Auscultating heart and breath sounds through patients’ gowns: who does this and does it matter?

Background Doctors are taught to auscultate with the stethoscope applied to the skin, but in practice may be seen applying the stethoscope to the gown. Objectives To determine how often doctors auscultate heart and breath sounds through patients’ gowns, and to assess the impact of this approach on the quality of the sounds heard. Methods A sample of doctors in the west of Scotland were sent an email in 2014 inviting them to answer an anonymous questionnaire about how they auscultated heart and breath sounds. Normal heart sounds from two subjects were recorded through skin, through skin and gown, and through skin, gown and dressing gown. These were played to doctors, unaware of the origin of each recording, who completed a questionnaire about the method and quality of the sounds they heard. Results 206 of 445 (46%) doctors completed the questionnaire. 124 (60%) stated that they listened to patients’ heart sounds, and 156 (76%) to patients’ breath sounds, through patients’ gowns. Trainees were more likely to do this compared with consultants (OR 3.39, 95% CI 1.74 to 6.65). Doctors of all grades considered this practice affected the quality of the sounds heard. 32 doctors listened to the recorded heart sounds. 23 of the 64 (36%) skin and 23 of the 64 (36%) gown recordings were identified. The majority of doctors (74%) could not differentiate between skin or gown recordings, but could tell them apart from the double layer recordings (p=0.02). Trainees were more likely to hear artefactual added sounds (p=0.04). Conclusions Many doctors listen to patients’ heart and breath sounds through hospital gowns, at least occasionally. In a short test, most doctors could not distinguish between sounds heard through a gown or skin. Further work is needed to determine the impact of this approach to auscultation on the identification of murmurs and added sounds

Global Response of the Space Shuttle External Tank with the Presence of Intertank Stringer Cracks and Radius Blocks

After propellant was loaded into the external tank (ET), the November 5, 2010 launch of Space Shuttle mission STS-133 was scrubbed due to a gaseous hydrogen leak located in a vent line near the ground umbilical and ET connection. Subsequent visual inspections identified cracks in the sprayed-on foam insulation in the forward end of the ET intertank segment, adjacent to the liquid oxygen (LOX) tank, as shown in Figure 1. These cracks necessitated repair of the foam due to debris concerns that violated launch constraints. As part of the repair process, the affected foam was removed to reveal cracks in the underlying external hat stiffeners on the intertank, as shown in Figure 2. Ultimately, five stiffeners were discovered to be cracked adjacent to the LOX tank. As the managing center for the ET Project, NASA Marshall Space Flight Center (MSFC) coordinated failure investigation and repair activities among multiple organizations, which included the ET prime contractor (Lockheed Martin Space Systems Michoud Operations), the Space Shuttle Program Office at the NASA Johnson Space Center (JSC), the NASA Kennedy Space Center (KSC), and the NASA Engineering and Safety Center (NESC). STS-133 utilized the external tank designated as ET-137. Many aspects of the investigation have been reported previously in Refs. 1-7, which focus on the root cause of the failures, the flight readiness rationale and the local analyses of the stringer failures and repair. This paper summarizes the global analyses that were conducted on ET-137 as part of the NESC effort during the investigation, which was conducted primarily to determine if the repairs that were introduced to the stringers would alter the global response of the ET. In the process of the investigation, a new STAGS tabular input capability was developed to more easily introduce the aerodynamic pressure loads using a method that could easily be extended to incorporate finite element property data such as skin and stiffener thicknesses and beam cross-sectional properties

Post-operative atrial fibrillation is influenced by beta-blocker therapy but not by pre-operative atrial cellular electrophysiology

We investigated whether post-cardiac surgery (CS) new-onset atrial fibrillation (AF) is predicted by pre-CS atrial cellular electrophysiology, and whether the antiarrhythmic effect of beta-blocker therapy may involve pre-CS pharmacological remodeling. Atrial myocytes were obtained from consenting patients in sinus rhythm, just prior to CS. Action potentials and ion currents were recorded using whole-cell patch-clamp technique. Post-CS AF occurred in 53 of 212 patients (25%). Those with post-CS AF were older than those without (67 ± 2 vs 62 ± 1 years, P = 0.005). In cells from patients with post-CS AF, the action potential duration at 50% and 90% repolarization, maximum upstroke velocity, and effective refractory period (ERP) were 13 ± 4 ms, 217 ± 16 ms, 185 ± 10 V/s, and 216 ± 14 ms, respectively (n = 30 cells, 11 patients). Peak L-type Ca2+ current, transient outward and inward rectifier K+ currents, and the sustained outward current were −5.0 ± 0.5, 12.9 ± 2.4, −4.1 ± 0.4, and 9.7 ± 1.0 pA/pF, respectively (13-62 cells, 7-19 patients). None of these values were significantly different in cells from patients without post-CS AF (P > 0.05 for each, 60-279 cells, 29-86 patients), confirmed by multiple and logistic regression. In patients treated >7 days with a beta-blocker pre-CS, the incidence of post-CS AF was lower than in non-beta-blocked patients (13% vs 27%, P = 0.038). Pre-CS beta-blockade was associated with a prolonged pre-CS atrial cellular ERP (P = 0.001), by a similar degree (∼20%) in those with and without post-CS AF. Conclusion: Pre-CS human atrial cellular electrophysiology does not predict post-CS AF. Chronic beta-blocker therapy is associated with a reduced incidence of post-CS AF, unrelated to a pre-CS ERP-prolonging effect of this treatment

Carvedilol alone or in combination with digoxin for the management of atrial fibrillation in patients with heart failure?

AbstractObjectivesThis study examined the relative merits of digoxin, carvedilol, and their combination for the management of patients with atrial fibrillation (AF) and heart failure (HF).BackgroundIn patients with AF and HF, both digoxin and beta-blockers reduce the ventricular rate, and both may improve symptoms, but only beta-blockers have been shown to improve prognosis. If combined therapy is not superior to beta-blockers alone, treatment of patients with HF and AF could be simplified by stopping digoxin.MethodsWe enrolled 47 patients (29 males; mean age 68 years) with persistent AF and HF (mean left ventricular ejection fraction [LVEF] 24%) in a randomized, double-blinded, placebo-controlled study. In the first phase of the study, digoxin was compared with the combination of digoxin and carvedilol (four months). In the second phase, digoxin was withdrawn in a double-blinded manner in the carvedilol-treated arm, thus allowing a comparison between digoxin and carvedilol (six months). Investigations were undertaken at baseline and at the end of each phase.ResultsCompared with digoxin alone, combination therapy lowered the ventricular rate on 24-h ambulatory electrocardiographic monitoring (p < 0.0001) and during submaximal exercise (p < 0.05), whereas LVEF (p < 0.05) and symptom score (p < 0.05) improved. In phase 2, there was no significant difference between digoxin alone and carvedilol alone in any variable. The mean ventricular rate rose and LVEF fell when patients switched from combination therapy to carvedilol alone. Six-minute walk distance was not significantly influenced by any therapy.ConclusionsThe combination of carvedilol and digoxin appears generally superior to either carvedilol or digoxin alone in the management of AF in patients with HF

Delving into Institutional Diversity Messaging A Cross-Institutional Analysis of Student and Faculty Interpretations of Undergraduate Experiences of Equity, Diversity, and Inclusion in University Websites

Recognizing that university statements about equity, diversity, and inclusion are often cosmetic, performative, or at best, aspirational, rather than indicative of on-campus realities, this project analyzes interpretations of student identity and diversity through publicly available materials. The primary purpose of this research was to investigate how university messages about equity, diversity, and inclusion, available through public websites, are interpreted by faculty and students. Using a students-as-partners approach, we identified and analyzed themes based on our own perceptions and understandings of each of five university websites University of Calgary (Canada), University of Alabama (USA), Deakin University (Australia), University of Exeter (UK), and Portland State University (USA). While equity, diversity, and inclusion are signature initiatives at many universities, we found that analyses of their websites suggest that the ways in which those are operationalized differ. The patterns identified suggest that messaging through university websites can promote or detract from equity, diversity, and inclusion in university settings, and we observed differences in the ways in which institutions operationalized and represented initiatives related to equity, diversity, and inclusion. Exploring how these efforts at our five institutions are messaged to and interpreted by students provides a better understanding of the institutional priorities and the assumed values identified by student co-researchers. The use of student co-researchers proved an especially valuable contribution to this analysis to gain perspectives about presentations of student identity and diversity. Using this form of embedded research, we identify the limited presentations of and perceptions around diversity at institutions of higher education cited by student co-researchers

Rate-dependency of action potential duration and refractoriness in isolated myocytes from the rabbit AV node and atrium

During atrial fibrillation, ventricular rate is determined by atrioventricular nodal (AVN) conduction, which in part is dependent upon the refractoriness of single AVN cells. The aims of this study were to investigate the rate-dependency of the action potential duration (APD) and effective refractory period (ERP) in single myocytes isolated from the AV node and atrium of rabbit hearts, using whole cell patch clamping, and to determine the contribution of the 4-aminopyridine (4-AP)-sensitive current, ITO1to these relationships in the two cell types. AVN cells had a more positive maximum diastolic potential (-60&#177;1 v-71&#177;2 mV), lower Vmax(8&#177;2 v 144&#177;17 V/s) and higher input resistance [420&#177;46 v 65&#177;7 MOHgr (mean±s.eP&#60;0.05n=9–33)], respectively, than atrial myocytes. Stepwise increases in rate from 75 beats/min caused activation failure and Wenckebach periodicity in AVN cells (at around 400 beats/min), but 1:1 activation in atrial cells (at up to 600 beats/min). Rate reduction from 300 to 75 beats/min shortened the ERP in both cell types (from 155&#177;7 to 135&#177;11 ms in AVN cells [P&#60;0.05, n=6] and from 130±8 to 106&#177;7 ms in atrial cells [P&#60;0.05, n=10]). Rate increase from 300 to 480 and 600 beats/min shortened ERP in atrial cells, by 12&#177;4% (n=8) and 26&#177;7% (n=7), respectively (P&#60;0.05). By contrast, AVN ERP did not shorten at rates &#62;300 beats/min. In atrial cells, rate reduction to 75 beats/min caused marked shortening of APD50(from 51&#177;6 to 29&#177;6 ms, P&#60;0.05). 4-AP (1 mm) significantly prolonged atrial APD50at 75 beats/min (P&#60;0.05, n=7), but not at 300 or 400 beats/min. In AVN cells, in contrast, there was less effect of rate change on APD, and 4-AP did not alter APD50at any rate. 4-AP also did not affect APD90or ERP in either cell type. In conclusion, a lack of ERP-shortening at high rates in rabbit single AVN cells may contribute to ventricular rate control. ITO1contributed to the APD50rate relation in atrial, but not AVN cells and did not contribute to the ERP rate relation in either cell type

Electrophysiological effects of 5-hydroxytryptamine on isolated human atrial myocytes, and the influence of chronic beta-adrenoceptor blockade

&lt;b&gt;1.&lt;/b&gt; 5-Hydroxytryptamine (5-HT) has been postulated to play a proarrhythmic role in the human atria via stimulation of 5-HT&lt;sub&gt;4&lt;/sub&gt; receptors. &lt;b&gt;2.&lt;/b&gt; The aims of this study were to examine the effects of 5-HT on the L-type Ca&lt;sup&gt;2+&lt;/sup&gt; current (&lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt;) action potential duration (APD), the effective refractory period (ERP) and arrhythmic activity in human atrial cells, and to assess the effects of prior treatment with &#946;-adrenoceptor antagonists. &lt;b&gt;3.&lt;/b&gt; Isolated myocytes, from the right atrial appendage of 27 consenting patients undergoing cardiac surgery who were in sinus rhythm, were studied using the whole-cell perforated patch-clamp technique at 37&#186;C. &lt;b&gt;4.&lt;/b&gt; 5-HT (1 n-10 &#956;M) caused a concentration-dependent increase in &lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt;, which was potentiated in cells from &#946;-blocked (maximum response to 5-HT, E&lt;sub&gt;max&lt;/sub&gt;=299&#177;12% increase above control) compared to non-&#946;-blocked patients (E&lt;sub&gt;max&lt;/sub&gt;=220&#177;6%, P&#60;0.05), but with no change in either the potency (log EC&lt;sub&gt;50&lt;/sub&gt;: -7.09&#177;0.07 vs -7.26&#177;0.06) or Hill coefficient (&lt;i&gt;n&lt;/i&gt;&lt;sub&gt;H&lt;/sub&gt;: 1.5&#177;0.6 vs 1.5&#177;0.3) of the 5-HT concentration-response curve. &lt;b&gt;5.&lt;/b&gt; 5-HT (10 &#956;M) produced a greater increase in the APD at 50% repolarisation (APD50) in cells from &#946;-blocked patients (of 37&#177;10 ms, i.e. 589&#177;197%) vs non-&#946;-blocked patients (of 10&#177;4 ms, i.e. 157&#177;54%; P&#60;0.05). Both the APD&lt;sub&gt;90&lt;/sub&gt; and the ERP were unaffected by 5-HT. &lt;b&gt;6.&lt;/b&gt; Arrhythmic activity was observed in response to 5-HT in five of 17 cells (29%) studied from &#946;-blocked, compared to zero of 16 cells from the non-&#946;-blocked patients (P&#60;0.05). &lt;b&gt;7.&lt;/b&gt; In summary, the 5-HT-induced increase in calcium current was associated with a prolonged early plateau phase of repolarisation, but not late repolarisation or refractoriness, and the enhancement of these effects by chronic &#946;-adrenoceptor blockade was associated with arrhythmic potential

Electrophysiological and arrhythmogenic effects of 5-hydroxytryptamine on human atrial cells are reduced in atrial fibrillation

5-Hydroxytryptamine (5-HT) is proarrhythmic in atrial cells from patients in sinus rhythm (SR) via activation of 5-HT&lt;sub&gt;4&lt;/sub&gt; receptors, but its effects in atrial cells from patients with atrial fibrillation (AF) are unknown. The whole-cell perforated patch-clamp technique was used to record L-type Ca&lt;sup&gt;2+&lt;/sup&gt; current (&lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt;), action potential duration (APD) and arrhythmic activity at 37 °C in enzymatically isolated atrial cells obtained from patients undergoing cardiac surgery, in SR or with chronic AF. In the AF group, 5-HT (10 μM) produced an increase in &lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt; of 115 ± 21% above control (&lt;i&gt;n&lt;/i&gt; = 10 cells, 6 patients) that was significantly smaller than that in the SR group (232 ± 33%; &lt;i&gt;p&lt;/i&gt; 0.05; &lt;i&gt;n&lt;/i&gt; = 27 cells, 12 patients). Subsequent co-application of isoproterenol (1 μM) caused a further increase in &lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt; in the AF group (by 256 ± 94%) that was greater than that in the SR group (22 ± 6%; p &#60; 0.05). The APD at 50% repolarisation (APD&lt;sub&gt;50&lt;/sub&gt;) was prolonged by 14 ± 3 ms by 5-HT in the AF group (&lt;i&gt;n&lt;/i&gt; = 37 cells, 14 patients). This was less than that in the SR group (27 ± 4 ms; &lt;i&gt;p&lt;/i&gt; &#60; 0.05; &lt;i&gt;n&lt;/i&gt; = 58 cells, 24 patients). Arrhythmic activity in response to 5-HT was observed in 22% of cells in the SR group, but none was observed in the AF group (p &#60; 0.05). Atrial fibrillation was associated with reduced effects of 5-HT, but not of isoproterenol, on &lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt; in human atrial cells. This reduced effect on &lt;i&gt;I&lt;/i&gt;&lt;sub&gt;CaL&lt;/sub&gt; was associated with a reduced APD&lt;sub&gt;50&lt;/sub&gt; and arrhythmic activity with 5-HT. Thus, the potentially arrhythmogenic influence of 5-HT may be suppressed in AF-remodelled human atrium