Transfer of knowledge, skills and confidence from a faculty development programme for health professions educators into practice.

BACKGROUND: Faculty development programmes should incorporate the transfer of knowledge, skills, and confidence from the training to educational practice. However, there is a risk that transfer may fail due to inadequate integration of knowledge, skills, and confidence. The study evaluated transfer levels, guided by learned principles from a faculty development programme. METHOD: The submitted self-reports on a pedagogical intervention of 92 out of 190 health professions educators who participated in a mandatory teaching and learning training programme, were analysed by a mixed-method approach guided by a structured conceptual framework. RESULTS: Overall 93.4% reported the successful transfer of learning. Participants incorporated sustainable changed practice (level A, 57.6%), showed reflection on the impact of changed practice (level B, 21.7%), and performed effect analysis (level C, 14.1%). The rest planned application of learning (level D, 4.4%) and identified gaps in current practice or developed an idea for educational intervention but did not implement (level E, 2.2%). CONCLUSION: The majority of participants transferred their learning. Faculty development programmes must ensure successful transfer of knowledge, skills, and confidence from the training to educational practice to ensure sustainable development of teaching and learning practices.

Severe complications during the management of a child with late presentation of a diaphragmatic hernia.

We report on a 3-year-old boy with late presentation of congenital diaphragmatic hernia who developed cardiac arrest after induction of anaesthesia. The paper discusses the anaesthetic technique, in particular ventilation during and after induction, how these techniques contributed to the complication, and how they might have been avoided.

Hydrogen peroxide production in leukocytes during cerebral hypoxia and reoxygenation with 100% or 21% oxygen in newborn piglets.

The aim of this study was to investigate whether reoxygenation with 21% O2 rather than 100% O2 results in reduced hydrogen peroxide (H2O2) concentrations in neutrophils (PMN). Piglets (2-4 d old) exposed to severe hypoxia (inspired fraction of oxygen, 0.08) were randomized to resuscitation with 21 (n = 13) or 100% O2 (n = 12). Five animals served as controls. H2O2 concentrations in PMN in terms of rhodamine 123 (Rho 123) fluorescence intensity from arterial and superior sagittal sinus blood were quantified by flow cytometry. Laser Doppler flowmetry (LDF) was used to assess cortical blood perfusion. During hypoxia, Rho 123 increased in arterial PMN in both study groups by 15 and 32%, respectively (p < 0.05). In cerebral venous PMN, the increase was less dominant (p = 0.06). Reoxygenation with 100 or 21% O2 had no different effect on Rho 123 in arterial PMN. In cerebral venous PMN, Rho 123 was approximately 40% higher after 60 min and 30% higher after 120 min compared with corresponding data in the 21% O2 group (p < 0.05), which were close to baseline levels. Further, O2 treatment in both groups induced PMN accumulation in arterial blood (p < 0.05). Laser Doppler flowmetry signals increased during transient hypoxia (p < 0.0001 compared with baseline) and were normalized after reoxygenation in both study groups. In conclusion, arterial and cerebral venous H2O2 concentration in PMN tended to increase during hypoxia. During reoxygenation, H2O2 concentration in PMN in the cerebral circulation was low with 21% O2 but remained high with 100% O2 ventilation. We speculate that oxygen should be reintroduced with more caution during neonatal resuscitation.

Cerebral hypoxemia-ischemia and reoxygenation with 21% or 100% oxygen in newborn piglets: effects on extracellular levels of excitatory amino acids and microcirculation.

OBJECTIVE: To determine whether reoxygenation with 21% oxygen is preferable to 100% oxygen in normalizing extracellular levels of excitatory amino acids in the brains of hypoxic-ischemic newborn piglets and to compare this model of combined hypoxemia-ischemia to a previously used model of global hypoxemia. DESIGN: Prospective, randomized animal study. SETTING: Surgical research laboratory. SUBJECTS: Twenty-four anesthetized piglets, 1-3 days old. INTERVENTIONS: Hypoxemia-ischemia was achieved by normoventilation with 8% oxygen and temporary occlusion of the common carotid arteries. After 20 mins, reoxygenation-reperfusion was started with 21% oxygen (HI 21% group, n = 12) or 100% oxygen (HI 100% group, n = 12) for 30 mins followed by 21% oxygen. All piglets were observed for 2 hrs. MEASUREMENTS AND MAIN RESULTS: We measured extracellular concentrations of amino acids in striatum and hypoxanthine in cerebral cortex (microdialysis), microcirculation in cerebral cortex (laser Doppler), plasma hypoxanthine, and mean arterial pressure. During the 2-hr reoxygenation-reperfusion period, levels of amino acids were significantly higher in the HI 21% group compared with the HI 100% group (glutamate, p = 0.02; aspartate, p = 0.03). Mean arterial pressure was significantly lower in the HI 21% group (p = 0.04). Microcirculation decreased to <10% of baseline during hypoxemia-ischemia and normalized during reoxygenation-reperfusion in the HI 100% group, but it remained at a significantly lower level in the HI 21% group (p = 0.03). CONCLUSIONS: Significantly higher levels of excitatory amino acids in striatum, significantly lower mean arterial pressure, and a significantly greater degree of hypoperfusion in cerebral cortex were found after reoxygenation with 21% oxygen compared with 100% oxygen in normocapnic, hypoxemic-ischemic newborn piglets. This suggests a less favorable outcome in the group receiving room air.

Effects of adenosine on extravascular lung water content in endotoxemic pigs.

OBJECTIVE: To investigate whether adenosine protects against endotoxin-induced increments in extravascular lung water content. DESIGN: Prospective, randomized, animal study. SETTING: University research laboratory. SUBJECTS: Twenty-one anesthetized juvenile pigs. INTERVENTIONS: The animals were divided into two groups subjected to endotoxin infusion: Endotoxin alone (n = 7), or endotoxin combined with adenosine infusion (n = 7) administered during the whole experimental period. Two other groups were exposed to anesthesia alone (n = 4) or adenosine infusion alone (n = 3), respectively. MEASUREMENTS AND MAIN RESULTS: Central hemodynamic variables and extravascular lung water, as assessed by the thermal dye dilution double indicator technique, were monitored. Plasma endothelin-1 concentrations were measured hourly. Extravascular lung water increased significantly in response to endotoxemia (p <.001) along with an increase in pulmonary microvascular pressure (P(mv) [p <.01]). Although the Pmv increased less in endotoxemic animals exposed to adenosine infusion, no intergroup difference was found. From 4 through 6 hrs, adenosine-treated pigs displayed only half of the extravascular lung water content of nontreated animals (p <.01). The latter did not differ from that of anesthetized controls receiving anesthesia or adenosine alone. Adenosine administered alone had no effect on P(mv). In pigs receiving adenosine alone, extravascular lung water content reached nadir after 3 hrs. In both endotoxin groups, plasma endothelin-1 concentration increased two-fold, peaking 4-6 hrs after the start of endotoxin infusion (p <.001). CONCLUSIONS: The endotoxin-induced increase in lung extravascular water was hampered by intravenously infused adenosine in the presence of a nonsignificantly reduced microvascular pressure. This leaves reduced microvascular permeability the most likely reason for the beneficial effect of adenosine.

Cerebral nitric oxide concentration and microcirculation during hypercapnia, hypoxia, and high intracranial pressure in pigs.

Intracerebral nitric oxide (NO) concentration was measured to establish the technique and to investigate the response of the NO concentration to CO(2)variations, hypoxia, and reduced cerebral perfusion pressure. An intracerebral nitric oxide sensor was used in 10 pigs. Cerebral microcirculation was measured by laser Doppler flowmetry. Five pigs received 40 mg/kg nitro-1-arginine methyl ester (L-NAME). Baseline NO concentration was 246 +/- 42 nM. Hypercapnia increased cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05). Hypoxia decreased NO concentration (P< 0.05). During high intracranial pressure, cerebral microcirculation decreased (P< 0.05) before the NO concentration decreased (P< 0.05), and after normalisation of the intracranial pressure the NO concentration increased, but more slowly than the cerebral microcirculation. L-NAME caused a decrease in cerebral microcirculation (P< 0.05) and NO concentration (P< 0.05) to a new steady state, and L-NAME attenuated the changes in NO concentration after hypoxia (P< 0.05) and high intracranial pressure (P< 0.05). In conclusion, the electrochemical sensor appears to reliably detect changes in localised intracerebral NO concentration and seems to be a promising tool for direct measurement of this chemically unstable substance.

Hemodynamic changes and systemic activation of coagulation and fibrinolysis during controlled endotoxemia in pigs.

In this study, we have established a pig model that can combine extensive hemodynamic monitoring with simultaneous repetitive (serial) blood sampling for the study of multiple variables related to the hemostatic system. Sixteen healthy young pigs were studied to evaluate the influence of continuous endotoxin infusion on hemodynamic patterns and activation of coagulation and fibrinolysis. The chief aim of the study was to investigate the applicability of analytical methods primarily developed for use with human plasma samples in quantification of factors and reaction products of the porcine coagulation and fibrinolytic systems, and further, to use these methods to study the longitudinal changes in the plasma levels of these hemostatic variables as a consequence of endotoxin infusion. We found that acute, controlled endotoxemia induced a hemodynamic state of shock and reduced pulmonary gas exchange. Simultaneously, a gradual increase in peripheral blood mononuclear cell tissue factor activity was demonstrated, and increased maximally 5.5-fold 4 hours after onset of endotoxin infusion. Thrombin-antithrombin complexes increased in plasma to maximum levels after 3 hours, accompanied by an ethanol gelation test that was regularly positive after 1 to 2 hours, and fibrin monomer levels that gradually increased maximally 3.8-fold after 6 hours. These changes were followed by gradual decreases of both fibrinogen and factor VII levels, mainly due to consumption. Plasma levels of tissue type plasminogen activator activity peaked at 1.5 hours (11.3-fold increase), whereas the peak of plasminogen activator inhibitor-1 activity (14-fold increase at 4.5 hours) was delayed compared to tissue plasminogen activator and completely extinguished plasma tissue plasminogen activator activity. The sequential activation of coagulation and fibrinolysis established a procoagulant state favoring disseminated intravascular coagulation and microthrombus formation, potentially leading to multiple organ dysfunction.

Effects of hypoxia and reoxygenation with 21% and 100%-oxygen on cerebral nitric oxide concentration and microcirculation in newborn piglets.

Bioelectric sensors for continuous registration of nitric oxide (NO) concentrations in tissues provide a new tool for invasive measurement of this gaseous molecule. This study sought to validate cerebral NO measurements using an amperiometric sensor. A series of experiments in 1- to 3-day-old piglets was carried out to study the response of NO and microcirculation during hypoxia (F(i)O(2) 0.06) and reoxygenation with 100% and 21% oxygen. Two-channel laser Doppler flowmetry was performed in the forebrain cortex. Significant decreases of NO levels were observed immediately after induction of hypoxemia (p < 0.05). During reoxygenation with 21 or 100% O(2) for 30 min, NO increased significantly compared to the values at the end of hypoxia (p < 0.05). The increase of NO levels in the 100% oxygen group was greater than the increase in the 21% oxygen group (p < 0. 05). There were no significant differences between the two groups during the following 3.5 h of observation. A significant increase in CBF was found in the first 2 min of hypoxia (p < 0.05), it then continued to fall to values significantly lower than baseline values at the end of hypoxemia (p < 0.05). During reoxygenation CBF normalised and there were consistent but no significant differences between the two reoxygenation groups. We conclude that NO concentration decreased during the course of hypoxia. Hypoxia-induced cerebral hyperaemia occurred in spite of significantly lower NO concentrations. Reoxygenation with 21 or 100% O(2) restored CBF in both groups similarly, although values were higher after reoxygenation with 100% O(2) compared to air. In fact, reoxygenation with 100% O(2) led to supranormal levels of NO by contrast to 21% O(2).