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In recent years, there has been a dramatic rise in the use of echocardiography in perioperative and critical care medicine. It is now recommended widely as a first-line diagnostic tool when approaching patients in shock, due to its ability to identify shock etiology and response to treatment noninvasively. To match the increasing training demand, and to ensure maintenance of high-quality and reproducible scanning, several accreditation pathways have been developed worldwide. Critical care echocardiography training pathways can include both transthoracic and transesophageal scanning and range from basic focused protocols to advanced comprehensive scans. The complexity of each individual training program is reflected in its accreditation process. While basic accreditations may require only course attendance and a relatively brief logbook, comprehensive accreditations often require extensive logbooks and written and practical examinations. Currently, the use of transoesophageal echocardiography remains restricted largely to cardiothoracic anesthesia and critical care; however, its use in the general intensive care setting is growing. This narrative review summarizes the most common training pathways, their curricula, and accreditation requirements. The authors initially focus on echocardiography training in the United Kingdom, and then go on to describe similar international accreditations available in Europe, North America, and Australasia.

In this work, an open-source ROS interface based on KUKAVARPROXY for control of KUKA robots is compared to the commercial closed-source Robot Sensor Interface available from KUKA. This comparison looks at the difference in how these two approaches communicate with the KUKA robot controller, the response time and tracking delay one can expect with the different interfaces, and the difference in use cases for the two interfaces. The investigations showed that the KR16 with KRC2 has a 50 ms response time, and RSI has a 120 ms tracking delay, with negligible delay caused by the ROS communication stack. The results highlight that the commercial inferface is more reliable for feedback control tasks, but the proposed interface gives read and write access to variables on the controller during execution, and can be used for simple motion and tooling control. The work reported in this paper was based on activities within centre for research based innovation SFI Manufacturing in Norway, and is partially funded by the Research Council of Norway under contract number 237900.

Purpose To evaluate the characteristics and practice of predatory journals in critical care medicine (CCM). Methods We checked a freely accessible online and constantly updated version of the Beall lists of potential predatory publishers/journals in the field of CCM. We checked the journals' websites to retrieve the following data such as: 1) Country and address (checked by Google maps); 2) Article processing charges (APC); 3) Indexing; 4) Editor-in-chief and the Editorial Board (EB) members; 5) Number of published articles; 6) Review time (lapse submission-acceptance); 7) English form. Results We identified 86 CCM journals from 48 publishers. Most journals' reported address was in the US (52%). The address was unreliable in 43%. English form was low/very-low in 72% of cases. Three journals were indexed in PubMed. Several journals reported false indexing in the Committee on publication ethics (COPE), International Committee of Medical Journal Editors (ICMJE), Directory of Open Access Journals (DOAJ) and Google Scholar. Median APCs for research article was 909.5 USD. Name of the Editor-in-chief and EB lists were reported by 29% and 81%, respectively. Median lapse submission-acceptance for published articles was 32 days. Conclusions We found a relevant number of probable predatory CCM journals. Scientists should carefully check journal's characteristics to avoid selecting predatory journals as editorial target.

Background Myocardial dysfunction may contribute to circulatory failure in sepsis. There is growing evidence of an association between left ventricular diastolic dysfunction (LVDD) and mortality in septic patients. Utilizing echocardiography, we know that tissue Doppler imaging (TDI) variables e′ and E/e′ are reliable predictors of LVDD and are useful measurements to estimate left ventricular (LV) filling pressures. Methods We conducted a systematic review and meta-analysis to investigate the association of e′ and E/e′ with mortality of patients with severe sepsis or septic shock. In the primary analysis, we included studies providing transthoracic TDI data for e′ and E/e′ and their association with mortality. Subgroup analyses were conducted according to myocardial regional focus of TDI assessment (septal, lateral or averaged). Three secondary analyses were performed: one included data from a transoesophageal study, another excluded studies reporting data at a very early ( 48 h) stage following diagnosis, and the third pooled data only from studies excluding patients with heart valve disease. Results The primary analysis included 16 studies with 1507 patients with severe sepsis and/or septic shock. A significant association was found between mortality and both lower e′ [standard mean difference (SMD) 0.33; 95% confidence interval (CI): 0.05, 0.62; P=0.02] and higher E/e′ (SMD –0.33; 95% CI: –0.57, –0.10; P=0.006). In the subgroup analyses, only the lateral TDI values showed significant association with mortality (lower e′ SMD 0.45; 95% CI: 0.11, 0.78; P=0.009; higher E/e′ SMD –0.49; 95% CI: –0.76, –0.22; P=0.0003). The findings of the primary analysis were confirmed by all secondary analyses. Conclusions There is a strong association between both lower e′ and higher E/e′ and mortality in septic patients.

Guidelines for treatment of out-of-hospital cardiac arrest (OOH-CA) with shockable rhythm recommend amiodarone, while lidocaine may be used if amiodarone is not available. Recent underpowered evidence suggests that amiodarone, lidocaine or placebo are equivalent with respect to survival at hospital discharge, but amiodarone and lidocaine showed higher hospital admission rates. We undertook a systematic review and meta-analysis to assess efficacy of amiodarone vs lidocaine vs placebo.We included studies published in PubMed and EMBASE databases from inception until May 15th, 2016. The primary outcomes were survival at hospital admission and discharge in OOH-CA patients enrolled in randomized clinical trials (RCT) according to resuscitation with amiodarone vs lidocaine vs placebo. If feasible, secondary analysis was performed including in the analysis also patients with in-hospital CA and data from non-RCT.A total of seven findings were included in the metanalysis (three RCTs, 4 non-RCTs). Amiodarone was as beneficial as lidocaine for survival at hospital admission (primary analysis odds ratio-OR 0.86-1.23, p=0.40) and discharge (primary analysis OR 0.87-1.30, p=0.56; secondary analysis OR 0.86-1.27, p=0.67). As compared with placebo, survival at hospital admission was higher both for amiodarone (primary analysis OR 1.12-1.54, p0.0001; secondary analysis OR 1.07-1.45, p0.005) and lidocaine (secondary analysis only OR 1.14-1.58, p=0.0005). With regards to hospital discharge there were no differences between placebo and amiodarone (primary outcome OR 0.98-1.44, p=0.08; secondary outcome OR 0.92-1.33, p=0.28) or lidocaine (secondary outcome only OR 0.97-1.45, p=0.10).Amiodarone and lidocaine equally improve survival at hospital admission as compared with placebo. However, neither amiodarone nor lidocaine improve long-term outcome.

Patients resuscitated from cardiac arrest develop a pathophysiological state named "post-cardiac arrest syndrome." Post-resuscitation myocardial dysfunction is a common feature of this syndrome, and many patients eventually die from cardiovascular failure. Cardiogenic shock accounts for most deaths in the first 3 days, when post-resuscitation myocardial dysfunction peaks. Thus, identification and treatment of cardiovascular failure is one of the key therapeutic goals during hospitalization of post-cardiac arrest patients. Patients with hemodynamic instability may require advanced cardiac output monitoring. Inotropes and vasopressors should be considered if hemodynamic goals are not achieved despite optimized preload. If these measures fail to restore adequate organ perfusion, a mechanical circulatory assistance device may be considered. Adequate organ perfusion should be ensured in the absence of definitive data on the optimal target pressure goals. Hemodynamic goals should also take into account targeted temperature management and its effect on the cardiovascular function.

Aim The prediction of return of spontaneous circulation (ROSC) during resuscitation of patients suffering of cardiac arrest (CA) is particularly challenging. Regional cerebral oxygen saturation (rSO 2 ) monitoring through near-infrared spectrometry is feasible during CA and could provide guidance during resuscitation. Methods We conducted a systematic review and meta-analysis on the value of rSO 2 in predicting ROSC both after in-hospital (IH) or out-of-hospital (OH) CA. Our search included MEDLINE (PubMed) and EMBASE, from inception until April 4th, 2015. We included studies reporting values of rSO 2 at the beginning of and/or during resuscitation, according to the achievement of ROSC. Results A total of nine studies with 315 patients (119 achieving ROSC, 37.7%) were included in the meta-analysis. The majority of those patients had an OHCA ( n =225, 71.5%; IHCA: n =90, 28.5%). There was a significant association between higher values of rSO 2 and ROSC, both in the overall calculation (standardized mean difference, SMD –1.03; 95%CI –1.39,–0.67; p 2 at the beginning of resuscitation: SMD –0.79; 95%CI –1.29,–0.30; p =0.002; averaged rSO 2 value during resuscitation: SMD –1.28; 95%CI –1.74,–0.83; p Conclusions Higher initial and average regional cerebral oxygen saturation values are both associated with greater chances of achieving ROSC in patients suffering of CA. A note of caution should be made in interpreting these results due to the small number of patients and the heterogeneity in study design: larger studies are needed to clinically validate cut-offs for guiding cardiopulmonary resuscitation.

This study was to evaluate the usefulness of hepato-biliary ultrasound (HBUS) for the investigation of isolated liver function tests (LFTs) abnormalities.We retrospectively reviewed HBUS reports in traumatic brain injury (TBI) patients admitted to our tertiary neuro-critical care unit (NCCU; January 2005-June 2011). We included patients receiving an HBUS for isolated LFTs derangement, excluding pre-existing hepato-biliary diseases or trauma. We assessed the temporal profile of alanine aminotransferase (ALT), bilirubin (Bil), and alkaline phosphatase (ALP).Of 511 patients, 58 received an HBUS. Of these, 47 were investigated for isolated LFTs derangement; HBUS always failed to identify a cause for these abnormalities. The HBUS was performed on day 18 (range 6-51) with the following mean values: 246 IU litre(-1) [ALT, 95% confidence interval (CI) 183-308], 24 μmol litre(-1) (Bil, 95% CI 8-40), and 329 IU litre(-1) (ALP, 95% CI 267-390); only ALT (72, 95% CI 36-107) and ALP (73, 95% CI 65-81) were deranged from admission values (both P0.01). At NCCU discharge, both ALT (160, 95% CI 118-202) and ALP (300, 95% CI 240-360) were higher than at admission (P0.01). Compared with HBUS-day value, only ALT improved by NCCU discharge (P0.05), while both were recovering by hospital discharge (ALT 83, 95% CI 59-107; ALP 216, 95% CI 181-251; P0.01). At hospital discharge, ALP remained higher than at admission (P0.01).In TBI patients, HBUS did not appear sensitive in detecting causes for isolated LFT abnormalities. Both ALT and ALP worsened and gradually recovered. Their abnormalities did not prevent NCCU discharge. ALP recovered more slowly than ALT. TBI and its complications, critical illness, and pharmacological strategies may explain the LFTs derangement.

To the Editor: Khemasuwan et al. retrospectively evaluated a cohort of 211 patients admitted to intensive care units (ICUs) with acute pulmonary embolism (PE). The investigators examined the correlation between echocardiographic parameters and clinical outcomes, in particular ICU, hospital, and long-termmortality. Several simple echocardiographic parameters were associated with ICU, hospital, and long-termmortality in this group of patients, while right ventricular (RV) strain analysis was not, although optimal data were available for only 54% of the patients. However, the study findings are partly flawed. The investigators performed adjusted analyses for Acute Physiology and Chronic Health Evaluation score (ICU mortality), Pulmonary Embolism Severity Index score (hospital mortality), or age and gender (longterm mortality), but they did not consider two important issues. First, intravenous thrombolytic therapy was administered to 9% of the study population. Thrombolytic therapy has been previously associated with significant early improvements in echocardiographic parameters of RV function compared with heparin alone in patients with acute massive or submassive PE. Therefore, patients receiving thrombolysis may have had more pronounced improvement in all or some of the parameters that were positively correlated with clinical outcomes in this study. Unfortunately, the investigators did not present a subgroup analysis of the echocardiographic findings in the subgroup of patients who received thrombolysis, and thrombolysis was not considered in the regression analysis. Second, absence of $50% inferior vena cava (IVC) collapsibility was correlated with ICU and hospital mortality. Nonetheless, 26% of the patients in this study required mechanical ventilation, which in turn significantly influences changes in IVC diameter (IVC distensibility for ventilated patients) and its value as an indicator of RV preload. The investigators did not adjust for this variable in the binary logistic regression analyses, and this can introduce a degree of bias when considering IVC collapsibility as predictor of outcome. Therefore, before the data can be correctly interpreted, an adjustment of the analysis for such variables (thrombolysis and mechanical ventilations) is needed. Finally, it would be interesting if the investigators could look into the echocardiographic follow-up of survivors, evaluating both early (within weeks) and late (after a few months) improvements in RV function and looking for predictors of good functional RV recovery. By reporting these data, the investigators would greatly contribute in providing further valuable insight on this interesting topic.

In May, 2012, a 46year-old woman reported chest pain before having an out-of-hospital cardiac arrest. Para medics successfully resuscitated her. The pre-arrest rhythm strip showed a sinus tachycardia only. A 12-h troponin I was raised at 5·9 μg/L (normal values 0–0·04 μg/L) A year earlier, she had been admitted with a similar history of chest pain, which had developed after taking sumatriptan for a migraine. A 12-lead electrocardiograph (ECG) showed transient inferior and lateral ST elevation. A 12-h troponin was negative. At this time, coronary angiography showed a normal left coronary system and a dominant right coronary artery, with minor ostial spasm and slow fl ow. A bubble study was negative for right to left shunting. She was diagnosed with vasospastic angina and started oral diltiazem. On advice, she stopped smoking and sumatriptan was discontinued. She continued to have occasional episodes of chest pain responsive to sublingual glycerol trinitrate. At the time of her cardiac arrest, her regular medications were oral diltiazem, nicorandil, lansoprazole, and a beclometasone inhaler. In the 48 h after the cardiac arrest she had fi ve additional pulseless electrical activity (PEA) arrests while intubated and ventilated in the intensive care unit. These were characterised by transient ST elevation (fi gure) and progressive hypotension, cul minating in loss of car diac output. Each episode responded to about 15–25 min of resuscitation. In between episodes, left ven tricular size and function was normal on echocardi ography. Electro cardiography was unremarkable. Repeat coronary angi ography showed normal coronary arteries, though of smaller luminal diameter than a year earlier. An intra-aortic balloon pump and a temporary tunnelled dual cham ber pacemaker were placed, which permitted potent vaso dilator therapy (intra venous glyceryl trinitrate and verapa mil, with nifedipine via a nasogastric tube) to be estab lished without the need for prolonged use of ino tropes. During this time, one episode of ST elevation and brady cardia was ter minated with a bolus of intravenous verapamil. The patient had a full neurological recovery; however it was complicated by the development of compartment syndrome in her left leg which necessitated removal of the intra-aortic balloon pump and a fasciotomy. She was converted to oral medications and underwent a cardiac magnetic resonance scan which was normal. At review in July, 2013, she remains entirely well. Although ventricular arrhythmia is recognised as the main cause of cardiac arrest in these patients, isolated cases of PEA have been reported. However, only one case has been described fully and did not feature the type of aggressive disease, with recurrent PEA arrests, detailed here. Patients with vasospastic angina are at higher risk of cardiac arrest than the background population. In a recent study of 1429 patients with vaso spastic angina, 35 (2·4%) had an out-of-hospital arrest and were younger (mean age 58 years) and more likely to have spasm of the left anterior descending coronary artery than were patients who had not had cardiac arrest. Since predicting which patients will have recurrent events is diffi cult, one suggestion is that all patients with vasospastic angina and a history of life-threatening arrhyth mia could benefi t from an automated implantable cardioverter-defi brillator alongside calcium channel blockers. In the absence of ventricular arrhythmias in our patient, an implantable cardioverter-defi brillator was not felt to be benefi cial. That this patient developed compart ment syndrome with no history of peripheral vascular disease is note worthy. We postulated that this was directly related to vasospasm provoked by the intra-aortic balloon pump. This case also highlights the value of intravenous calcium channel blockade to abort ST elevation and progression to PEA arrest. Our patient has been reminded to treat any further chest pain promptly with sublingual glyceryl trinitrate and seek immediate medical attention. Maintenance of vasodilator therapy has been strongly recommended.