Effect of self-regulated learning and technology-enhanced activities on anatomy learning, engagement, and course outcomes in a problem-based learning program.

Problem-based learning (PBL) offers advantages for teaching anatomy and physiology for physical therapy students as clinical cases provide a scaffold for a comprehensive review of body systems. Although the utilization of interactive anatomy software greatly contributes to an active learning environment and efficient use of time, simply providing textbook readings, access to anatomy software, and models is not enough to engage students to become active in reaching their learning goals. Time constraints, meaningful technology implementation, resource abundance, and unfamiliarity are challenges that decrease the effectiveness of both facilitating and learning anatomy. The present study investigated the use of three supplemental learning tools to support anatomy instruction in a self-regulated manner. Friedman test results demonstrated significant differences for perceived engagement [χ2(2) = 15.74, P < 0.001, W = 0.23] but not for perceived learning. Survey responses demonstrated that perceived engagement was greatest with the nondigital supplemental learning tool compared with the two technology-enhanced learning tools (iBooks Author + SoftChalk and SoftChalk alone). Multivariate regression analyses demonstrated statistically significant relationships between the nondigital supplemental learning tool and anatomy practical scores (P < 0.001). The technology-enhanced supplemental learning tools did not further increase learning outcomes as measured by practical scores compared with nondigital learning tools. Incorporation of instructor-created instructional materials independent of technology is an efficient method to drive self-regulated learning, enhance engagement, and improve anatomy course outcomes and may overcome barriers associated with a purely self-directed PBL model.

Pediatric clinical simulation: a pilot project.

With increased enrollment, nursing faculty are finding clinical placement for students more difficult, especially in clinical areas such as child health. Simulation using moderate-fidelity and high-fidelity manikins offers evidence-based and innovative approaches to augment traditional clinical experiences. However, few studies quantitatively examine student outcomes associated with clinical simulation. This article describes student learning outcomes related to traditional and hybrid (part simulation and part traditional clinical) undergraduate clinical experiences in a baccalaureate nursing program. In addition, the use of faculty-developed simulation scenarios integration of Quality and Safety Education for Nurses (QSEN) competencies into four pediatric scenarios, as well as the educational development of faculty at a simulation center, are presented.

Evidence for a higher risk of hypovolemia-induced hemodynamic instability in females: implications for decision support during prehospital triage.

Lower body negative pressure (LBNP) simulates hemorrhage, and tolerance to LBNP (time to presyncope [TTP]) is indicative of tolerance to blood loss. The purpose of this study was to predict TTP based on demographic characteristics (sex, age, height, and body mass index) and physiological variables (heart rate [HR], systolic arterial pressure, diastolic arterial pressure [DAP], pulse pressure, stroke volume, total peripheral resistance [TPR], and baroreflex sensitivity [BRS]) at baseline, and during 2 levels of LBNP (-15, -30 mm Hg). Multiple linear regression analysis was used to create a model to predict TTP (range: 670 to 2516 seconds, n=187) based on demographic characteristics and physiological variables changes (Δ) from baseline to -30 mm Hg LBNP. The prediction model revealed that TTP (seconds)=1667.5+(5.1×Age)+(61.1×Sex)-(21.5×ΔHR)+(55.3×ΔDAP)-(88.2×ΔTPR)-(4.9×ΔBRS). Most significantly, our analysis demonstrated a lesser survival trajectory for females given the same rate and magnitude of hemorrhage compared to males. Young age and female sex are predictors of low tolerance to blood loss, and should be considered for early triage in the prehospital setting.

Predictors of the Onset of Hemodynamic Decompensation During Progressive Central Hypovolemia: Comparison of the Peripheral Perfusion Index, Pulse Pressure Variability, and Compensatory Reserve Index.

INTRODUCTION: As technological advances allow for the development of more sophisticated measurement of the mechanisms that contribute to compensation for loss of circulating blood volume such as hemorrhage, it is important to compare the discriminative ability of these new measures to standard vital signs and other new physiologic metrics of interest. The purpose of this study was to compare the discriminative ability of the following three measures to predict the onset of hemodynamic decompensation: peripheral perfusion index (PPI), pulse pressure variability (PPV), and the compensatory reserve index (CRI). MATERIALS AND METHODS: There were 51 healthy participants who underwent a progressive simulated hemorrhage to induce central hypovolemia by lower body negative pressure (LBNP). The least-squares means and 95% confidence intervals for each measure were reported by LBNP level and stratified by tolerance status (high tolerance vs. low tolerance). Generalized estimating equations were used to perform repeated measures logistic regression analysis by regressing the onset of hemodynamic decompensation on each of the vital signs of interest. These probabilities were used to calculate sensitivity, specificity, and receiver-operating characteristic area under the curve (ROCAUC) for PPI, PPV, and CRI. RESULTS: Compared with both PPV (ROCAUC = 0.79) and PPI (0.56), the CRI (0.90) had superior discriminative ability (P ≤ 0.0001) to predict the onset of hemodynamic decompensation. This included higher sensitivity (0.86 vs. 0.78 and 0.71) and specificity (0.78 vs. 0.69 and 0.29) for the CRI compared with PPV and PPI, respectively. Further, CRI was the only measure with mean predicted probabilities of the onset of hemodynamic decompensation that progressively increased as the level of simulated hemorrhage increased. DISCUSSION: There are two potential rationales for why the CRI had superior discriminative ability to predict hemodynamic decompensation. First, the CRI more accurately predicted the onset of hemodynamic decompensation at all levels of simulated hemorrhage, but especially at lower levels of hemorrhage. Second, the CRI was better able to differentiate high versus low tolerant participants. CONCLUSION: Consistent with previous research, the CRI had superior discriminative ability to predict the onset of hemodynamic decompensation. For those patients at greatest risk for developing impending circulatory shock, identifying the most sensitive and specific measures of the onset of hemodynamic decompensation is critical for both the early recognition and implementation of life-saving interventions.

Validation of lower body negative pressure as an experimental model of hemorrhage.

Lower body negative pressure (LBNP), a model of hemorrhage (Hem), shifts blood to the legs and elicits central hypovolemia. This study compared responses to LBNP and actual Hem in sedated baboons. Arterial pressure, pulse pressure (PP), central venous pressure (CVP), heart rate, stroke volume (SV), and +dP/dt were measured. Hem steps were 6.25%, 12.5%, 18.75%, and 25% of total estimated blood volume. Shed blood was returned, and 4 wk after Hem, the same animals were subjected to four LBNP levels which elicited equivalent changes in PP and CVP observed during Hem. Blood gases, hematocrit (Hct), hemoglobin (Hb), plasma renin activity (PRA), vasopressin (AVP), epinephrine (EPI), and norepinephrine (NE) were measured at baseline and maximum Hem or LBNP. LBNP levels matched with 6.25%, 12.5%, 18.75%, and 25% hemorrhage were -22 ± 6, -41 ± 7, -54 ± 10, and -71 ± 7 mmHg, respectively (mean ± SD). Hemodynamic responses to Hem and LBNP were similar. SV decreased linearly such that 25% Hem and matching LBNP caused a 50% reduction in SV. Hem caused a decrease in Hct, Hb, and central venous oxygen saturation (ScvO2). In contrast, LBNP increased Hct and Hb, while ScvO2 remained unchanged. Hem caused greater elevations in AVP and NE than LBNP, while PRA, EPI, and other hematologic indexes did not differ between studies. These results indicate that while LBNP does not elicit the same effect on blood cell loss as Hem, LBNP mimics the integrative cardiovascular response to Hem, and validates the use of LBNP as an experimental model of central hypovolemia associated with Hem.