ObjectiveAn attempt to define pre-osteoarthritis (OA) versus early OA and definitive osteoarthritis.MethodsA group of specialists in the field of cartilage science and treatment was formed to consider the nature of OA onset and its possible diagnosis.ResultsLate-stage OA, necessitating total joint replacement, is the end stage of a biological process, with many previous earlier stages. Early-stage OA has been defined and involves structural changes identified by arthroscopy or radiography. The group argued that before the “early-stage OA” there must exist a stage where cellular processes, due to the presence of risk factors, have kicked into action but have not yet resulted in structural changes. The group suggested that this stage could be called “pre-osteoarthritis” (pre-OA).ConclusionsThe group suggests that defining points of initiation for OA in the knee could be defined, for example, by traumatic episodes or surgical meniscectomy. Such events may set in motion metabolic processes that could be diagnosed by modern MRI protocols or arthroscopy including probing techniques before structural changes of early OA have developed. Preventive measures should preferably be applied at this pre-OA stage in order to stop the projected OA “epidemic.”
In a circulation completely dependent on ECMO support, maximum achievable flow directly depended on the vascular factors governing venous return - i.e. closing conditions, stressed vascular volume and the elastance and resistive properties of the vasculature. Both treatments increased maximum achievable ECMO flow at stable DO2, via increases in stressed volume by different mechanisms. Vascular resistance and pump afterload decreased with Volume Expansion.
Background: Collapsibility of caval vessels and stroke volume and pulse pressure variations (SVV, PPV) are used as indicators of volume responsiveness. Their behavior under increasing airway pressures and changing right ventricular afterload is incompletely understood. If the phenomena of SVV and PPV augmentation are manifestations of decreasing preload, they should be accompanied by decreasing transmural right atrial pressures. Methods: Eight healthy pigs equipped with ultrasonic flow probes on the pulmonary artery were exposed to positive end-expiratory pressure of 5 and 10 cmH2O and three volume states (Euvolemia, defined as SVV < 10%, Bleeding and Retransfusion). SVV and PPV were calculated for the right and PPV for the left side of the circulation at increasing inspiratory airway pressures (15, 20, 25 cmH2O). Right ventricular afterload was assessed by surrogate flow profile parameters. Transmural pressures in the right atrium and the inferior and superior caval vessels (IVC and SVC) were determined. Results: Increasing airway pressure led to increases in ultrasonic surrogate parameters of right ventricular afterload, increasing transmural pressures in the right atrium and SVC, and a drop in transmural IVC pressure. SVV and PPV increased with increasing airway pressure, despite the increase in right atrial transmural pressure. Right ventricular stroke volume variation correlated with indicators of right ventricular afterload. This behavior was observed in both PEEP levels and all volume states. Conclusions: Stroke volume variation may reflect changes in right ventricle afterload, rather than changes in preload.
Studies performed in rabbit and mouse models and in a limited number of human subjects, show that transfused platelets bind thrombopoietin (TPO) and decrease its concentration in the circulation. The aim of the present study was to further examine this relationship. The material comprised 12 patients receiving a total of 21 transfusions, as part of the routine clinical treatment. Blood samples were collected from the patients immediately before and 30 min after completion of the platelet transfusion, and the corrected platelet count increment (CCI) was calculated. A commercially available ELISA kit was used to determine plasma TPO concentrations. Statistically significant reductions in median TPO concentration were observed in response to the platelet transfusions. Patients who were refractory to platelet transfusions showed the slightest decrease in TPO concentration. As for the linear regression between change in TPO level and CCI, only borderline significance was observed. Thus, our findings support the concept that platelets can remove TPO from the circulation.
Background
Stroke volume measurement should provide estimates of acute treatment responses. The current pulse contour method estimates left ventricle stroke volume. Heart-lung interactions change right ventricular stroke volume acutely. We investigated the accuracy, precision, and trending abilities of four calibrated stroke volume estimates based on pulmonary artery pulse contour analysis.
Results
Stroke volume was measured in 9 pigs with a pulmonary artery ultrasound flow probe at 5 and 10 cmH2O of PEEP and three volume states (baseline, bleeding, and retransfusion) and compared against stroke volume estimates of four calibrated pulmonary pulse contour algorithms based on pulse pressure or pressure integration. Bland-Altman comparison with correction for multiple measurements and trend analysis were performed. Heart rate and stroke volumes were 104 ± 24 bpm and 30 ± 12 mL, respectively. The stroke volume estimates had a minimal bias: − 0.11 mL (95% CI − 0.55 to 0.33) to 0.32 mL (95% CI − 0.06 to 0.70). The limits of agreement were − 8.0 to 7.8 mL for calibrated pulse pressure to − 10.4 to 11.5 mL for time corrected pressure integration, resulting in a percentage error of 36 to 37%. The calibrated pulse pressure method performed best. Changes in stroke volume were trended very well (concordance rates 73–100%, r2 0.26 to 0.987, for pulse pressure methods and 71–100%, r2 0.236 to 0.977, for integration methods).
Conclusions
Pulmonary artery pulse contour methods reliably detect acute changes in stroke volume with good accuracy and moderate precision and accurately trend short-term changes in cardiac output over time.
Background
Recent studies in haemodynamic management have focused on fluid management and assessed its effects in terms of increase in cardiac output based on fluid challenges or variations in pulse pressure caused by cyclical positive pressure ventilation. The theoretical scope may be characterised as Starling-oriented. This approach ignores the actual events of right-sided excitation and left-sided response which is consistently described in a Guyton-oriented model of the cardiovascular system.
Aim
Based on data from a previous study, we aim to elucidate the primary response to crystalloid and colloid fluids in terms of cardiac output, mean blood pressure and right atrial pressure as well as derived and efficiency variables defined in terms of Guyton venous return physiology.
Method
Re-analyses of previously published data.
Results
Cardiac output invariably increased on infusion of crystalloid and colloid solutions, whereas static and dynamic efficiency measures declined in spite of increasing pressure gradient for venous return.
Discussion
We argue that primary as well as derived and efficiency measures should be reported and discussed when haemodynamic studies are reported involving fluid administrations.
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