|
| ||
|
|
||
Blood Gas Values (blood + gas_value)
Selected AbstractsEffect of breathing a mixture of 92% O2 + 8% CO2 on flicker induced vasodilatationACTA OPHTHALMOLOGICA, Issue 2009M LASTA Purpose It has been shown that increased neural activity evoked by stimulation with diffuse luminance flicker increases retinal and optic nerve head blood flow. Beside others, an increased oxygen demand has been attributed to evoke the flicker response. This study seeks to investigate whether the flicker light induced increase in retinal vessel diameters is different in subjects breathing 92% O2 + 8% CO2 compared to breathing room air. Methods 24 healthy volunteers were included in the study. Diameters of retinal vessels were recorded continuously with a Retinal Vessel Analyzer. During this measurement flicker stimulation was applied at a frequency of 8 Hz. Subjects were breathing a combination of 92% O2 + 8% CO2 and room air in a randomized, two way cross over design. Flicker responses were assessed during the two breathing periods. Blood gas values were determined from capillary blood samples. Results Under room air conditions flicker stimulation significantly increased retinal venous diameters (p<0.05). Breathing of 92% O2 + 8% CO2 increased pO2 from 88±18 mmHg to 277±71 mmHg (p<0.05) and pCO2 from 37±3 mmHg to 46±6 mmHg (p<0.05). Breathing a combination of 92% O2 + 8% CO2 significantly increased flicker induced vasodilatation in retinal veins compared to room air (p<0.05). Conclusion Breathing of a combination of 92% O2 + 8% CO2 increases the response of retinal venous diameters to stimulation with flicker light. The reason for this effect has, however, yet to be clarified. [source] Evaluation of hematological, chemistry and blood gas values in dogs receiving hemoglobin glutamer-200JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2007DACVECC, DACVIM, Marie E. Kerl DVM Abstract Objective: To evaluate the degree of interference that administration of hemoglobin glutamer-200 (Hb-200) caused for complete blood counts (CBC), biochemical profiles, cooximetry, and point of care (POC) testing in healthy dogs. Design: Prospective, longitudinal experimental study. Setting: Veterinary medical teaching hospital. Animals: Six purpose-bred research hounds. Interventions: Dogs were administered FDA-approved hemoglobin-based oxygen carrier (Hb-200) intravenously at 7.5 mL/kg over 2 hours. Arterial and venous blood samples were obtained before administration (Time 0) and at 3, 8, 14, 26, 50, 74, 98, 122, and 146 hours following administration. Measurements and main results: No adverse health effects were observed in any of the dogs. Characteristic mucous membrane, serum, and plasma color changes occurred following administration of Hb-200. Laboratory values that were significantly lower than baseline included packed cell volume, red blood cell count, hemoglobin, hematocrit, creatinine, cholesterol, alanine aminotransferase, and alkaline phosphatase. Laboratory values that were significantly greater than baseline included mean corpuscular hemoglobin concentration, arterial pH, arterial total carbon dioxide, arterial bicarbonate, amylase, albumin, total protein, globulin, calcium, phosphorous, total bilirubin, carboxyhemoglobin, and methemoglobin. All values returned to baseline by the completion of the 146-hour monitoring period. Conclusions: In normal dogs, administration of Hb-200 resulted in statistically significant changes in multiple laboratory parameters; however, these changes are not likely to be clinically significant in the care of critically ill dogs. [source] Ventilator treatment in the Nordic countries.ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2002A multicenter survey Background: A 1-day point prevalence study was performed in the Nordic countries to identify ventilator-treatment strategies in the region. Material and methods: On 30 May 30 2001 all mechanically ventilated patients in 27 intensive care units (ICUs) were registered via the internet. The results are shown as medians (25th, 75th percentile). Results: ,One hundred and eight patients were included (69% male) with new simplified acute physiology score (SAPS) 48 (37,57) and 4.5 d (2,11) of ventilator treatment. The most frequent indication for ventilator treatment was acute respiratory failure (73%). Airway management was by endotracheal tube (64%), tracheostomy (32%) and facial mask (4%). Pressure regulated ventilator modes were used in 86% of the patients and spontaneous triggering was allowed in 75%. The tidal volume was 7 ml/kg (6,9), peak inspiratory pressure 22 cmH2O (18,26) and positive end-expiratory pressure (PEEP) 6 cmH2O (6,9). FiO2 was 40% (35,50), SaO2 97% (95,98), PaO2 11 kPa (10,13), PaCO2 5.4 kPa (4.7,6.3), pH 7.43 (7.38,7.47) and BE 2.0 mmol/l (, 0.5,5). The PaO2/FiO2 ratio was 220 mmHg (166,283). The peak inspiratory pressure (r=0.37), mean airway pressure (r=0.36), PEEP (r=0.33), tidal volume (r=0.22) and SAPS score (r=0.19) were identified as independent variables in relation to the PaO2/FiO2 ratio. Conclusion: The vast majority of patients were ventilated with pressure-regulated modes. Tidal volume was well below what has been considered conventional in recent large trials. Correlations between the parameters of gas exchange, respiratory mechanics, ventilator settings and physiological status of the patients was poor. It appears that blood gas values are the main tool used to steer ventilator treatment. These results may help to design future interventional studies of ventilator treatment. [source] Double-outlet right ventricle in a 10-month-old Friesian fillyAUSTRALIAN VETERINARY JOURNAL, Issue 5 2009LC Fennell A 10-month-old Friesian filly had a presentation that was consistent with chronic left- and right-sided congestive heart failure. Clinical pathology findings included abnormal haematological and biochemical variables, abnormal blood gas values and increased serum concentration of cardiac troponin I. Echocardiography revealed cardiac chamber dilation and dextropositioning of the aorta. Radiography revealed a generally enlarged heart and pulmonary interstitial infiltration. These findings were supported at necropsy and the diagnosis of double-outlet right ventricle was confirmed. The pathological changes and physiological responses subsequent to double-outlet right ventricle have not previously been described in detail in horses. Clinical progression closely resembles that seen in humans, in whom antemortem diagnosis relies on echocardiography. In horses, complex cardiac disease presents a diagnostic challenge to the clinician. Appropriate therapy must be based on an accurate diagnosis. [source] Respiratory muscle strength and muscle endurance are not affected by acute metabolic acidemiaCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2009Tessa A. C. Nizet Summary Respiratory muscle fatigue in asthma and chronic obstructive lung disease (COPD) contributes to respiratory failure with hypercapnia, and subsequent respiratory acidosis. Therapeutic induction of acute metabolic acidosis further increases the respiratory drive and, therefore, may diminish ventilatory failure and hypercapnia. On the other hand, it is known that acute metabolic acidosis can also negatively affect (respiratory) muscle function and, therefore, could lead to a deterioration of respiratory failure. Moreover, we reasoned that the impact of metabolic acidosis on respiratory muscle strength and respiratory muscle endurance could be more pronounced in COPD patients as compared to asthma patients and healthy subjects, due to already impaired respiratory muscle function. In this study, the effect of metabolic acidosis was studied on peripheral muscle strength, peripheral muscle endurance, airway resistance, and on arterial carbon dioxide tension (PaCO2). Acute metabolic acidosis was induced by administration of ammonium chloride (NH4Cl). The effect of metabolic acidosis was studied on inspiratory and expiratory muscle strength and on respiratory muscle endurance. Effects were studied in a randomized, placebo-controlled cross-over design in 15 healthy subjects (4 male; age 33·2 ± 11·5 years; FEV1 108·3 ± 16·2% predicted), 14 asthma patients (5 male; age 48·1 ± 16·1 years; FEV1 101·6 ± 15·3% predicted), and 15 moderate to severe COPD patients (9 male; age 62·8 ± 6·8 years; FEV1 50·0 ± 11·8% predicted). An acute metabolic acidemia of BE ,3·1 mmol.L,1 was induced. Acute metabolic acidemia did not significantly affect strength or endurance of respiratory and peripheral muscles, respectively. In all subjects airway resistance was significantly decreased after induction of metabolic acidemia (mean difference ,0·1 kPa.sec.L,1 [95%-CI: ,0·1 ,,0·02]. In COPD patients PaCO2 was significantly lowered during metabolic acidemia (mean difference ,1·73 mmHg [,3·0 ,,0·08]. In healthy subjects and in asthma patients no such effect was found. Acute metabolic acidemia did not significantly decrease respiratory or peripheral muscle strength, respectively muscle endurance in nomal subjects, asthma, or COPD patients. Metabolic acidemia significantly decreased airway resistance in asthma and COPD patients, as well as in healthy subjects. Moreover, acute metabolic acidemia slightly improved blood gas values in COPD patients. The results suggest that stimulation of ventilation in respiratory failure, by induction of metabolic acidemia will not lead to deterioration of the respiratory failure. [source] | ||||||||||