Performing Platform Governance: Facebook and the Stage Management of Data Relations.

Controversies surrounding social media platforms have provided opportunities for institutional reflexivity amongst users and regulators on how to understand and govern platforms. Amidst contestation, platform companies have continued to enact projects that draw upon existing modes of privatized governance. We investigate how social media companies have attempted to achieve closure by continuing to set the terms around platform governance. We investigate two projects implemented by Facebook (Meta)-authenticity regulation and privacy controls-in response to the Russian Interference and Cambridge Analytica controversies surrounding the 2016 U.S. Presidential Election. Drawing on Goffman's metaphor of stage management, we analyze the techniques deployed by Facebook to reinforce a division between what is visible and invisible to the user experience. These platform governance projects propose to act upon front-stage data relations: information that users can see from other users-whether that is content that users can see from "bad actors", or information that other users can see about oneself. At the same time, these projects relegate back-stage data relations-information flows between users constituted by recommendation and targeted advertising systems-to invisibility and inaction. As such, Facebook renders the user experience actionable for governance, while foreclosing governance of back-stage data relations central to the economic value of the platform. As social media companies continue to perform platform governance projects following controversies, our paper invites reflection on the politics of these projects. By destabilizing the boundaries drawn by platform companies, we open space for continuous reflexivity on how platforms should be understood and governed.

Adaptive social networks promote the wisdom of crowds.

Social networks continuously change as new ties are created and existing ones fade. It is widely acknowledged that our social embedding has a substantial impact on what information we receive and how we form beliefs and make decisions. However, most empirical studies on the role of social networks in collective intelligence have overlooked the dynamic nature of social networks and its role in fostering adaptive collective intelligence. Therefore, little is known about how groups of individuals dynamically modify their local connections and, accordingly, the topology of the network of interactions to respond to changing environmental conditions. In this paper, we address this question through a series of behavioral experiments and supporting simulations. Our results reveal that, in the presence of plasticity and feedback, social networks can adapt to biased and changing information environments and produce collective estimates that are more accurate than their best-performing member. To explain these results, we explore two mechanisms: 1) a global-adaptation mechanism where the structural connectivity of the network itself changes such that it amplifies the estimates of high-performing members within the group (i.e., the network "edges" encode the computation); and 2) a local-adaptation mechanism where accurate individuals are more resistant to social influence (i.e., adjustments to the attributes of the "node" in the network); therefore, their initial belief is disproportionately weighted in the collective estimate. Our findings substantiate the role of social-network plasticity and feedback as key adaptive mechanisms for refining individual and collective judgments.

Does big data serve policy? Not without context. An experiment with in silico social science.

The DARPA Ground Truth project sought to evaluate social science by constructing four varied simulated social worlds with hidden causality and unleashed teams of scientists to collect data, discover their causal structure, predict their future, and prescribe policies to create desired outcomes. This large-scale, long-term experiment of in silico social science, about which the ground truth of simulated worlds was known, but not by us, reveals the limits of contemporary quantitative social science methodology. First, problem solving without a shared ontology-in which many world characteristics remain existentially uncertain-poses strong limits to quantitative analysis even when scientists share a common task, and suggests how they could become insurmountable without it. Second, data labels biased the associations our analysts made and assumptions they employed, often away from the simulated causal processes those labels signified, suggesting limits on the degree to which analytic concepts developed in one domain may port to others. Third, the current standard for computational social science publication is a demonstration of novel causes, but this limits the relevance of models to solve problems and propose policies that benefit from the simpler and less surprising answers associated with most important causes, or the combination of all causes. Fourth, most singular quantitative methods applied on their own did not help to solve most analytical challenges, and we explored a range of established and emerging methods, including probabilistic programming, deep neural networks, systems of predictive probabilistic finite state machines, and more to achieve plausible solutions. However, despite these limitations common to the current practice of computational social science, we find on the positive side that even imperfect knowledge can be sufficient to identify robust prediction if a more pluralistic approach is applied. Applying competing approaches by distinct subteams, including at one point the vast TopCoder.com global community of problem solvers, enabled discovery of many aspects of the relevant structure underlying worlds that singular methods could not. Together, these lessons suggest how different a policy-oriented computational social science would be than the computational social science we have inherited. Computational social science that serves policy would need to endure more failure, sustain more diversity, maintain more uncertainty, and allow for more complexity than current institutions support.

Accuracy-Risk Trade-Off Due to Social Learning in Crowd-Sourced Financial Predictions.

A critical question relevant to the increasing importance of crowd-sourced-based finance is how to optimize collective information processing and decision-making. Here, we investigate an often under-studied aspect of the performance of online traders: beyond focusing on just accuracy, what gives rise to the trade-off between risk and accuracy at the collective level? Answers to this question will lead to designing and deploying more effective crowd-sourced financial platforms and to minimizing issues stemming from risk such as implied volatility. To investigate this trade-off, we conducted a large online Wisdom of the Crowd study where 2037 participants predicted the prices of real financial assets (S&P 500, WTI Oil and Gold prices). Using the data collected, we modeled the belief update process of participants using models inspired by Bayesian models of cognition. We show that subsets of predictions chosen based on their belief update strategies lie on a Pareto frontier between accuracy and risk, mediated by social learning. We also observe that social learning led to superior accuracy during one of our rounds that occurred during the high market uncertainty of the Brexit vote.

Resampling reduces bias amplification in experimental social networks.

Large-scale social networks are thought to contribute to polarization by amplifying people's biases. However, the complexity of these technologies makes it difficult to identify the mechanisms responsible and evaluate mitigation strategies. Here we show under controlled laboratory conditions that transmission through social networks amplifies motivational biases on a simple artificial decision-making task. Participants in a large behavioural experiment showed increased rates of biased decision-making when part of a social network relative to asocial participants in 40 independently evolving populations. Drawing on ideas from Bayesian statistics, we identify a simple adjustment to content-selection algorithms that is predicted to mitigate bias amplification by generating samples of perspectives from within an individual's network that are more representative of the wider population. In two large experiments, this strategy was effective at reducing bias amplification while maintaining the benefits of information sharing. Simulations show that this algorithm can also be effective in more complex networks.

Flexible social inference facilitates targeted social learning when rewards are not observable.

Groups coordinate more effectively when individuals are able to learn from others' successes. But acquiring such knowledge is not always easy, especially in real-world environments where success is hidden from public view. We suggest that social inference capacities may help bridge this gap, allowing individuals to update their beliefs about others' underlying knowledge and success from observable trajectories of behaviour. We compared our social inference model against simpler heuristics in three studies of human behaviour in a collective-sensing task. Experiment 1 demonstrated that average performance improved as a function of group size at a rate greater than predicted by heuristic models. Experiment 2 introduced artificial agents to evaluate how individuals selectively rely on social information. Experiment 3 generalized these findings to a more complex reward landscape. Taken together, our findings provide insight into the relationship between individual social cognition and the flexibility of collective behaviour.

Bayesian collective learning emerges from heuristic social learning.

Researchers across cognitive science, economics, and evolutionary biology have studied the ubiquitous phenomenon of social learning-the use of information about other people's decisions to make your own. Decision-making with the benefit of the accumulated knowledge of a community can result in superior decisions compared to what people can achieve alone. However, groups of people face two coupled challenges in accumulating knowledge to make good decisions: (1) aggregating information and (2) addressing an informational public goods problem known as the exploration-exploitation dilemma. Here, we show how a Bayesian social sampling model can in principle simultaneously optimally aggregate information and nearly optimally solve the exploration-exploitation dilemma. The key idea we explore is that Bayesian rationality at the level of a population can be implemented through a more simplistic heuristic social learning mechanism at the individual level. This simple individual-level behavioral rule in the context of a group of decision-makers functions as a distributed algorithm that tracks a Bayesian posterior in population-level statistics. We test this model using a large-scale dataset from an online financial trading platform.

Exposure to anaesthetic trace gases during general anaesthesia: CobraPLA vs. LMA classic.

BACKGROUND: To prospectively investigate the performance, sealing capacity and operating room (OR) staff exposure to waste anaesthetic gases during the use of the Cobra perilaryngeal airway (CobraPLA) compared with the laryngeal mask airway classic (LMA). METHODS: Sixty patients were randomly assigned to the CobraPLA or the LMA group. Insertion time, number of insertion attempts and airway leak pressures were assessed after induction of anaesthesia. Occupational exposure to nitrous oxide (N(2)O) and Sevoflurane (SEV) was measured at the anaesthetists' breathing zone and the patients' mouth using a photoacoustic infrared spectrometer. RESULTS: N(2)O waste gas concentrations differed significantly in the anaesthetist's breathing zone (11.7+/-7.2 p.p.m. in CobraPLA vs. 4.1+/-4.3 p.p.m. in LMA, P=0.03), whereas no difference could be shown in SEV concentrations. Correct CobraPLA positioning was possible in 28 out of 30 patients (more than one attempt necessary in five patients). Correct positioning of the LMA classic was possible in all 30 patients (more than one attempt in three patients). Peak airway pressure was higher in the CobraPLA group (16+/-3 vs. 14+/-2 cmH(2)O, P=0.01). The average leak pressure of the CobraPLA was 24+/-4 cmH(2)O, compared with 20+/-4 cmH(2)O of the LMA classic (P<0.001; all values means+/-SD). CONCLUSION: Despite higher airway seal pressures, the CobraPLA caused higher intraoperative N(2)O trace concentrations in the anaesthetists' breathing zone.

Characterization and distribution of endothelin receptors in the pulmonary circulation: investigation of isolated, perfused, and ventilated rabbit lungs.

The aim of the study was to investigate the distribution of 2 subtypes of endothelin-receptors, mediating the effects of endothelin-1 (ET-1) in the pulmonary circulation. Until now, it is still unclear, whether ET(A) receptors or ET(B) receptors or even both are localized in pulmonary vessels. The experiments were performed on 72 isolated and ventilated rabbit lungs that were perfused with a cell- and plasma-free buffer solution. The arterial pressure and the lung weight gain were continuously registered. Intermittently perfusate samples were taken for determination of thromboxane A2 (TXA2) and prostacyclin (PGI2). The injection of ET-1 (10(-8) M, n = 6) resulted in a biphasic increase in pulmonary arterial pressure (PAP) that was accompanied by the generation of TXA2 and PGI2. Pretreatment with the ET(A)-receptor antagonist LU135252 (10(-6) M, n = 6) suppressed the pressure response after ET-1 application (P < 0.01 at 120 min) and reduced the generation of TXA2 (P < 0.05 at 120 min) and PGI2 (P < 0.05 at 120 min). Pretreatment with the cyclooxygenase inhibitor diclofenac (10 microg/mL; n = 6) also reduced the PAP increase after ET-1 injection. In contrast to this, the pulmonary vascular pressure reaction after ET-1 application was elevated, when ET(B)-receptor antagonist BQ788 (10(-6) M; n = 6) was given. Furthermore, the PGI2 to TXA2 ratio was shifted from 2.3 to 0.9, reflecting a predominance of vasoconstrictive TXA2. The simultaneous application of LU135252 and BQ788 significantly reduced the PAP increase after ET-1 application, but no beneficial effects were observed compared with the application of LU135252 solely. The injection of the ET(B)-receptor agonist sarafotoxin S6c (S6c; 10(-8) M, n = 6) also induced an increase in PAP that was not attenuated by pretreatment with the ET(B)-receptor antagonist BQ788 (10(-6) M, n = 6). LU135252 (n = 6) as well as the application of LU135252 in combination with BQ788 (n = 6) failed to suppress the pressure response after S6c, whereas the cyclooxygenase inhibitor diclofenac (10 microg/mL, n = 6) alone and in combination with LU135252 and BQ788 (n = 6) was able to prevent the PAP increase after S6c injection (P < 0.001). The results demonstrate that the ET-1-induced increase in pulmonary vascular resistance is mainly mediated via ET(A) receptors, whereas ET(B) receptors seem to mediate vasodilation, which was shown by an imbalance of TXA2 and PGI2 generation. On the other hand, the ET(B)-receptor agonist S6c induced vasoconstriction, which was only attenuated by the cyclooxygenase inhibitor diclofenac. From the current results we conclude that, apart from vasoconstrictor ET(A) receptors, at least 2 ET(B)-receptor subtypes are expressed in the pulmonary circulation, one mediating vasoconstriction, which was not blocked by BQ788, and one mediating vasodilation, which was influenced by BQ788.

Mixed venous oxygen saturation in critically ill septic shock patients. The role of defined events.

STUDY OBJECTIVE: To investigate the frequency and extent of spontaneous changes ("events") in continuously measured mixed venous oxygen saturation (SvO2) in septic patients and to determine whether attention to individual event-frequency offers additional information for patient management. DESIGN: Nonrandomized prospective study. SETTING: General intensive care unit at a university hospital. PATIENTS: Fifteen patients suffering from septic shock and multiple organ dysfunction syndrome. MEASUREMENTS: For the continuous assessment of SvO2 a fiberoptic pulmonary artery catheter (Baxter Edwards) was inserted in all patients. A certain event was defined as a sudden change in SvO2 of > or = 5 percent lasting for > 10 min. All events were grouped as either moderate (< or = 10 percent changes in SvO2) or severe events (> 10 percent changes). Hemodynamics and inotropic support, oxygenation and ventilatory support, hemoglobin levels and body temperature were determined at the event and compared with the ultimate values registered before the event. RESULTS: We evaluated 377 events during an observation period of 1,575 h. Patients' mean SvO2 levels ranged between 72 +/- 7 and 82 +/- 4. Desaturations below 65 percent (39 out of 377 events) occurred in 11 patients. Overall, 74 percent of all events were moderate and 26 percent were severe. The incidence of events was 5.6 +/- 1.5 during 24 h in survivors (n = 10) and 6.3 +/- 1.6 during 24 h in nonsurvivors (n = 5). While in survivors only 20 percent of all events were severe events, this portion was significantly higher in nonsurvivors (34 percent; p = 0.03). In 67 percent of all events we observed changes in the registered physiologic parameters or therapeutic interventions probably causing the event. The cause of the remaining 33 percent of all events could not be elucidated. CONCLUSIONS: The SvO2 of septic shock patients is mainly normal or even supranormal. However, short-term changes in SvO2 do occur frequently in these patients. Nonsurvivors exhibit a higher frequency as well as a significantly greater severity of events, which may point toward a concealed mismatch of oxygen supply and demand. A high incidence of short-term SvO2 changes in a septic shock patient may be of diagnostic and prognostic significance. Therefore, we recommend the installation of a computerized alarm-function for the automatic detection and indication of frequent events.

Effectiveness of nitric oxide inhalation in septic ARDS.

STUDY OBJECTIVE: To evaluate the percentage of nitric oxide (NO) responders in septic shock patients with ARDS. Additionally, to investigate long-term NO effects on cardiac performance and oxygen kinetic patterns in NO responders vs nonresponders. DESIGN: Prospective cohort study. SETTING: ICU of a university hospital. PATIENTS: Twenty-five consecutive patients with a diagnosis of septic shock and established ARDS requiring inotropic and vasopressor support. INTERVENTIONS: After diagnosis of ARDS, NO was administered at 18 or 36 ppm. Patients demonstrating a NO-induced rise of arterial oxygen tension of 20% or more and/or a fall in mean pulmonary artery pressure of 15% or more were grouped as NO responders; others were grouped as nonresponders. MEASUREMENTS AND RESULTS: Ten patients (40%) were NO responders, while 15 patients (60%) were nonresponders. Mortality was 40% in NO responders and 67% in nonresponders (NS). NO responders developed a significantly lower mean pulmonary artery pressure (28 +/- 6 vs 33 +/- 6 mm Hg; p < 0.05), lower pulmonary vascular resistance (PVR: 258 +/- 73 vs 377 +/- 163 dyne.s.cm-5.m-2; p < 0.05), and higher PaO2/FIO2 ratio (192 +/- 85 vs 144 +/- 74 mm Hg; p < 0.05) within the study period. In responders, NO-induced afterload reduction resulted in increased right ventricular ejection fraction (RVEF: 40 +/- 7 vs 35 +/- 9%; p < 0.05), significantly higher cardiac index (CI: 4.5 +/- 1.1 vs 4.0 +/- 1.2 L.min-1.m-2; p < 0.05) and oxygen delivery (DO2: 681 +/- 141 vs 599 +/- 160 mL.min-1.m-2; p < 0.05) compared with nonresponders. In NO nonresponders, RVEF was correlated with PVR, CI, DO2, mixed venous oxygen saturation (SvO2), and oxygen extraction ratio (O2ER) (r = +/- 0.60 to +/- 0.69; p < 0.05). No significant correlation between RVEF and any of these parameters was observed in responders. SvO2 (75 +/- 7 vs 69 +/- 8%; p < 0.05) and O2ER (0.24 +/- 0.06 vs 0.27 +/- 0.06; p < 0.05) were significantly different between responders and nonresponders, while no difference in oxygen consumption was observed (161 +/- 41 vs 153 +/- 43 mL.min.m-2). CONCLUSIONS: Inhaled NO is effective in only a subgroup of septic ARDS patients, with a higher, but insignificantly different percentage of survivors in the responder group. NO responders were characterized by increased RVEF accompanied by higher CI, DO2, and lower O2ER. In nonresponders, RVEF remained depressed, with a close correlation between RVEF and CO as well as DO2 and O2ER. Thus, nonresponders seem to suffer from impaired cardiac reserves and correspondingly lower oxygen transport variables.

The acute respiratory distress syndrome: definitions, severity and clinical outcome. An analysis of 101 clinical investigations.

OBJECTIVE: To determine possible changes in outcome from acute respiratory distress syndrome (ARDS) and to compare severity of lung injury and methods of treatment from 1967 to 1994. DATA SOURCES: Computerized (Medline, Current Contents) and manual (Cumulated Index Medicus) literature search using the key word and/or title ARDS. STUDY SELECTION: Only clinical studies published as full papers reporting data on both patient mortality (survival) and oxygenation index (PaO2/FIO2) were included. Single case reports, abstracts, reviews and editorials were excluded from evaluation. DATA EXTRACTION: Relevant data were extracted in duplicate, followed by quality checks on approximately 80% of data extracted. DATA SYNTHESIS: 101 papers reporting on 3264 patients were included: 48 studies (2207 patients) were performed in the USA, 43 studies (742 patients) in Europe and 10 studies (315 patients) elsewhere. Mortality reported in these studies was 53 +/- 22% (mean +/- SD), with no apparent trend towards a higher survival (1994: 22 studies, mortality 51 +/- 19%). The mean PaO2/FIO2 ratio remained unchanged throughout the observation period (118 +/- 47 mmHg). No correlation could be established between outcome and PaO2/FIO2 or lung injury score. Patients who underwent pressure-limited ventilation had a significantly lower mortality (35 +/- 20%) than patients on volume-cycled ventilation (54 +/- 22%) or patients for whom there was no precise information on ventilatory support (59 +/- 19%). Significantly lower PaO2/FIO2 ratios (61 +/- 17 mmHg) were observed in patients prior to extracorporeal lung assist, together with mortality rates in the range of those for conventionally treated patients (55 +/- 22%). CONCLUSIONS: The mortality of ARDS patients remained constant throughout the period studied. Therefore, the standard for outcome in ARDS should be a mortality in the 50% range. Neither PaO2/FIO2 ratio nor lung injury score was a reliable predictor for outcome in ARDS. Patients might benefit from pressure-limited ventilatory support, as well as extracorporeal lung assist. Since crucial data were missing in most clinical studies, thus preventing direct comparison, we emphasize the importance of using standardized definitions and study entry criteria.

ET-1-induced pulmonary vasoconstriction shifts from ET(A)- to ET(B)-receptor-mediated reaction after preconstriction.

Endothelin-1 (ET-1) has been reported to induce pulmonary vasoconstriction via either ET(A) or ET(B) receptors, and vasorelaxation after ET-1 injection has been observed. Our study investigated the effects of ET-1 in isolated rabbit lungs, which were studied at basal tone (part I) and after preconstriction (U-46619; part II). Pulmonary arterial pressure (PAP) and lung weight gain were monitored continuously. In part I, ET-1 (10(-8) M; n = 6; control) was injected after pretreatment with the ET(A)-receptor antagonist BQ-123 (10(-6) M; n = 6) or the ET(B)-receptor antagonist BQ-788 (10(-6) M; n = 6). The same protocol was carried out in part II after elevation of pulmonary vascular tone. ET-1 induced an immediate PAP increase (DeltaPAP 4.3 +/- 0.4 mmHg at 10 min) that was attenuated by pretreatment with BQ-123 (P < 0.05 at 10 min and P < 0.01 thereafter) and that was more pronounced after BQ-788 (P < 0.01 at 10 min and P < 0.001 thereafter). In part II, ET-1 induced an immediate rise in PAP with a maximum after 5 min (DeltaPAP 6.3 +/- 1.4 mmHg), leveling off at DeltaPAP 3.2 +/- 0.2 mmHg after 15 min. Pretreatment with BQ-123 failed to attenuate the increase. BQ-788 significantly reduced the peak pressure at 5 min (0.75 +/- 0.4 mmHg; P < 0.001) as well as the plateau pressure thereafter (P < 0.01). We conclude that ET-1 administration causes pulmonary vasoconstriction independent of basal vascular tone, and, at normal vascular tone, the vasoconstriction seems to be mediated via ET(A) receptors. BQ-788 treatment resulted in even more pronounced vasoconstriction. After pulmonary preconstriction, ET(A) antagonism exerted no effects on PAP, whereas ET(B) antagonism blocked the PAP increase. Therefore, ET-1-induced pulmonary vasoconstriction is shifted from an ET(A)-related to an ET(B)-mediated mechanism after pulmonary vascular preconstriction.

Severity and outcome of ARDS: the present place of extracorporeal lung assist (ECLA).

Within the last decade extracorporeal lung assist has been recommended for the treatment of acute respiratory distress syndrome. However, this recommendation was challenged by several recent clinical studies and reviews. The goal of our analysis was therefore to investigate data on outcome and severity of gas exchange disturbance published from patients treated with ECLA. These data were compared to a historical control group consisting of ARDS patients treated conventionally. Computerized (MEDLINE 1967-95) literature search using the keywords ARDS, ECLA, ECMO, ECCO2R and HUMAN was performed. Only clinical studies published as full papers reporting data on both, patients mortality and oxygenation index (PaO2/FiO2) were included. Overall mean mortality reported was 53 +/- 22% in 17 studies (419 patients), with no apparent trend towards a higher survival within the last decade with a mean PaO2/FIO2 (14 papers; 61 +/- 17 mmHg). However, mean mortality rates of ARDS patients requiring ECLA was 52.3% and 44.9% if patients undergoing ECMO were excluded (3 papers). Therefore the mortality of these patients with severe lung injury was in the range of patients treated conventionally. Patient outcome observed in our analysis is in accordance with the mortality rates from the European ECLA centres published recently (49% in 1993). Therefore, we conclude that the mean mortality rate of patients suffering from severe ARDS treated with ECLA is in the 50% range and does not differ significantly from those of patients treated conventionally, despite significantly poorer pulmonary function.

Haemodynamic evaluation during small volume resuscitation in patients with acute respiratory failure.

In addition to the invasive haemodynamic monitoring procedures, an on-line assessment of cardiac performance by means of transoesophageal echocardiography might have a certain role in small volume resuscitation of patients with acute respiratory failure or Adult Respiratory Distress Syndrome (ARDS). The goal of this investigation was therefore to determine the effects of a hypertonic hyperoncotic solution, hypertonic hydoxyethl-starch (HHES), (HHES = HES [200.000/0.6-0.66; 60 g l-1; Leopold, Graz; Austria] combined with NaCl [75 g l-1) on haemodynamics and cardiac performance using the transoesophageal echocardiography. After institutional approval we investigated 23 patients suffering from septic ARDS after trauma or major surgery during four periods of resuscitation. Phase I = control values after infusion of 20 ml kg-1 crystalloid solution, phase II = 50% hypertonic hydroxyethyl-starch solution (2 ml kg-1), phase III = at the end of HHES (4 ml kg-1), IV = 30 min after the end of HHES. Before HHES-infusion, all patients showed arterial hypotension with mean arterial pressures of 64 +/- 2 mmHg. The infusion of 2 ml kg-1 HHES resulted in a significant increase of systemic and pulmonary arterial pressures over the study period. A significant improvement in cardiac output was associated with increasing stroke volumes, oxygen delivery and oxygen consumption (see Tables 1 and 2). Small volume resuscitation also resulted in significant increases of endsystolic and endiastolic left ventricular areas and the corresponding calculated wall stress (Figs 1-3). We conclude from our preliminary data that when using HHES, only modest fluid resuscitation was sufficient to restore adequate preload and oxygen delivery in patients with sepsis-related acute respiratory failure.

[The difficult airway]. / Der schwierige Atemweg.

Management of the difficult airway has gained increasing interest, because hypoxia is one of the leading causes of death and of severe neurological sequelae related to anesthesia or resuscitation. The difficult airway algorithm of the American Society of Anesthesiologists as well as the guidelines of the European Resuscitation Council provide recommendations for the prevention of difficulties in tracheal intubation and/or mask ventilation. Especially preoperative patient evaluation is of major importance. Patients history, oral and maxillofacial anatomy, pharyngeal and laryngeal structures as well as cervical spine mobility have to be assessed and awake fiberoptic intubation has to be performed in all cooperative patients with indices pointing towards difficult airways. If problems in intubating the trachea are encountered after induction of anesthesia and mask ventilation is adequate, one must call for help and decide rapidly whether to awaken the patient or to proceed with alternative intubation techniques (e.g. different laryngoscope blades, flexible fiberoptic scope or other fiberoptic techniques, lighted wand, retrograde intubation or surgical airway). In the potentially life-threatening "cannot intubate--cannot ventilate" situation either transtracheal jet ventilation, laryngeal mask airway, the esophageal-tracheal Combitube or a surgical airway have to be performed or have to be inserted immediately. These alternative methods have to be appropriately taught and--as far as possible--to be trained under routine conditions in order to master emergency situations.

Assessing a murmur, saving a life: current trends in the management of hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy, formerly called idiopathic hypertrophic subaortic stenosis (IHSS), is the leading cause of sudden cardiac death in young people. Hypertrophic cardiomyopathy is a non-dilated cardiomyopathy primarily affecting the left ventricle, left atria, intraventricular septum, and mitral valve. It is an autosomal dominant genetic disorder that impairs diastolic and systolic function. Diagnosis is complex due to the heterogeneity of the disease. Symptoms and morphology are not always related and clinical signs may be absent or limited to a soft systolic murmur. The first symptom of hypertrophic cardiomyopathy is frequently sudden cardiac death. Echocardiogram is an accurate diagnostic tool. Asymptomatic patients are generally not treated. Treatment for symptomatic patients begins with beta or calcium channel blockers. Antiarrhythmics may be added to protect against sudden cardiac death. Surgical intervention is done if other treatments fall and involves removal of a portion of the obstructive septum. Operative mortality is 5% with a 60% reduction in symptoms. A promising alternative to surgery is dual-chamber pacemakers. Patient and family teaching is the emphasis of long-term management.