and 0.6% (-8.3 to 9.5%) for flank oxygen saturation and somatic reference values, respectively, and 7.7% and -4.9% (-15.0 to 5.2%) for flank oxygen saturation and renal reference values. The kidney depth was 3.1 ± 0.9 cm below the skin. CONCLUSION: O3 regional oximetry can be used on the quadriceps and flank to monitor somatic saturation, yet has a saturation-level dependent bias. O3-derived values obtained at the flank underestimated renal reference values. Additionally, it is unlikely that the flank sensors did directly measure renal tissue. TRIAL REGISTRATION: Clinicaltrials.gov (NCT04584788): registered October 6th, 2020.

Mitral Valve Coaptation Reserve Index: A Model to Localize Individual Resistance to Mitral Regurgitation Caused by Annular Dilation.

OBJECTIVES: The objective of this study was to develop a mathematical model for mitral annular dilatation simulation and determine its effects on the individualized mitral valve (MV) coaptation reserve index (CRI). DESIGN: A retrospective analysis of intraoperative transesophageal 3-dimensionalechocardiographic MV datasets was performed. A mathematical model was created to assess the mitral CRI for each leaflet segment (A1-P1, A2-P2, A3-P3). Mitral CRI was defined as the ratio between the coaptation reserve (measured coaptation length along the closure line) and an individualized correction factor. Indexing was chosen to correct for MV sphericity and area of largest valve opening. Mathematical models were created to simulate progressive mitral annular dilatation and to predict the effect on the individual mitral CRI. SETTING: At a single-center academic hospital. PARTICIPANTS: Twenty-five patients with normally functioning MVs undergoing cardiac surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Direct measurement of leaflet coaptation along the closure line showed the lowest amount of coaptation (reserve) near the commissures (A1-P1 0.21 ± 0.05 cm and A3-P3 0.22 ± 0.06 cm), and the highest amount of coaptation (reserve) at region A2 to P2 0.25 ± 0.06 cm. After indexing, the A2-to-P2 region was the area with the lowest CRI in the majority of patients, and also the area with the least resistance to mitral regurgitation (MR) occurrence after simulation of progressive annular dilation. CONCLUSIONS: Quantification and indexing of mitral coaptation reserve along the closure line are feasible. Indexing and mathematical simulation of progressive annular dilatation consistently showed that indexed coaptation reserve was lowest in the A2-to-P2 region. These results may explain why this area is prone to lose coaptation and is often affected in MR.

What is new in microcirculation and tissue oxygenation monitoring?

Ensuring and maintaining adequate tissue oxygenation at the microcirculatory level might be considered the holy grail of optimal hemodynamic patient management. However, in clinical practice we usually focus on macro-hemodynamic variables such as blood pressure, heart rate, and sometimes cardiac output. Other macro-hemodynamic variables like pulse pressure or stroke volume variation are additionally used as markers of fluid responsiveness. In recent years, an increasing number of technological devices assessing tissue oxygenation or microcirculatory blood flow have been developed and validated, and some of them have already been incorporated into clinical practice. In this review, we will summarize recent research findings on this topic as published in the last 2 years in the Journal of Clinical Monitoring and Computing (JCMC). While some techniques are already currently used as routine monitoring (e.g. cerebral oxygenation using near-infrared spectroscopy (NIRS)), others still have to find their way into clinical practice. Therefore, further research is needed, particularly regarding outcome measures and cost-effectiveness, since introducing new technology is always expensive and should be balanced by downstream savings. The JCMC is glad to provide a platform for such research.

Cerebral monitoring in surgical ICU patients.

PURPOSE OF REVIEW: To give an overview of cerebral monitoring techniques for surgical ICU patients. RECENT FINDINGS: As the burden of postsurgical neurological and neurocognitive complications becomes increasingly recognized, cerebral monitoring in the surgical ICU might gain a relevant role in detecting and possibly preventing adverse outcomes. However, identifying neurological alterations in surgical ICU patients, who are often sedated and mechanically ventilated, can be challenging. Various noninvasive and invasive techniques are available for cerebral monitoring, providing an assessment of cortical electrical activity, cerebral oxygenation, blood flow autoregulation, intracranial pressure, and cerebral metabolism. These techniques can be used for the diagnosis of subclinical seizures, the assessment of sedation depth and delirium, the detection of an impaired cerebral blood flow, and the diagnosis of neurosurgical complications. SUMMARY: Cerebral monitoring can be a valuable tool in the early detection of adverse outcomes in surgical ICU patients, but the evidence is limited, and clear clinical indications are still lacking.

Inflammation and primary graft dysfunction after lung transplantation: CT-PET findings.

BACKGROUND: The leading cause of early mortality after lung transplantation is Primary graft dysfunction (PGD). We assessed the lung inflammation, inflation status and inhomogeneities after lung transplantation. Our purpose was to investigate the possible differences between patients who did or did not develop PGD. METHODS: We designed a prospective observational study enrolling patients who underwent a CT-PET study within 1 week after lung transplantation. Twenty-four patients (10 after double- and 14 after single-lung) were enrolled. Respiratory and hemodynamic data were collected before, during and after lung transplantation. Each patient underwent computed tomography-positron emission tomography (CT-PET) scan early after surgery. Broncho-alveolar lavage (BAL) fluid collection was performed to analyze inflammatory mediators. RESULTS: The grafts showed a [18F]fluoro-2-deoxy-D-glucose ([18F]FDG) uptake rate of 26[18-33]*10-4 mLblood/mLtissue/min (reference values 11[7-15]*10-4). Three double- and six single-lung recipients developed PGD. The grafts of patients who developed PGD had similar [18F]FDG uptake than grafts of patients who did not (28[18-26]*10-4 versus 26[22-31]*10-4, P=0.79). Not-inflated tissue fraction was significantly higher (28[20-38]% versus 14[7-21]%, P=0.01) while well-inflated fraction was significantly lower (29[25-41]% versus 53[39-65]%, P<0.01). Inhomogeneity extent was higher in patients who developed PGD (23[18-26]% versus 14[10-20]%, P=0.01)The lung weight was 650[591-820]g versus 597[480-650]g (P=0.09)). BAL fluid analysis for inflammatory mediators did not detect a difference between the study groups. CONCLUSIONS: Compared to healthy lungs, all the grafts showed increased [18F]FDG uptake rate, but there were no differences between patients who developed PGD and patients who did not. Of note, the PGD patients showed a worse inflation status of lungs and a higher inhomogeneity extent.

Mechanical Power and Development of Ventilator-induced Lung Injury.

BACKGROUND: The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung. METHODS: Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. RESULTS: In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r = 0.41, P = 0.001) and lung elastance (r = 0.33, P < 0.01) and decrease in PaO2/FIO2 (r = 0.40, P < 0.001) at the end of the study. CONCLUSION: In piglets, VILI develops if a mechanical power threshold is exceeded.

Lung inhomogeneities, inflation and [18F]2-fluoro-2-deoxy-D-glucose uptake rate in acute respiratory distress syndrome.

The aim of the study was to determine the size and location of homogeneous inflamed/noninflamed and inhomogeneous inflamed/noninflamed lung compartments and their association with acute respiratory distress syndrome (ARDS) severity.In total, 20 ARDS patients underwent 5 and 45 cmH2O computed tomography (CT) scans to measure lung recruitability. [(18)F]2-fluoro-2-deoxy-d-glucose ([(18)F]FDG) uptake and lung inhomogeneities were quantified with a positron emission tomography-CT scan at 10 cmH2O. We defined four compartments with normal/abnormal [(18)F]FDG uptake and lung homogeneity.The homogeneous compartment with normal [(18)F]FDG uptake was primarily composed of well-inflated tissue (80±16%), double-sized in nondependent lung (32±27% versus 16±17%, p<0.0001) and decreased in size from mild, moderate to severe ARDS (33±14%, 26±20% and 5±9% of the total lung volume, respectively, p=0.05). The homogeneous compartment with high [(18)F]FDG uptake was similarly distributed between the dependent and nondependent lung. The inhomogeneous compartment with normal [(18)F]FDG uptake represented 4% of the lung volume. The inhomogeneous compartment with high [(18)F]FDG uptake was preferentially located in the dependent lung (21±10% versus 12±10%, p<0.0001), mostly at the open/closed interfaces and related to recruitability (r(2)=0.53, p<0.001).The homogeneous lung compartment with normal inflation and [(18)F]FDG uptake decreases with ARDS severity, while the inhomogeneous poorly/not inflated compartment increases. Most of the lung inhomogeneities are inflamed. A minor fraction of healthy tissue remains in severe ARDS.

Lung inhomogeneities and time course of ventilator-induced mechanical injuries.

BACKGROUND: During mechanical ventilation, stress and strain may be locally multiplied in an inhomogeneous lung. The authors investigated whether, in healthy lungs, during high pressure/volume ventilation, injury begins at the interface of naturally inhomogeneous structures as visceral pleura, bronchi, vessels, and alveoli. The authors wished also to characterize the nature of the lesions (collapse vs. consolidation). METHODS: Twelve piglets were ventilated with strain greater than 2.5 (tidal volume/end-expiratory lung volume) until whole lung edema developed. At least every 3 h, the authors acquired end-expiratory/end-inspiratory computed tomography scans to identify the site and the number of new lesions. Lung inhomogeneities and recruitability were quantified. RESULTS: The first new densities developed after 8.4 ± 6.3 h (mean ± SD), and their number increased exponentially up to 15 ± 12 h. Afterward, they merged into full lung edema. A median of 61% (interquartile range, 57 to 76) of the lesions appeared in subpleural regions, 19% (interquartile range, 11 to 23) were peribronchial, and 19% (interquartile range, 6 to 25) were parenchymal (P < 0.0001). All the new densities were fully recruitable. Lung elastance and gas exchange deteriorated significantly after 18 ± 11 h, whereas lung edema developed after 20 ± 11 h. CONCLUSIONS: Most of the computed tomography scan new densities developed in nonhomogeneous lung regions. The damage in this model was primarily located in the interstitial space, causing alveolar collapse and consequent high recruitability.