Sure. So I do want to start by just reminding listeners that talking about trauma, learning about trauma, can bring up some feelings, which is a very normal reaction to that. So I just want to remind people, if you notice that, that it’s okay to take a rain check on listening and engaging in this conversation. I also do recommend that even if you feel okay to engage with a discussion about trauma that it’s recommended that you do so in small doses, especially during these very challenging times.

Long-Term Care Outbreaks

cute coronary syndrome (ACS)4/81(4.94%)

Malignant arrhythmia2/81(2.47%)

Patients presented with functional damage involving multiple vital organs, including respiratory failure (80 [94.1%]), shock (69 [81.2%]), ARDS (63 [74.1%]) arrhythmia (51 [60.0%]), acute myocardial injury (38 [44.7%]), acute liver injury (30 [35.3%]) and sepsis (28 [32.9%]) (Table 5)

Most patients had abnormal myocardial zymograms characterized by increased creatine kinase in 31 (36.5%) and increased lactate dehydrogenase in 70 (82.4%) patients.

The most common cause of death in 81 of the 85 patients was respiratory failure (38, 46.91%), followed by septic shock (16, 19.75%), multiple organ failure (13, 16.05%) and cardiac arrest (7, 8.64%).

In the epicenter of the current Italian epidemic, sudden cardiac death (SCD) likely occurred in many non-hospitalized patients with mild symptoms who were found dead home while in quarantine.

Even after hospital discharge, we should consider that myocardial injury might result in atrial or ventricular fibrosis, the substrate for subsequent cardiac arrhythmias

However, a recent pathological study found scarce interstitial mononuclear inflammatory infiltrates in heart tissue without substantial myocardial damage in a patient with COVID-19,13 suggesting that COVID-19 might not directly impair the heart.

ompared with patients without cardiac injury, patients with cardiac injury presented with more severe acute illness, manifested by abnormal laboratory and radiographic findings, such as higher levels of C-reactive protein, NT-proBNP, and creatinine levels; more multiple mottling and ground-glass opacity; and a greater proportion requiring noninvasive or invasive ventilation.

Consistently, our study also found 19.7% of patients with cardiac injury and first demonstrated that cardiac injury was independently associated with an increased risk of mortality in patients with COVID-19.

After adjusting for age, preexisting cardiovascular diseases (hypertension, coronary heart disease, and chronic heart failure), cerebrovascular diseases, diabetes mellitus, chronic obstructive pulmonary disease, renal failure, cancer, ARDS, creatinine levels greater than 133 μmol/L, and NT-proBNP levels greater than 900 pg/mL, the multivariable adjusted Cox proportional hazard regression model showed a significantly higher risk of death in patients with cardiac injury than in those without cardiac injury, either during time from symptom onset (hazard ratio [HR], 4.26 [95% CI, 1.92-9.49]) or time from admission to study end point (HR, 3.41 [95% CI, 1.62-7.16]) (Table 3).

The mortality rate was higher among patients with vs without cardiac injury (42 [51.2%] vs 15 [4.5%]; P < .001) as shown in Table 2 and the Kaplan-Meier survival curves in Figure 2. The mortality rate increased in association with the magnitude of the reference value of hs-TNI

Patients with cardiac injury vs those without cardiac injury had shorter durations from symptom onset to follow-up (mean, 15.6 [range, 1-37] days vs 16.9 [range, 3-37] days; P = .001) and admission to follow-up (6.3 [range, 1-16] days vs 7.8 [range, 1-23] days; P = .039).

Of patients with cardiac injury, only 22 (26.8%) underwent examination of electrocardiogram (ECG) after admission, and 14 of 22 ECGs (63.6%) were performed during the periods of elevation of cardiac biomarkers. All 14 ECGs were abnormal, with findings compatible with myocardial ischemia, such T-wave depression and inversion, ST-segment depression, and Q waves. The ECG changes in 3 patients with representative cardiac injury are shown in eFigure 2 in the

In terms of radiologic findings, bilateral pneumonia (75 of 82 patients [91.5%] vs 236 of 334 patients [70.7%]) and multiple mottling and ground-glass opacity (53 [64.6%] vs 15 [4.5%]) were more prevalent in patients with than those without cardiac injury (both P < .001, Table 1).

The duration of hospitalization before testing was longer in patients with cardiac injury than those without cardiac injury (median [range] time, 3 [1-15] days vs 2 [1-8] days; P < .001).

The laboratory and radiologic findings are shown in Table 1. In the overall study population of 416 patients, median (IQR) levels of C-reactive protein (4.5 [1.4-8.5] mg/dL; to convert to milligrams per liter, multiply by 10) and procalcitonin (0.07 [0.04-0.15] ng/L) were elevated, while the median values of other laboratory indicators were within the normal range, such as counts of leukocytes, lymphocytes, platelets, erythrocytes; hemoglobin level; cardiac indicators

In the present study, we also found that markers of inflammatory response, such as C-reactive protein, procalcitonin, and leukocytes, were significantly increased among patients who suffered from cardiac injury. The activation or enhanced release of these inflammatory cytokines can lead to apoptosis or necrosis of myocardial cells.

Thus, because of the current limited evidence, the question of whether the SARS-CoV-2 virus can directly injure the heart requires further demonstration.

In terms of laboratory findings, patients with cardiac injury compared with patients without cardiac injury showed higher median leukocyte count (median [IQR], 9400 [6900-13 800] cells/μL vs 5500 [4200-7400] cells/μL), and levels of C-reactive protein (median [IQR], 10.2 [6.4-17.0] mg/dL vs 3.7 [1.0-7.3] mg/dL), procalcitonin (median [IQR], 0.27 [0.10-1.22] ng/mL vs 0.06 [0.03-0.10] ng/mL), CK-MB (median [IQR], 3.2 [1.8-6.2] ng/mL vs 0.9 [0.6-1.3] ng/mL), myohemoglobin (median [IQR], 128 [68-305] μg/L vs 39 [27-65] μg/L), hs-TNI (median [IQR], 0.19 [0.08-1.12] μg/L vs <0.006 [<0.006-0.009] μg/L), N-terminal pro-B-type natriuretic peptide (NT-proBNP) (median [IQR], 1689 [698-3327] pg/mL vs 139 [51-335] pg/mL),

Greater proportions of patients with cardiac injury required noninvasive mechanical ventilation (38 of 82 [46.3%] vs 13 of 334 [3.9%]; P < .001) or invasive mechanical ventilation (18 of 82 [22.0%] vs 14 of 334 [4.2%]; P < .001) than those without cardiac injury.

creatinine kinase–myocardial band (median [IQR], 3.2 [1.8-6.2] vs 0.9 [0.6-1.3] ng/mL)

N-terminal pro-B-type natriuretic peptide (median [IQR], 1689 [698-3327] vs 139 [51-335] pg/mL)

Moreover, hypoxemia caused by COVID-19 may bring about atrial fibrillation, which is the most common arrhythmia among elderly individuals, and atrial fibrillation could be refractory before the pulmonary function is improved.

100 nM MLN-4760did not interfere with immunoprecipitation of ACE2 by S1-Ig,nor did this inhibitor interfere with S-protein-mediated infec-tion (Figure 4B and C)

There were numerous differences in laboratory findings between patients admitted to the ICU and those not admitted to the ICU (Table 2), including higher white blood cell and neutrophil counts, as well as higher levels of D-dimer, creatine kinase, and creatine.

Thirty-six patients (26.1%) were transferred to the intensive care unit (ICU) because of complications, including acute respiratory distress syndrome (22 [61.1%]), arrhythmia (16 [44.4%]), and shock (11 [30.6%]).

Heart rate, respiratory rate, and mean arterial pressure did not differ between patients who received ICU care and patients who did not receive ICU care. These measures were recorded on day of hospital admission for all patients, then divided into those who were later admitted to the ICU or not.

Common complications among the 138 patients included shock (12 [8.7%]), ARDS (27 [19.6%]), arrhythmia (23 [16.7%]), and acute cardiac injury (10 [7.2%]). Patients who received care in the ICU were more likely to have one of these complications than non-ICU patients.

The mortality during hospitalization was 7.62% (8 of 105) for patients without underlying CVD and normal TnT levels,

for those without underlying CVD but elevated TnT levels, and 69.44% (25 of 36) for those with underlying CVD and elevated TnTs.

Plasma TnT levels demonstrated a high and significantly positive linear correlation with plasma high-sensitivity C-reactive protein levels (β = 0.530, P < .001) and N-terminal pro–brain natriuretic peptide (NT-proBNP) levels (β = 0.613, P < .001). Plasma TnT and NT-proBNP levels during hospitalization (median [interquartile range (IQR)], 0.307 [0.094-0.600]; 1902.00 [728.35-8100.00]) and impending death (median [IQR], 0.141 [0.058-0.860]; 5375 [1179.50-25695.25]) increased significantly compared with admission values (median [IQR], 0.0355 [0.015-0.102]; 796.90 [401.93-1742.25]) in patients who died (P = .001; P < .001), while no significant dynamic changes of TnT (median [IQR], 0.010 [0.007-0.019]; 0.013 [0.007-0.022]; 0.011 [0.007-0.016]) and NT-proBNP (median [IQR], 352.20 [174.70-636.70]; 433.80 [155.80-1272.60]; 145.40 [63.4-526.50]) was observed in survivors

During hospitalization, patients with elevated TnT levels had more frequent malignant arrhythmias, and the use of glucocorticoid therapy (37 [71.2%] vs 69 [51.1%]) and mechanical ventilation (41 [59.6%] vs 14 [10.4%]) were higher compared with patients with normal TnT levels.

that the levels of the last test of neutrophils (14/16, 87.5%), PCT (11/11, 100%), CRP (11/13, 84.6%), cTnI (7/9, 77.8%),

In severe cases, COVID-19 may present as pneumonia, the acute respiratory distress syndrome (ARDS), with or without both distributive and cardiogenic shock, to which elderly populations with preexisting medical comorbidities are the most vulnerable

No study has described the incidence of ST-segment elevation myocardial infarction in COVID-19, but it appears to be low. Similarly, the incidence of left ventricular systolic dysfunction, acute left ventricular failure and cardiogenic shock have also not been described.

However, an elevation of high-sensitivity cardiac troponin I (cTnI) above 99th percentile upper reference limit is the most commonly used definition

We describe the first case of acute cardiac injury directly linked to myocardial localization of severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) in a 69‐year‐old patient with flu‐like symptoms rapidly degenerating into respiratory distress, hypotension, and cardiogenic shock.

An intra‐aortic balloon pump (IABP) was placed on top of adrenaline (0.07 μg/kg/min), and noradrenaline (0.1 μg/kg/min) was added for worsening hypotension (systolic blood pressure: 80/67/60 mmHg).

The first echocardiography showed a dilated left ventricle [left ventricular (LV) end‐diastolic diameter 56 mm], severe and diffuse LV hypokinesia (LV ejection fraction 34%). Three hours later, LV ejection fraction dropped to 25% and estimated cardiac index was 1.4 L/min/m2. Coronary angiography findings were unremarkable.

Vice versa, we did not observe viral particles in cardiac myocytes and, therefore, we cannot infer on viral cardiotropism. Cardiac myocytes showed non‐specific damage that was mainly characterized by focal myofibrillar lysis. In addition, we did not observe cytopathic endothelia and small intramural vessel inflammation or thrombosis. Other cases are needed to confirm this observation.

Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets. We did not observe viral particles in myocytes and endothelia. Small intramural vessels were free from vasculitis and thrombosis. EMB did not show significant myocyte hypertrophy or nuclear changes; interstitial fibrosis was minimal, focal, and mainly perivascular

The pathologic study showed low‐grade interstitial and endocardial inflammation (Figure 1A and 1B). Large (>20 μm), vacuolated, CD68‐positive macrophages were seen with immune‐light microscopy (Figure 1C and 1D); they were ultrastructurally characterized by cytopathy, with membrane damage and cytoplasmic vacuoles (Figure 1E). The ultrastructural study demonstrated single or small groups of viral particles with the morphology (dense round viral envelope and electron‐dense spike‐like structures on their surface) and size (variable between 70 and 120 nm) of coronaviruses (Figure 2). COVID‐19 infected Vero cells were used as control. The viral particles were observed in cytopathic, structurally damaged interstitial cells that demonstrated loss of the cytoplasmic membrane integrity (Figure 3)

By the end of Jan 25, 31 (31%) patients had been discharged and 11 (11%) patients had died; all other patients were still in hospital (table 1). The first two deaths were a 61-year-old man (patient 1) and a 69-year-old man (patient 2). They had no previous chronic underlying disease but had a long history of smoking.

The final diagnosis was acute virus-negative lymphocytic myocarditis associated with SARS-CoV-2 respiratory infection

EMB (Panel E, day 7) documented diffuse T-lymphocytic inflammatory infiltrates (CD3+ >7/mm2) with huge interstitial oedema and limited foci of necrosis. No replacement fibrosis was detected, suggesting an acute inflammatory process. Molecular analysis showed absence of the SARS-CoV-2 genome within the myocardium. No contraction band necrosis or TTS-associated microvascular abnormalities were observed.

CMR (day 7) showed a recovery of systolic function (from 52% by CTA to 64% by CMR), although with persistence of a mild hypokinesia at basal and mid left ventricular segments; at the same sites, diffuse myocardial oedema, determining wall pseudo-hypertrophy, was observed on short T1 inversion recovery (STIR) sequences (Panel D) and confirmed by T1 and T2 mapping (average native T1 = 1188 ms, normal value <1045; average T2 = 61 ms, normal value <50). Late gadolinium enhancement sequences demonstrated absence of detectable myocardial scar/necrotic foci.

Although the first clinical suspicion was myocarditis, coronary computed tomography angiography (CTA) was acquired to rule out coronary artery disease (CAD). Baseline chest scan (Panel B) confirmed bilateral patchy ground-glass opacities; CTA showed no aortic dissection, pulmonary embolism, or epicardial CAD (Panel C). Dynamic 3D volume-rendering reconstruction demonstrated a clear hypokinesia of the left ventricle mid and basal segments, with normal apical contraction, suggesting a reverse Tako-Tsubo syndrome (TTS) pattern

ECG (Panel A) showed low atrial ectopic rhythm, mild ST-segment elevation in leads V1–V2 and aVR, reciprocal ST depression in V4–V6, and QTc 452 ms with diffuse U-waves. The high-sensitivity troponin T curve was 135–107–106 ng/L (normal value <14), NT-proBNP 512 pg/mL (normal value <153), and C-reactive protein 18 mg/L (normal value <6). Transthoracic echocardiogram showed mild left ventricular systolic dysfunction (LVEF 43%) with inferolateral wall hypokynesis; neither ventricle was dilated and there was no pericardial effusion.

Itis likely that cardiac troponin measurements wererequested in those who were more unwell or where there wasreasonable suspicion of myocardial ischemia or myocardial dysfunction. Only systematic testing of both symptomatic and asymptomatic patients infected with SARS-CoV-2 will provide an accurate estimate of the prevalence of myocardial injuryin this condition.

In a cohort of 191 patients with confirmed COVID-19 based on SARS-CoV-2 RNA detection, the univariable odds ratio for death when hs-cTnI concentrations were above the 99thpercentile upper reference limit was 80.1 (95% confidence interval [CI]10.3 to 620.4, P<0.0001).[4]This was higher than the odds ratios observed for all other biomarkerstested,including D-Dimer and lymphocyte count.

While the spectrum of clinical manifestation is highly related to the inflammation process of the respiratory tract, this case provides evidence of cardiac involvement as a possible late phenomenon of the viral respiratory infection. This process can be subclinical with few interstitial inflammatory cells, as reported by an autopsy study,10 or can present with overt manifestations even without respiratory symptoms, as in the present case.

A 12-lead electrocardiogram (ECG) showed low voltage in the limb leads, minimal diffuse ST-segment elevation (more prominent in the inferior and lateral leads), and an ST-segment depression with T-wave inversion in lead V1 and aVR

Chest radiography was repeated on day 4 and showed no thoracic abnormalities. Transthoracic echocardiography, performed on day 6, revealed a significant reduction of LV wall thickness (interventricular septum, 11 mm; posterior wall, 10 mm), an improvement of LVEF to 44%, and a slight decrease of pericardial effusion (maximum, 8-9 mm). At the time of submission, the patient was hospitalized with progressive clinical and hemodynamic improvement.

During the first days of her hospitalization, the patient remained hypotensive (systolic blood pressure less than 90 mm Hg) and required inotropic support (dobutamine) in the first 48 hours, during which there was a further increase in levels of NT-proBNP (8465 pg/mL), high-sensitivity troponin T (0.59 ng/mL), and creatine kinase–MB (39.9 ng/mL), with a progressive stabilization and reduction during the following days (Table). Blood pressure progressively stabilized, although systolic pressure remained less than 100 mm Hg, and dobutamine treatment was weaned on day 4.

Transthoracic echocardiography revealed normal left ventricular (LV) dimensions with an increased wall thickness (interventricular septum, 14 mm, posterior wall, 14 mm) and a diffuse echo-bright appearance of the myocardium. There was diffuse hypokinesis, with an estimated LV ejection fraction (LVEF) of 40%. There was no evidence of heart valve disease. Left ventricular diastolic function was mildly impaired with mitral inflow patterns, with an E/A ratio of 0.7 and an average E/e′ ratio of 12. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers (maximum, 11 mm) without signs of tamponade. Cardiac magnetic resonance imaging (MRI) confirmed the increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe LV dysfunction (LVEF of 35%) (Video 1 and Video 2). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema. Phase-sensitive inversion recovery sequences showed diffuse late gadolinium enhancement extended to the entire biventricular wall (Figure 2). The myocardial edema and pattern of late gadolinium enhancement fulfilled all the Lake Louise criteria for the diagnosis of acute myocarditis.6 The circumferential pericardial effusion was confirmed, especially around the right cardiac chambers (maximum, 12 mm).

Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe left ventricular dysfunction (left ventricular ejection fraction of 35%). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers. These findings were all consistent with acute myopericarditis.

In addition, repeated floods of catecholamines due to anxiety and the side effects of medication can also lead to myocardial damage.

Third, Huang’s study noted that high concentration of IL-1β, IFN-γ, IP-10 and MCP-1 could be detected in patients infected with 2019-nCoV, which might lead to activated T-helper-1 (Th1) cell responses [4]. Furthermore, they also found that ICU patients had much higher concentrations of inflammatory factors than those non-ICU patients, suggesting that the cytokine storm was associated with disease severity

Second, hypoxaemia may be also an important reason of cardiac injury. In Huang’s study, 32% COVID-19 patients had various degree of hypoxaemia and need required high-flow nasal cannula or higher-level oxygen support. In Chen’s study, up to 76% of patients require oxygen therapy. Due to severe 2019-nCoV infection, the pneumonia may cause significant gas exchange obstruction, leading to hypoxaemia, which significantly reduces the energy supply by cell metabolism, and increases anaerobic fermentation, causing intracellular acidosis and oxygen free radicals to destroy the phospholipid layer of cell membrane. Meanwhile, hypoxia-induced influx of calcium ions also leads to injury and apoptosis of cardiomyocytes.

The data again showed a significant higher incidence of acute cardiac injury in ICU/severe patients compared to the non-ICU/severe patients [RR = 13.48, 95% CI (3.60, 50.47), Z = 3.86, P = 0.0001]

Another two studies only gave the data of creatine kinase, if it can be seen as a biomarker of cardiac injury, the proportion might be 11.5% (95% CI 7.8–15.2%).

Two studies that gave clear data were statistically analyzed, and the data showed that 8.0% (95% CI 4.1–12.0%) patients might be suffered from an acute cardiac injury.

It is reasonable to expect that severe and critical cases have more severe effects on the cardiovascular system owing to more robust inflammatory response. At this early stage, our knowledge is mainly based on available numerators data, and the exact population-level denominators are not known. Also, it is likely that the asymptomatic and mildly symptomatic cases are missing from most reports, which further skews our understanding of the disease.

There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart

There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue

Based on the analysis of the clinical data, we confirmed that some patients died of fulminant myocarditis. In this study, we first reported that the infection of SARS-CoV-2 may cause fulminant myocarditis.

Among the 68 fatal cases, 36 patients (53%) died of respiratory failure, five patients (7%) with myocardial damage died of circulatory failure, 22 patients (33%) died of both, and five remaining died of an unknown cause

There were a few interstitial mononuclear inflammatory infiltrates, but no other substantial damage in the heart tissue

Among survivors, secondary infection, acute kidney injury, and acute cardiac injury were observed in one patient each, occurring 9 days (acute kidney injury), 14 days (secondary infection), and 21 days (acute cardiac injury) after illness onset.

Creatine kinase, U/L≤1851 (ref)......>1852·56 (1·03–6·36)0·043....High-sensitivity cardiac troponin I, pg/mL≤281 (ref)......>2880·07 (10·34–620·36)<0·0001....

In this study, increased high-sensitivity cardiac troponin I during hospitalisation was found in more than half of those who died.

Heart failure44 (23%)28 (52%)16 (12%)<0·0001Septic shock38 (20%)38 (70%)0<0·0001Coagulopathy37 (19%)27 (50%)10 (7%)<0·0001Acute cardiac injury33 (17%)32 (59%)1 (1%)<0·0001Acute kidney injury28 (15%)27 (50%)1 (1%)<0·0001

COVID‐19 prognosis is related to age and sex. The expression of ACE2 decreases with increasing age. ACE2 expression is higher in young people than in elderly individuals and higher in females than in males.11, 12 This pattern does not match the characteristic of severely ill COVID‐19 patients being mostly elderly males. We believe that whether the level of ACE2 expression is high or low is not a key factor affecting the prognosis of patients with COVID‐19. The relationship between sex and prognosis requires additional data to verify.

Duration from onset of symptoms to radiological confirmation of pneumonia, days5 (3–9)5 (3–7)Duration from onset of symptoms to ICU admission, days9 (6–12)11 (7–14)Heart rate, beats per min89 (20)89 (15)Systolic blood pressure, mm Hg133 (20)140 (21)

Cardiac injury3 (15%)9 (28%)12 (23%)

By Jan 26, 2020, 710 patients had been admitted to Wuhan Jin Yin-tan hospital with confirmed SARS-CoV-2 pneumonia, of whom 658 (93%) were considered ineligible, including three patients who had cardiac arrest immediately after admission.

A raised troponin (hypersensitive-troponin I (hs-cTnI)) was detected in five patients, possibly suggestive of virus-associated myocardial injury.

The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury.

Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells

Among the people who died from COVID-19 reported by the NHC, 11.8% of patients without underlying CVD had substantial heart damage, with elevated levels of cTnI or cardiac arrest during hospitalization.

and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardial cells.

some of the patients first went to see a doctor because of cardiovascular symptoms. The patients presented with heart palpitations and chest tightness rather than with respiratory symptoms, such as fever and cough, but were later diagnosed with COVID-19.

where the dragon is an enchanted prince, where the handsome prince is a nasty thief, and where the thief saves the day

We find Alper et al.'s (2000) concept of "conflict efficacy" useful: it says that conflict should be measured not by its nature or origin, but by its contribution to the perception among group members that conflicts can and are dealt with productively.

Ravn (1998) poses the interesting possibility that Thomas' definition of conflict includes in it both productive and unproductive conflict, because productive conflict stops before it gets to the third phase of non-acceptance, instead using the energy of conflict as a positive force.

Skule (1999) describes how an inter-organisational group of workers from five food-and-drink companies were taken through a training program that included "practice in other companies". Says Skule, "Most of the skilled operators described [the experience] in terms like "see things differently", “opened my eyes”, “think more about what I am doing”, “more alert” and “think more about the consequences”. These new perspectives or ways of seeing in turn made operators attend to features in their work situation in a new way. From a former habitual way of working according to minimum standards, many skilled operators developed a more reflectively skilled way of performing their job, within the limits of existing job structures and routines." We believe this kind of benefit may not be as often used as is possible.

The strength of unwritten rules is that they are habitual within the group and thus both adaptive and resilient. Good management practice creates habits rather than rules. Coming

Inter-organisational networks help organisations sustain productive rule networks

In rejecting managerialism, we can equally discover the tyranny of the expert, as in Orwell’s nightmare the animals look through the window of the farm to see the pigs dressed as men.

What inter-organisational networks provide is the opportunity for employees to discover this paradox for themselves through learning about the experiences of people at other organisations, and in the process to change how they manage their own constellation of identities in relation to their organisation.

The most effective systems leave a sufficient level of inefficiency in order that they can be resilient in changing contexts.

Idealistic approaches tend to privilege expert knowledge, analysis and interpretation. Naturalistic approaches emphasise the inherent un-knowability of current and future complexities, and thus they de-privilege expert interpretation in favor of enabling emergent meaning at the ground level.

In China, where the mortality rate for men was almost twice as high as that for women, nearly half of men over 15 smoke, compared with just 2 percent of women.

we face two particularly important choices. The first is between totalitarian surveillance and citizen empowerment. The second is between nationalist isolation and global solidarity. 

Entire countries serve as guinea-pigs in large-scale social experiments. What happens when everybody works from home and communicates only at a distance? What happens when entire schools and universities go online? In normal times, governments, businesses and educational boards would never agree to conduct such experiments. But these aren’t normal times. 

Instead of every country trying to do it locally and hoarding whatever equipment it can get, a co-ordinated global effort could greatly accelerate production and make sure life-saving equipment is distributed more fairly.

When people are told the scientific facts, and when people trust public authorities to tell them these facts, citizens can do the right thing even without a Big Brother watching over their shoulders. A self-motivated and well-informed population is usually far more powerful and effective than a policed, ignorant population.

But temporary measures have a nasty habit of outlasting emergencies, especially as there is always a new emergency lurking on the horizon.

One of the problems we face in working out where we stand on surveillance is that none of us know exactly how we are being surveilled, and what the coming years might bring. Surveillance technology is developing at breakneck speed, and what seemed science-fiction 10 years ago is today old news.

But with coronavirus, the focus of interest shifts. Now the government wants to know the temperature of your finger and the blood-pressure under its skin. 

This kind of technology is not limited to east Asia.

Welcome to ACUE’s Online Teaching Toolkit

Management of Critically Ill Adults With COVID-19

Passano le stagioni, ma solo quelle di Netflix.

wearing simple face masks which exert a barrier function that blocks those big projectile droplets that land in the nose or throat may substantially reduce the production rate R, to an extent that may be comparable to social distancing and washing hands.

Make sure to discard or launder after use without touching the outward surface

CDC suggests use of scarf by health care providers as last resort when no face masks are available

avoiding large droplets, which cannot enter the lung anyway but land in the upper respiratory tracts, could be the most effective means to prevent infection. Therefore, surgical masks, perhaps even your ski-mask, bandanas or scarf

The molecular analysis also show that the SARS-Cov2 virus is active and replicates already in the nasopharynx, unlike other respiratory viruses that dwell in deeper regions of the lung.

Surprisingly, ACE2 expression in the lung is very low: it is limited to a few molecules per cell in the alveolar cells (AT2 cells) deep in the lung. But a just published paper by the Human Cell Atlas (HCA) consortium reports that ACE2 is highly expressed in some type of (secretory) cells of the inner nose!

SARS-Cov-2 virus, like any virus, must dock onto human cells using a key-lock principle, in which the virus presents the key and the cell the lock that is complementary to the key to enter the cell and replicate. For the SARS-Cov-2 virus, the viral surface protein “Spike protein S” is the “key” and it must fit snugly into the “lock” protein that is expressed (=molecularly presented) on the surface of the host cells. The cellular lock protein that the SARS-Cov-2 virus uses is the ACE2 protein

Filtering effect for small droplets (aerosols) by various masks; home-made of tea cloth, surgical mask (3M “Tie-on”) and a FFP2 (N95) respirator mask. The numbers are scaled to the reference of 100 (source of droplets) for illustrative purposes, calculated from the PF (protection factor) values

The tacit notion at the CDC that the alveolae are the destination site for droplets to deliver the virus load (the alveolae are after all the anatomical site of life-threatening pneumonia), has elevated the apparent importance of N95 masks and led to the dismissal of surgical masks.

In the case of the SARS-Cov-2 virus it is not known what the minimal infectious load is (number of viral particles needed to start the pathogenesis cascade that causes a clinical disease).

Of course many aerosol droplets in the exhalation or cough spray may not contain the virus, but some will do.

droplets of a typical cough expulsion have a size distribution such that approximately half of the droplet are in the categories of aerosols, albeit they collectively represent only less than 1/100,000 of the expelled volume

For airborne particles to be inspired and reach deep into the lung, through all the air ducts down to the alveolar cells where gas-exchange takes place, it has to be small

Droplets can (for this discussion) be crudely divided in two large categories based on size

Droplet larger than aerosols, when exhaled (at velocity of <1m/s), evaporate or fall to the ground less than 1.5 m away. When expelled at high velocity through coughing or sneezing, especially larger droplets (> 0.1 micrometers), can be carried by the jet more than 2m or 6m, respectively, away.

The official recommendation by CDC, FDA and others that masks worn by the non-health-care professionals are ineffective is incorrect at three levels: In the logic, in the mechanics of transmission, and in the biology of viral entry.

Flattening the curve”. Effect of mitigating interventions that would decrease the initial reproduction rate R0 by 50% when implemented at day 25. Red curve is the course of numbers of infected individuals (”case”) without intervention. Green curve reflects the changed (”flattened”) curve after intervention. Day 0 (March 3, 2020) is the time at which 100 cases of infections were confirmed (d100 = 0).

we must abide by the voluntary quarantine rules verbatim

Turkey’s government says it is not disclosing the location of cases to prevent the risk of increasing transmission rates by encouraging people to move from areas with high rates to places where there are no or few cases.

Coronavirus at a Glance

He referred to a viral video posted by a critical care nurse who implored shoppers to stop stripping supermarkets of essential items, leaving little behind for NHS workers coming off long shifts. It is an undeniably emotive and valid issue, but widespread calls for shoppers to exercise restraint have so far mirrored the government’s own narrow framing of the necessary response to coronavirus more broadly: namely, the absolute personalisation of responsibility over scrutiny of the infrastructure we all depend on.

Comment se connecter à l’ENT (espace numérique de travail)? En début de l’année scolaire, chaque parent et chaque élève ont été destinataires des identifiants permettant d’accéder à l’ENT. Si vous avez perdu ces codes d’accès, l’établissement restera à votre disposition pendant sa fermeture pour vous les redonner et vous communiquer le livret de prise en main de l’outil.

Où peut-il trouver les cours et les exercices? Chaque lycée met à disposition des élèves un espace numérique de travail (ENT) où se trouvent, dans le cadre du cahier de texte numérique, des cours et des devoirs déposés par chaque professeur concernant sa discipline ainsi queles dates de remise des travaux. L’élève y télécharge les documents (sujets, supports de cours, exercices...) à travailler. Si le professeur lui demande, l’élèvedépose ses devoirs une fois faits et il y récupère les copies corrigées avec les annotations duprofesseur.

Pendant la fermeture de l’établissement, mon enfant a-t-il du travail à faire? Dans le cadre de la fermeture aux élèves de toutes les écoles et de tous établissements à compter du lundi 16 mars, la continuité pédagogique doit être assurée pour tous les élèves c’est-à-dire que des cours et des exercices doivent leur être proposés ainsi qu’un accompagnement pédagogique par leurs professeurs. Pendant cette période, les élèves auront des activités à réaliser (cours à suivre, exercices à réaliser) et des devoirs à rendre dans les délais fixés par leurs professeurs.

JE SUIS PARENT D’UN ENFANT DE LYCEEGENERAL,TECHNOLOGIQUE OU PROFESSIONNEL

Si je suis convoquépar la direction ou un professeur, suis-je obligéde me déplacer? Non, les déplacements et réunions non indispensables doivent être évités. Des moyens adaptés d’échanges avec l’équipe pédagogique qui suit votre enfant vous seront proposés.

Mon enfant doit-il faire la séquence d’observation prévue sur une des semaines à venir?La santé des Français est la priorité du gouvernement. Au nom du principe de précaution, il est préconisé d’annuler ces séquences d’observation ou de les reporteren lien avec la structure d’accueil du stage.

Comment mon enfant va-t-il être accompagné dans ses choix d’orientation?Afin d’accompagner votre enfant dans ses choix d’orientation, des contacts réguliers, par téléphone ou messagerie, seront organisés avec le professeur principal de la classe.

Le calendrier d’orientation est-il modifié?La priorité est donnée aux conseils de classe qui ont une incidence sur la suite du parcours des élèves: en classe de 3è, avis sur les choix initiaux de la famille en termes de poursuite d’études (voie d’orientation, éventuellement spécialité envisagée en voie professionnelle).A ce jour, le calendrier d’orientationest maintenu.

Que se passe-t-il pour l’orientation de mon enfant après la classe de troisième?La continuité du suivi du parcours de l’élève et de la vie scolaire est assurée. Si besoin, vous pouvez contacter le professeur principal ou le chef d’établissement.

Mon fils ou ma fille vont-ilspouvoir passer les épreuves écrites du DNB? A quelle date?Les dates des épreuves écrites terminales du DNB ont été publiées: il s’agit des 29 et 30 juin 2020 pour la métropole. A ce jour, ce calendrier est maintenu. Mais évidemment les choses peuvent évoluer en fonction des évolutions de la situation. Une idée préside à toutes les décisions: ne pas léser les élèves.

Les sujets du DNB vont-ils être adaptés à la situation?(programmes allégés?)A ce jour, aucune suppression ou modification des examens nationaux, ni aucun allègement de programmes ne sont prévus. En tout état de cause, il sera tenu compte des circonstances exceptionnelles que notre pays traverse.

Mon fils ou ma fille vont-ilspasser son épreuve orale du DNB? A quelle date?Les parents d’élèves seront informés régulièrement de l’évolution de la situation et des prescriptions applicables via tous les canaux usuels (courriels, SMS, affichages extérieurs à l’entrée de l’établissement ainsi qu’en mairie).La situation étant évolutive, vous êtes invités à consulter régulièrement l’ENT, la messagerie et/ou le site de l’établissement.

Je suis représentant de parent d’élèves. Y a-t-il un maintien des conseils de classe?Oui, les conseils de classe sont maintenus, notamment en priorité ceux de troisième, uniquement en visio conférence ou en audioconférence. Vous en serez informé par le chef d’établissement.

Comment peut-on avoir les téléphones des professeurs?Il faut consulter régulièrement l’espace numérique de travail (ENT) du collège pour disposer d’informations pour contacter les professeurs. Vous pouvez communiquer via l’ENT avec les professeurs ou leur envoyer un courriel sur la messagerie professionnelle.

Mon enfant doit-il faire et rendre tous les devoirs qui vont lui être donnés en ligne?L’objectif est de maintenir les acquis déjà développés par votre enfant depuis le début de l’année, de les consolider et de les enrichir par des exercices. Ces derniers sont indispensables pour assurer le retour en classe. Les devoirs donnés en ligne ont un rôle identique à celui des devoirs donnés en période scolaire normale

Combien de temps cette fermeture du collège va durer? Qu’est-ce qui est prévu en termes pédagogiques? Mon enfant pourra-t-il continuer à apprendre si cela dure plusieurs semaines?La fermeture du collège esteffective jusqu’à nouvel ordre.La situation étant évolutive, vous êtes invités à consulter régulièrement l’ENT, la messagerie et/ou le site de l’établissement. Vous pouvez aussi vous connecter au site de l’académie ou de l’inspection académique pour recevoir les consignes.Les ressources pédagogiques à disposition des professeurs et des élèves sont nombreuses et permettent de répondre aux besoins sur une longue période. Ma classe à la maison comporte à ce stade 4 semaines complètes de travaux. Ces ressources seront complétées si nécessaire.

Je n’ai pas d’ordinateur chez moi. Comment va faire mon enfant pour continuer à étudier? Comment puis-je récupérer des supports papier de cours?La continuité pédagogique peut se poursuivre sans outil numérique. Vous devez prendre contact avec le chef d’établissement ou le professeur principal de votre enfant pour recevoir les consignes. Il vous précisera les modalités de diffusion des documents pédagogiques sur support papier.

Comment dois-je faire pour accompagner mon enfant dans cette période?Vous devez vous connecter sur le site du collège ou l’ENT pour récupérer et suivre les consignes et conseils des professeurs. Il est recommandé de respecter un temps régulier quotidien de travail et de veiller à conserver un rythme biologique de sommeil proche du temps scolaire. Vouspouvez aider votre enfant en le rassurant sur la situation, en veillant à la régularité de son travail, en vous intéressant à ses apprentissages et en lui assurant, autant que possible, des conditions propices à sa concentration.Si vous ne disposez pas d’équipement numérique adapté, contactez le chef d’établissement pour avoir accès aux documents sous des formats adaptés.

Je n’ai plus les codes pour accéder à l’ENT. Comment faire?Vous pouvez adresser par messagerie ou par téléphone à votre établissement une demande pour obtenir les codes. Ils vous seront personnellement fournis par messagerie ou SMS

Peut-on se rendre au collège de notre enfant pour avoir une information à partir du lundi 16 mars?Afin de lutter contre la propagation du covid19, tout déplacement non indispensable doit être proscrit. Consultez régulièrement l’espace numérique de travail (ENT) du collège pour disposer d’informations.Vous pouvezaussi vous connecter sur le site du collège, contacter par messagerie ou téléphone l’équipe de direction du collège de votre enfant, ainsi que la cellule académique de suivi.

JE SUIS PARENT D’UN ENFANT AU COLLEGE

L’objectif de la continuité pédagogique est de s’assurer que les élèves poursuivent des activités scolaires leur permettant de progresser, s’appuyant plus spécifiquement sur des compétences variées adossées au travail autonome des élèves. A cette fin, le professeur soumet un ensemble de travaux et d’activités dont l’élève s’empare dans le cadre de son travail personnel.Le professeur coordonne, supervise et identifie les travaux qu’il souhaite évaluer afin de s’assurer de l’acquisition et/ou de la consolidation de notions ou de compétences.Le travail demandé doit être régulier.

Est-ce que je peux évaluer les élèves et attribuer des notes durant cette période ?Il s’agit de prévoir des séquences compatibles avec des enseignements à distance et d’adapter le travail demandé aux élèves aux contraintes des ENT. Les travaux demandés s’appuient plus spécifiquement sur des compétences variées adossées au travail autonome.

Comment savoir si les ressources privées que j’utilise sont conformes aux usages ?La continuité pédagogique mobilise les supports usuels: -Les manuels scolaires en possession des élèves. -Les ressources de l’espace numérique de travail; -Des supports numériques, ressources créées par les professeurs et les ressources éditoriales disponibles (BRNE, Eduthèque...); -La plateforme du CNED «Ma classe à la maison»; -La plateforme «Jules» du CNED pour consolider le travail personnel de l’élève;-Les ressources disciplinaires ou transversales du site académique et des autres sites institutionnels. Il convient de ne pas utiliser des solutions privées non conformes aux usages professionnels et au règlement général sur la protection des données personnelles (RGPD). Les corps d’inspection ainsi que les délégations académiques au numérique éducatif (DANE) sont disponibles en appui et en conseil. Il convient de se rapprocher de son chef d’établissement afin de connaître l’adresse mail ou la hotline dédiée.

Les programmes seront-ils allégés pour le brevet ?A ce jour, il n’est prévu aucune suppression ou modification desexamens nationaux, ni aucun allègement de programmes. Si la situation le nécessite, des dispositions seront prises au niveau national et vous en serez informé directement par le chef d’établissement.

Comment aborder la démarche expérimentale en sciences à distance?L’objectif de la continuité pédagogique est de maintenir les acquis déjà développés depuis le débutde l’année (consolidation, enrichissement...) et d’acquérir des compétences nouvelles lorsque les modalités d’apprentissage le permettent. Dans cette perspective, dans la mesure du possible, le professeur de sciences peut aborder la démarche expérimentale et proposer un ensemble de documents, interactifs ou non, qui permettent aux élèves de comprendre les situations choisies. En aucun cas, il n’est demandé à l’élève de mener des expériences seul chez lui et qui puissent présenter un quelconque danger. Le recours à des vidéos pédagogiques, montrant des expériences, sur lesquelles l’élève est ensuite interrogé, peut constituer un complément utile.

Comment travailler avec les élèves en EPS ?L’objectif de la continuité pédagogique est de maintenir les acquis déjà développés depuis le début de l’année (consolidation, enrichissement...) et d’acquérir des compétences nouvelles lorsque les modalités d’apprentissage le permettent. Sur le plan de la motricité, le professeurpeut mettre à disposition des ressources vidéos choisies ou construites par lui-même afin de favoriser une pratique physique quotidienne, individuelle et adaptée aux consignes de confinement (routine échauffement, stretching commenté, renforcement musculaire guidé...). En respectant le principe d’une activité physique de 30 minutes par jour, les élèves pourront consolider un ensemble de techniques et savoir-faire nécessaires à l’entretien de soi, et, plus largement mieux faire face au stress lié à cette nouvelle forme de travail scolaire et aux nécessaires mesures de confinement.Par ailleurs, le professeur des écoles et le professeur d’EPS peuvent proposer des documents àvisionner ou à écouter en lien avec les activités physiques pratiquées pendant l’année.

Comment accorder un accompagnement spécifique aux élèves ?L’objectif de la continuité pédagogique est de maintenir les acquis déjà développés depuis le début de l’année (consolidation, enrichissement...) et d’acquérir des compétences nouvelles lorsque les modalités d’apprentissage le permettent. Dans cette perspective, dans la mesure du possible, le professeur peut recueillir les besoins d’un élève et répondre de manière individualisée et personnalisée grâce aux outils qu’il a à sa disposition.

Comment savoir si l’élève fait son travail tout seul?La continuité pédagogique est destinée à s’assurer que les élèves poursuivent des activités scolaires leur permettant de progresser dans leurs apprentissages. Il s’agit d’attirer l’attention des élèves sur l’importance et la régularité du travail personnel quelle que soit l’activité, même si elle est réalisée avec l’aide d’un pair ou d’un tiers. Des travaux réguliers et évalués régulièrement y contribuent. Toutefois, le professeur ne peut contrôler l’assiduité dans ce cadre, ni sanctionner son éventuel défaut.

Puis-je m’adresser directement aux corps d’inspection ?Les corps d’inspection sont disponibles en appui et en conseil. Les équipes de professeurs ne doivent pas hésiter à les solliciteraprès en avoir informé le directeur de l’école ou le chef d’établissement. Des dispositifs d’accompagnement des professeurs sont prévus à l’échelle académique avec notamment l’organisation de cellules d’aide à la mise en œuvre de la continuité pédagogique. Le plus simple consiste à se rapprocher de son chef d’établissement qui contactera la cellule de son académie.

Ai-je le droit de rencontrer les parents ou les élèves en dehors de mon établissement ?Afin de limiter les risques de propagation du coronavirus, l’accompagnement des familles devra reposer sur des solutions à distance pour permettre le lien continu avec les élèves et les familles (téléphone, courriel, point de dépôt de documents...). Il convient de se référer aux préconisations du ministère des Solidarités et de la Santé, régulièrement actualisées.

Dois-je me relier à la classe uniquement selon mon emploi du temps ?Les professeurs restent responsables de la conception de leur enseignement et prennent appui sur les personnels de direction chargés de la mise en cohérence des initiatives de chaque professeur. En outre, le lien avec la classe peut être maintenu sous des formes différentes (envoi de devoirs par messagerie, classes virtuelles, lecture de documents, recherches...). Une attention particulière devra être portée aux élèves qui ne disposent pas d’équipement adapté au format numérique. Des documents sous format papier seront alors mis à disposition de ces élèves.

Comment adapter ses enseignements à la situation? Les professeurs doivent prévoir des séquences compatibles avec un enseignement à distance et adapter le travail demandé aux élèves à la situation et à ses contraintes, par exemple si l’ENT est utilisé à travers des productions écrites. Si des classes virtuelles sont organisées, il s’agitde réfléchir à leur articulation avec le travail en autonomie de l’élève.Au-delà des outils déjà disponibles soit via l’ENT, soit via le CNED, les professeurs peuvent mettre à disposition des documents non interactifs qui permettent de poursuivre l’activité dans une discipline donnée (recherche documentaire, exercicesà réaliser, textes à lire et à commenter...)

Les conseils de classe vont-ils avoir lieu? Comment faire ?Les conseils de classe sont maintenus, notamment en priorité ceux de troisième, en visioconférence ou en audioconférence. Les personnels de direction en informent les équipes.

Dans mes consignes aux élèves, dois-je faire des révisions ou dois-je poursuivre ma progression pédagogique ?Sur le plan pédagogique, l’objectif est demaintenir les acquis déjà développés depuis le début del’année (consolidation, enrichissements, exercices...) et d’acquérir des compétences nouvelles lorsque les modalités d’apprentissage à distance le permettent. Les activités proposées s’inscrivent naturellement dans le prolongement de ce qui s’est fait en classe auparavant et/ou dans une préparation possible de ce qui sera fait dès le retour dans l’établissement.Le travail demandé doit être régulier. Il doit pouvoir être réalisé dans un temps raisonnable, indiqué explicitement. Le temps consacré à chaque discipline ne doit pas dépasser les horaires habituels, en tenant compte des conditions, notamment en termes de concentration, qui sont celles des élèves à la maison. Les travaux proposés sont adaptés auniveau d’enseignement et aux capacités des élèves. Ils pourront être l’occasion de s’appuyer plus spécifiquement sur des compétences variées adossées au travail autonome.

Quels sont les outils dont je dispose pour assurer la continuité pédagogique?Pour assurer la continuité pédagogique, les professeurs s’appuientsur :-Lessupports papiers usuels comme les manuels scolairesen possession des élèves, dont la plupart sont désormais accessibles en ligne gratuitement.-Les supports numériques usuelstels que:oLes ressources de l’espace numérique de travail de leur école ou établissement; oDes supports numériques, ressources créées par les professeurs et les ressources éditoriales disponibles (BRNE, Eduthèque...); oLa plateforme du CNED «Ma classe à la maison»; oLa plateforme «Jules» du CNED pour consolider le travail personnel de l’élève;oLes ressources disciplinaires ou transversales du site académique et des autres sites institutionnels. En cas de besoin, il est possible de se rapprocher de ses collègues professeurs référents pour les usages du numérique, de se former avec les ressources sur le site de la DANE afin de s’assurer de la maîtrise des outils.

Je suis professeur principal, comment faire pour suivre l’orientation de mes élèves ?Afin de permettre la continuité du suivi du parcours de l’élève, différentes ressources relatives à l’orientation sont disponibles sur les sites académiques, nationaux et régionaux.L’’échange demeure souhaitable avec l’élève et sa famille, notamment par téléphone.

Dois-je être physiquement présent dans le collègeou le lycéependant la période de fermeturede l’accès aux élèves?L’accès aux collègesest fermé aux élèves. S’agissant des adultes, ne doivent être présents que les personnels strictement et absolument nécessaires. La continuité pédagogique est assurée uniquement à distance. L’ENT et/ou le site du collège, s’il y en a un, doit être actualisé en fonction de l’évolution de la situation.