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Can your lungs explode: Dance music can make your lungs collapse › News in Science (ABC Science)

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Dance music can make your lungs collapse › News in Science (ABC Science)

News in Science

Tuesday, 21 September 2004 Catriona Purcell
ABC


Dance music, and other loud music, has been linked to a lung condition that can send you to the emergency department (Image: iStockphoto)

Dance music can make your lungs collapse even if you have no obvious health problems, say European researchers.

They say loud music, like dance or heavy metal music, can trigger a condition known as spontaneous pneumothorax, where air can leak out of the lungs into the surrounding cavity.

Young, tall people who smoke are particularly at risk of the condition, which leaves you breathless and with chest pain.

But Dr Marc Noppen from the Academic Hospital AZ-ZUB in Brussels, Belgium, and his colleagues said their study was the first report of loud music as a trigger.

Three of the patients were next to speakers at a rock concert or nightclub when the pneumothorax occurred. The fourth was in his car, which had 1000-watt bass box speakers.

The researchers outlined the cases recently in the journal Thorax.

When a pneumothorax occurs there is an abnormal build-up of air in the space around the lungs that causes the lung to collapse. Symptoms include breathlessness and chest pain on the affected side.

Large explosions have been known to cause lung damage because of the change in environmental air pressure around the lungs.

But Noppen suggested loud music produces a series of smaller “repetitive blasts” resulting in lung collapse.

The researchers also suspected the repetitive booming bass frequency sound waves that vibrate through the body can cause the lungs to vibrate, tear and leak air into the pleural cavity.

Underlying risk factors

Australian respiratory specialist Dr Christine Jenkins from the Woolcock Institute of Medical Research in Sydney said the report was interesting but not conclusive.

“We know for example that high-frequency, high-energy noise such as you get on building sites can cause ear damage,” she said. “But this is talking about the effects of low-frequency, high-energy sound characteristic of the type of rock music they were listening to.”

It was important to note that all the patients in the study had risk factors for pneumothorax, Jenkins said.

All were tall, thin young males in their late teens and early 20s, and three were heavy smokers.

Two had medical histories that suggested connective tissue disorders, which may also weaken their lung tissue and make it susceptible to damage, she said.

Holding your breath while twisting or straining to lift a heavy weight could also bring on a spontaneous pneumothorax, she said.

“It could be a combination of factors including a predisposition to pneumothorax and an environmental insult such as loud noise may be a cause,” she said.

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My lungs felt like they were going to explode if I coughed

Nikki, a physiotherapist who helps people with breathing problems, shares her experience of having Covid and recovering.

Just before lockdown, I developed symptoms that felt like I was getting a cold. Or it could have been I was very tired after a weekend away with friends to celebrate my birthday! From time to time I was shivering, and I lost my appetite. I didn’t want any food because everything tasted very metallic.

The next day I developed a temperature which fluctuated from 37.5 to 39.9 degrees, a sinus-type painful headache and lots of episodes of diarrhoea despite having had no food. Trying to eat anything made me gag – my throat felt so dry it was difficult to swallow. At this stage, my GP thought I had gastric flu and when I called NHS 111, they didn’t reckon I had COVID-19 either, because I didn’t have a cough.

I drifted in and out of heavy sleep for 20 hours a day

During the next week, I drifted in and out of heavy sleep for about 20 hours every day – and when I woke up I was shivering and had a temperature of 39.9 degrees. The most food I could manage was a small biscuit or a few spoonfuls of jelly. In the end, it was so much effort, I stopped trying to force the food down and didn’t eat at all. During the night I’d struggle downstairs to get a cold drink, but would get severely dizzy and have to lie on the sofa or floor before I could try to get back upstairs.

In the light of this, my GP was now sure I had COVID-19. I went to A&E, as I felt so unwell. My daughter took me in her car at 6 in the morning. The usually bustling A&E (where I had worked) was empty and I was seen straightaway. I was so grateful they got me in so quickly, as I felt so unwell and I couldn’t have sat in a waiting room for long. They gave me fluids intravenously for around 2-3 hours and I was sent home feeling slightly better. Once home, I had a bath and went to bed. 

I hadn’t really believed I actually had COVID-19 and was shocked when the doctor told me. But even at this point, I wasn’t too worried, as I thought I would recover quickly, because the fluids had made me feel better.

I had pain all over my body

I’d now had COVID-19 for 7 to 10 days, and my physical strength was continuing to decline. I still had diarrhoea and no appetite. In the early hours of Monday morning, I began vomiting up fluids and knew I needed medical help. I felt extremely uncomfortable and had pain all over my body. I felt so weak, so I went back to A&E. This time I was admitted into hospital because I had low blood pressure. Blood tests showed I was low in potassium, had markers for inflammation and had low oxygen levels, as well as having pneumonia in both my lungs.

I was in hospital for 7 days

I was looked after in a side room on my own on a ward for the elderly. I was in hospital for 7 days, 5 of those days on oxygen given through nasal cannulas. This dried out my nose and gave me nosebleeds. When I got out of bed to go to the toilet, I needed to connect to an oxygen cylinder and lift it with me, which was a big effort.

I found it difficult mentally. It was then just before lockdown and each morning on the news, I’d hear about the number of deaths overnight. That was tough to listen to while I was in hospital and felt so unwell.

The second day I was in hospital (day 11), I really noticed just how bad my breathing was. I could not get out of bed without using the control to raise the top of the bed and help me sit up. My lungs felt like they were going to explode if I sneezed or coughed. I wasn’t breathless in the way you get out of breath running for a bus. I felt a real heaviness in my chest that felt like my lungs were going to collapse in on themselves. Even getting to the commode or having a wash was a massive effort.

I’d gone from being an active 49-year-old woman to someone who couldn’t even change her position in bed without a lot of difficulty. Being a physiotherapist, I had to become my own personal physio using techniques to help me shift around in bed or get in and out of the bed with least effort. Although I felt – and was – very unwell, I did bed exercises, as I knew how important they were to do to stop my muscles from wasting away. I did things like moving my legs, circling my ankles, and punching my arms up in the air and out in front of me. Even moving to sit on the edge of the bed became an exercise.

I was told I could go home 48 hours after I was breathing room air and the level of oxygen in my blood was above 90%. I managed this for 24 hours, but then felt quite low and depressed about being so isolated. I just wanted my own home and to be with my daughter. No visitors were allowed. Knowing lockdown was now being enforced, I just wanted to be home. The doctor agreed I could go home, as I had good awareness of what to do in terms of my breathing, due to my job as a respiratory physiotherapist.

Getting washed and dressed took me a couple of hours

The first week at home was the hardest, as I was so weak and had lost all my fitness and muscle tone.  My legs were like jelly. Getting washed and dressed in the morning would take me a couple of hours. I also had lots of pain in my legs that I believe was caused by being so weak.

I became anxious about being on my own, in case I suddenly deteriorated or died. Fortunately, this only lasted a few days. Once I could get downstairs more easily and do more for myself, this anxiety went.

I had difficulty finding words

For the first couple of weeks recovering from COVID-19, I had difficulty finding words. I would be talking, but couldn’t remember a name or a word to describe something. Even if I paused and waited, I just couldn’t remember the word I wanted to use. Numbers weren’t an issue – it just words.

Every few days I set myself a goal, like being able to cook breakfast or being able to do my washing. At first, I had to sit down to do these jobs, because I could only stand for 10 minutes. I took each day as it came and after 2 weeks, I was able to do most things again. I was just slower doing them.

When the hay fever season started, I had one relapse with breathlessness, but afterwards I was able to return to work.  In all, I was off work for 7 weeks, then had a phased return over 4 weeks.

I found COVID-19 relentless

My experience of COVID-19 is that it’s painful, relentless and makes you feel so unwell. But people do recover.

Fatigue is a big factor. As I recovered, I was not only dealing with breathlessness and anxiety, but also not being able to do everyday things for myself.

I was fortunate that I was not ill with COVID-19 itself for long and that I recovered quite speedily. But I can just imagine how much tougher it could be for people with long-term conditions, or who were treated in intensive care. And as you do recover, life is different. You’re recovering in lockdown. It’s all strange and unsettling. Work life is different too, due to the pandemic, but it feels so good being back in my job.


Share your story

If you’d like to share your story of recovering from Long COVID, please get in touch.


Blast injuries to the lung: epidemiology and management

Philos Trans R Soc Lond B Biol Sci. 2011 Jan 27; 366(1562): 295–299.

Iain M. J. Mackenzie

1Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, UK

2School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

Bill Tunnicliffe

1Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, UK

1Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham B15 2WB, UK

2School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

*Author for correspondence.

Copyright This journal is © 2011 The Royal SocietyThis article has been cited by other articles in PMC.

Abstract

Lung injury is frequently a component of the polytrauma sustained by military personnel surviving blast on the battlefield. This article describes a case series of the military casualties admitted to University Hospital Birmingham’s critical care services (role 4 facility), during the period 1 July 2008 to 15 January 2010. Of the 135 casualties admitted, 107 (79.2%) were injured by explosive devices. Plain chest films taken soon after arrival in the role 4 facility were reviewed in 96 of the 107 patients. In 55 (57.3%) films a tracheal tube was present. One or more radiological abnormalities was present in 66 (68.75%) of the films. Five patients met the consensus criteria for the definition of adult respiratory distress syndrome (ARDS). The majority of casualties with blast-related lung injury were successfully managed with conventional ventilatory support employing a lung protective strategy; only a small minority received non-conventional support at any time in the form of high-frequency oscillatory ventilation. Of those casualties who survived to be received by the role 4 facility, none subsequently died as a consequence of lung injury.

Keywords: blast injuries, blast lung, radiology of blast lung injury, conventional mechanical ventilation in blast lung injury, HFOV in blast lung injury

1. Introduction

Medical support for UK military personnel is provided in 4 tiers or ‘roles’; in-field physician-delivered first-aid (role 1), in-field medical post (role 2), deployed field hospitals (role 3) and UK-based specialist hospital care (role 4). In the past, role 4 was provided by a combination of military and National Health Service hospitals, but with the rationalization of the Armed Forces medical services over the last 20 years all acute trauma has been admitted to the University Hospital’s Birmingham (UHB) NHS Foundation Trust (Selly Oak site) since 2001, where care is delivered by both military and NHS personnel. Military casualties surviving to role 3 receive world-class resuscitation and stabilization, including imaging and surgery as required, and those requiring further hospitalization are returned to the UK as soon as it is clinically safe to do so. Repatriation is coordinated by the Royal Air Force’s tactical medical wing and effected by their ‘critical care air support teams’, that are able to provide advanced critical care support during transfer in one of the Royal Air Force’s specially equipped C-17 Globemasters. Most of the patients evacuated in this way represent intensive care unit (ICU) to ICU transfers and in the period between 1 July 2008 and 15 January 2010 a total of 135 patients were admitted to UHB’s critical care services, of which 107 (79.2%) were injured by explosive devices, mostly improvised explosive devices (IEDs).

2. Blast injuries

The origin of the mixture of powdered charcoal, sulphur and potassium nitrate known as black powder, or gunpowder, is commonly attributed to China in the period between the eleventh and thirteenth centuries but may have arisen independently at about the same time in the Middle East and Europe. Blast injuries have, therefore, been a feature of human activity for almost 1000 years. Injuries from explosions arise in a number of ways. In temporal order these include tissue damage from; the blast shock wave (primary blast injury), material propelled into the casualty (secondary), the casualty propelled against other objects (tertiary), heat, chemicals and toxins delivered by the device (quaternary) and finally the systemic inflammatory response provoked in the host (quinary) [1]. Injury from the shock wave is thought to arise from three distinct mechanisms—spallation, implosion and inertia. Spallation arises at the interface between media of high (tissue) and low (gas) densities where the high-density material has nothing to which it can transfer the kinetic energy received, causing it to accelerate like the last ball in a Newton’s cradle. Implosion damage is caused by the rapid compression and expansion of gas-filled tissues, originally postulated in 18121 [2]; while inertial damage is generated by shearing between tissues of different densities that are subject to differential acceleration by the shock wave. The key roles of density contrasts and gas in the mechanism of primary blast injury explain why the lungs are particularly susceptible to damage. The first formal descriptions of blast lung were made in air-raid victims of the second world war [3], but shock wave injuries were alluded to in the descriptions of injuries ascribed to the ‘wind of a [cannon] ball’ by Gilbert Blane, Physician to the Fleet, in 1785 [4]. More recently, our understanding of this condition has been informed by terrorist activity in the Middle East [5–8], the UK [9,10] and Europe [11,12].

3. Blast lung

Fatal blast lung injury (BLI) can be sustained in the absence of any other external signs of trauma, thoracic [13] or otherwise [3,14–16]. Our series derives from 517 blast casualties, of which 95 (18.4%) were immediately fatal and 13 of the 412 surviving to role 3 (3.1%) died before they could be evacuated to the UK (). In a series arising from the battle of Monte Cassino in spring 1944 evidence of BLI was found in 34. 5 per cent of a series of 87 autopsies performed in soldiers who died with no external evidence of thoracic injury [13], while diffuse pulmonary contusions were found in 47 per cent of the fatalities in Northern Ireland in the period between 1969 and 1974 [10]. The incidence of blast lung injury in fatalities in this series awaits the results of autopsy investigations.

Flow diagram illustrating the fate of 517 military personnel injured by explosive devices in the period 1 July 2008 and 15 January 2010.

The clinical diagnosis of blast lung is based on context, clinical symptoms and radiology. Symptoms may include respiratory distress, restlessness, and in some cases haemoptysis, associated with cyanosis and hypoxaemia. In some patients symptoms may be significantly delayed [3]. With respect to radiological features most of the available data are based on plain chest films [5,17–19] rather than computerized tomography (CT). Typical findings described to date include unilateral or bilateral focal opacities, diffuse unilateral or bilateral loss of lung translucency which, if unilateral, may be associated with reduced rib-expansion, and radiological evidence of barotrauma. The latter may include pneumothorax, pneumomediastinum, pneumopericardium, surgical emphysema, interstitial emphysema and haemothorax secondary to pulmonary parenchymal lacerations. Abnormalities on plain chest films have been reported in 52 per cent [17] to 91.7 per cent [5] of patients whereas respiratory symptoms are only reported in 22 per cent [17] to 50 per cent [5]. In the setting of this series of cases symptoms of chest pain and dyspnoea were not recorded and would, in any case, have been impossible to disentangle from similar symptoms arising from other injuries, shock or, in the case of patients who were unconscious or had severe head injuries, could not have been elicited. For example, in this series of 107 patients, 39 patients suffered one or more traumatic limb amputations, 20 suffered severe head injuries, and three suffered both. Symptoms would thus have been unreliable as a marker of blast lung in 62 (57.9%). Radiological examinations were performed in all patients, but were not available on UHB’s picture archiving and communications system (PACS) in 19 (17. 7%) cases. In the 88 patients for whom role 3 pulmonary imaging was available, 21 (23.9%) only had plain chest films taken, 11 (12.5%) only had CT and 56 (63.6%) had both. Most patients that had both examinations (87.5%) had plain chest films taken 1.6 (0.74 to 3.6) h prior to CT, the remaining eight patients had their chest films taken 4 (1.25 to 9.65) h after their CT. Overall, the two examinations were performed a median of 1.8 (0.75 to 4.2) h apart. Forty-two (47.7%) patients had a tracheal tube in place at the time of the first radiological examination ().

Table 1.

Proportion of patients in whom a tracheal tube was present at the time of their first radiological examination.

examination tracheal tube total
CT first 7 (87. 5%) 8
CT only 7 (63.6%) 11
CXR first 20 (41.7%) 48
CXR only 8 (38.1%) 21
at first examination 42 (47.7%) 88

4. Initial radiographic examination

Plain chest radiographs were abnormal in 48 of the 69 cases (69.5%) in which it was the first examination. The commonest abnormality was diffuse loss of translucency present in 43 (89.6%) and as a single abnormality in 34 (70.8%). Focal opacities were present in 13 (27.1%), usually in combination with diffuse loss of translucency in 10 (20.8%, two of these also associated with mediastinal displacement), although in three cases (6. 25%) this was the single abnormality. Mediastinal displacement was apparent in seven (14.6%) cases, but never as an isolated finding. One patient’s film showed the deep sulcus sign [20] in association with mediastinal displacement.

Thoracic CT was abnormal in 11 of the 19 cases (57.9%) in which it was the first examination, with abnormalities detected including pulmonary contusion in 10 (30.5%), surgical emphysema in five (26.3%), pneumothorax in four (21.0%), haemothorax in four (21.0%), and pneumomediastinum in three (15.8%).

Overall, pulmonary abnormalities were detected radiographically in 59 of the 88 patients (67%) for whom role 3 radiology was available and given that these examinations were performed relatively early in the process of resuscitation it is probable that these changes were blast-related, rather than the consequence of trauma-related acute respiratory distress syndrome (ARDS).

5. Role 4

Demographic data for the 107 casualties who were evacuated to role 4 is presented in . No plain chest radiogram was performed on arrival in the UK in 11 patients. Three of these patients had head injuries and spent 84.6, 171.1 and 102.5 h, respectively, on intensive care; the remaining eight patients spent a median of 11.1 h on intensive care (range 1.5–49.9). One of these patients died within 2 h of ICU admission, the other 10 all survived to hospital discharge.

Table 2.

Demographic data for 107 military blast casualties admitted to UHB’s intensive care services in the period 1 July 2008 to 15 January 2010.

survived


blast lung by JTTR criteria


all yes no yes no
n 107 103 4 14 93
age (years)a 25. 5 (5.7) 25.6 (5.8) 24.5 (2.1) 24.0 (4.3) 25.8 (5.9)
males 106 (99.1%) 102 (99.0%) 4 (100%) 14 (100%) 92 (98.9%)
JTTR ‘blast lung’ 14 (13.1%) 13 (12.6%) 1 (25%)
rhVIIa 22/84 (26.2%) 19/80 (23.75%)b 3 (75%)b 6 (42.8%) 16/70 (22.8%)
massive transfusion protocol 46 (43. 0%) 43 (41.7%) 3 (75%) 7 (50%) 39 (41.9%)
injury to role 4 (hrs)c 38 (30, 51) 37.5 (30.1, 50.0) 49.0 (12.4, 59.4) 40.3 (37.3, 60.1) 37.0 (29.6, 49.9)
ICU length of stay (days)c 7.8 (4.2, 14.6) 7.8 (4.25, 14.6) 6.0 (0.9, 31.0) 11.8 (6.6, 17.7) 7.2 (0.3, 17.7)
APACHE II scorec 9 (5.75, 12) 9 (5, 12) 12 (8. 75, 21.25) 8 (6.5, 14) 9 (5, 11.5)
days of ventilationc 4 (1, 8) 4 (1, 8) 6.5 (1.75, 31.5) 6.5 (3.75, 11.5)d 3 (0.5, 7)d
survival 103 (96.3%) 13 (92.8%) 90 (96.8%)

Plain chest films were taken in the remaining 96 patients within a median of 3 (1.6–10.7) h of admission to the ICU. In 55 (57.3%) a tracheal tube was present. One or more radiological abnormalities was present in 66 (68.75%) of the films. Not surprisingly, the number of abnormalities on plain chest radiographs was loosely associated with the average PF ratio2 over the first 24 h of intensive care, and the duration of mechanical ventilation (). Five patients met the consensus criteria for the definition of ARDS.

Table 3.

Relationship between plain chest radiology, PF ratio during first 24 h and duration of mechanical ventilation.

number of radiological abnormalities on plain chest films taken on admission to role 4 intensive care


1 2 3
PF ratio (kPa) 45.9 (35.2, 54.2) 38.4 (28.5, 45.3) 36.8 (25.4, 44.4)
days of ventilation 2.5 (0, 5.75) 6 (3.75, 9. 5) 6 (2.25, 15.75)

6. Ventilatory management

Lung protective ventilation is the cornerstone of ventilatory management in the intubated blast injured casualties evacuated to role 4. Given that the vast majority of these casualties do not have isolated lung injuries, this forms only one component of their care, alongside management of their wounds and other injuries. Beyond an initial, brief (2–4 days), requirement for slightly more aggressive respiratory support3 in a minority, in the majority, the presence of blast lung injury is almost an epiphenomenon and has little impact on the casualties’ care, in that their need for respiratory support, particularly its duration, is determined by other factors. In others, its presence has more important effects and on occasions dominates the clinical picture; of the 107 casualties in this series, two were formerly referred to us for urgent consideration of extracorporeal membrane oxygenation (ECMO) although on both occasions this proved unnecessary, each being successfully managed with high-frequency oscillatory ventilation (HFOV) from the time of their arrival. This contrasts to blast lung in civilian terrorist events where the incidence of severe respiratory distress is higher, a phenomenon that may reflect the impact of explosions in enclosed spaces.

The principles of the lung protective conventional ventilation that we employ are based on the ARDS network protocol [21], with low tidal volumes (6 to 8 ml kg lbw−1), the application of PEEPe and limitation of plateau pressures to less than 30 cm H2O. Permissive hypercapnia is deliberately variably pursued dependent on the presence or absence of concerns around cerebral perfusion/raised intracranial pressure related to other injuries. In general, in the absence of concerns and metabolic acidosis, our target pH is 7.25–7.3. When concerns are present, particularly, where the trade-off between potential ventilator-induced lung injury and the need for control of PaCO2 are critical, we have used intracranial pressure monitoring to help guide our decisions. We recognize that the use of PEEPe in the management of blast lung injury is controversial; while a detailed review of our PEEPe selection in this series is beyond the remit of this paper, we have in general adopted the ARDS network approach and have to date avoided complications associated with air-leaks. This is in contrast to our management of lung injury consequent to penetrating and ballistic injury where we have adopted a more conservative approach to the application of PEEPe.

In most cases, conventional lung protective ventilation as outlined above has proved more than adequate for the respiratory support of the blast injured casualties in this series. In a small proportion of casualties, predominantly in the presence of ongoing sepsis with a profound systemic inflammatory response syndrome response where lung injury is likely to reflect more than just the consequences of blast, we have instituted HFOV as rescue ventilation when conventional ventilation is failing. Failure of conventional ventilation in our hands has predominantly been on the basis of failure of oxygenation (defined as a requirement for an FiO2 more than 0.6 for 4 or more hours when being expertly ventilated). In each event HFOV has proved highly effective and successful.

When using HFOV in this setting, either as rescue or ab initio, we have conceptually seen it as an extension of the concept of lung protective ventilation, and have aimed to exploit permissive hypercapnia to the same degree, accepting similar targets as we would during conventional ventilation. Where practical, we have also used controlled cuff deflation of the endotracheal tube to further enhance lung protection by reducing the need to drive CO2 clearance through changes in frequency and amplitude. In those casualties with the most profound lung injury receiving HFOV, hypercapnia rather than problems with oxygenation has presented challenges; to date when this has arisen active cooling, following the exclusion of a partially occluded endotracheal tube and detailed review of the oscillatory parameters, has proven effective. Contingency planning, should these measures have proved ineffective, has included the use of tris-hydroxymethyl aminomethane (THAM), extra corporeal CO2 removal and ECMO, but fortunately none has been required to date.

7. Conclusions

Blast lung injury appears to be a relatively common accompaniment to the polytrauma experienced by military casualties exposed to blast. In this series, of those casualties who survived to be received by the role 4 facility, none subsequently died as a consequence of lung injury. In our experience the majority of casualties with blast-related lung injury have been very successfully managed with conventional ventilatory support employing a lung protective strategy with only a small minority requiring non-conventional support in the form of HFOV.

Acknowledgements

The Royal Centre for Defence Medicine has funded the audit of this patient series.

Endnotes

1‘When a ball then passes close…there is, in the first place, a great addition to the pressure…from the condensation of the air: as soon as the ball is passed, this pressure, with a great part of the atmosphere, is taken off; the consequence of which is a sudden expansion of all the fluids in the stomach and the blood in its blood vessels, and the rupture of both. ’.

2Calculated as the arterial partial pressure of oxygen (PaO2) divided by the fractional inspired oxygen concentration (FiO2).

3Increased fractional inspired oxygen concentration, higher positive end-expiratory pressure (PEEP), and increase in the inspiratory to expiratory ratio.

One contribution of 20 to a Theme Issue ‘Military medicine in the 21st century: pushing the boundaries of combat casualty care’.

References

4. Blane G. 1785. Observations on the diseases incident to seamen, 1st edn. London, UK: Joseph Cooper [Google Scholar]12. de Ceballos J. P., Turegano-Fuentes F., Perez-Diaz D., Sanz-Sanchez M., Martin-Llorente C., Guerrero-Sanz J. E. 2005. 11 March 2004: The terrorist bomb explosions in Madrid, Spain—an analysis of the logistics, injuries sustained and clinical management of casualties treated at the closest hospital. Crit. Care 9, 104–11110.1186/cc2995 (doi:10.1186/cc2995) [PMC free article] [PubMed] [CrossRef] [Google Scholar]17. Dean D. M., Thomas A. R., Allison R. S. 1940. Effects of high-explosive blast on the lungs. Br. Med. J. 2, 224–226 [Google Scholar]18. Adler O. B., Rosenberger A. 1988. Blast injuries. Acta Radiol. 29, 1–5 [PubMed] [Google Scholar]21. The Acute Respiratory Distress Syndrome Network 2000. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N. Engl. J. Med. 342, 1301–130810.1056/NEJM200005043421801 (doi:10.1056/NEJM200005043421801) [PubMed] [CrossRef] [Google Scholar]

Music: a new cause of primary spontaneous pneumothorax

Primary spontaneous pneumothorax is defined as the spontaneous occurrence of pneumothorax in patients without apparent underlying pulmonary disease. It typically occurs in young, tall, thin, smokers. Although no apparent underlying lung disease is present, most patients present with some abnormalities in the affected (and sometimes also at the contralateral) lung. Subpleural blebs or bullae (emphysema-like changes, ELCs) are seen in most of the patients, as shown by high resolution CT scanning1 or during thoracoscopy or thoracotomy.2 The actual site of air leakage, however, can be located at the ELCs which may be ruptured in some cases,3 or elsewhere at the lung surface (“pleural porosity”).4 Alternatively, air can enter after alveolar rupture with an air leak into the peribronchovascular interstitium (causing pneumomediastinum) and ultimately into the pleural space.5 Whatever the exact site of the air leak, some kind of transpulmonary pressure difference between the alveolar space and pleural space—resulting in rupture of the alveolo-pleural barrier and penetration of air into the pleural space—has to be present.

We report four patients in whom five episodes of spontaneous pneumothorax occurred after exposure to loud music, a specific form of air pressure variation.

CASE HISTORIES

Case 1

A 23 year old non-smoking man of Tunisian origin was transferred to our clinic for management of a first episode of primary spontaneous pneumothorax. Five days before his admission he had experienced a sudden right sided pleuritic chest pain and dyspnoea while attending a pop concert, standing quietly within a few metres of several large loud speakers. His medical history was negative except for a familial myopathy characterised by generalised Ehlers-Danlos like ligamentary hyperlaxicity and muscle weakness. He was treated with a 24 Fr chest tube drain but was transferred for thoracoscopic pleurodesis because of a persistent (72 hours) air leak. At thoracoscopy several apical blebs were visualised, one of which was ruptured. The ruptured bleb was coagulated and a thoracoscopic talcage with 3 g sterile, asbestos-free talc was performed. The postoperative recovery was uneventful and persistent pleurodesis was obtained. Three days later the patient was discharged. Two months later a small partial recurrence of a right sided pneumothorax occurred. Because there was only a 1 cm air rim around the right lower lobe, no active treatment was proposed. After 5 days the pneumothorax had resolved completely. There have been no recurrences during a 3 year follow up period.

Case 2

A 25 year old man of Moroccan origin was transferred to our clinic for management of a first episode of primary spontaneous pneumothorax. The day before admission he had experienced a sudden pleuritic left sided chest pain while visiting a dance hall. The pain occurred when he was standing quietly in the vicinity of a loud speaker. His past medical history included asthma, retinal loosening, and a perforated tympanum after otitis media. He was an active smoker (20–30 cigarettes per day for 7 years). He was treated with manual aspiration using a 16 G catheter.6 After radiographic confirmation of re-expansion of the left lung, he was discharged the same day. There have been no recurrences in a 1 year period of follow up.

Case 3

A 23 year old white male smoker (10 pack years) was first seen with an episode of left sided primary spontaneous pneumothorax in November 1998. Because he mentioned that he had experienced two similar episodes of left sided pleuritic chest pain and dyspnoea in the past (which had resolved spontaneously), the diagnosis of recurrent pneumothorax was made and a thoracoscopic talcage was performed. Follow up was uneventful until February 2002 when he presented with a first episode of right sided spontaneous pneumothorax. A CT scan showed apical ELCs at both lung apices. A general work-up including measurement of α1-antitrypsin was negative. At the patient’s request a right sided thoracoscopic talcage was performed. In July 2002 a very small right sided recurrence of pneumothorax occurred while on holiday in Spain. No active treatment was proposed since there was only a small rim of air around the lower lobe. While discussing the pathogenesis and precipitating causes of recurrent spontaneous pneumothorax during a follow up visit, we mentioned having seen two patients in whom exposure to loud music was associated with the occurrence of a pneumothorax. At that moment the patient also recalled that both his first left sided pneumothorax and second right sided pneumothorax had occurred while attending a heavy metal rock concert.

Case 4

A 19 year old white male smoker had suffered a first right sided pneumothorax when driving a 125 cc monocylinder motorbike. A chest radiograph showed a complete pneumothorax which was successfully treated by simple aspiration. Two years later he had bought a car in which he installed a 1000 Watt base box in the boot as he liked to listen to loud music in his car. While doing this he experienced a sudden pain in the right side of his chest followed by breathlessness. He immediately knew that his pneumothorax had recurred and this was subsequently confirmed radiographically. He is convinced that the very loud music in his car triggered this recurrent pneumothorax. He was advised to undergo thoracoscopic pleurodesis but elected to await events.

DISCUSSION

This is the first report of primary spontaneous pneumothorax occurring after exposure to very loud music. Although the occurrence of spontaneous pneumothorax in these young men may have been coincidental, the exact temporal relationship between the symptoms and the exposure to loud music suggests this may have been the cause.

Sound is a form of mechanical energy characterised by wave front propagation through a physical medium. Propagation of sound pressure waves through the respiratory system is a complex three-dimensional problem, but it is bound to result in pressure differences at the interface between media of different densities. (air, alveolar surface water and tissue). These pressure differences could tear the alveolar or ELC walls resulting in an air leak into the pleural space. We propose three types of mechanism that could be involved in this process.

Firstly, primary blast damage to gas containing organs such as ears or lungs can occur if the mechanical energy of sound is very high, as in blasts or explosions.7 Very loud sounds at close range, as in our patients, could be considered as a miniature variant of “repetitive blasts”, causing a lung blast injury (pneumothorax). Blast injury has generally been attributed to direct mechanical damage—that is, rapid compression/decompression forcing air against various usually delicate compartments such as the alveolar septa, causing them to rupture.8 Besides its direct mechanical impact on the lung, blast injury has also been shown to induce biochemical changes such as antioxidant depletion and lipid peroxidation, both correlating with blast peak overpressure9 which may last for hours after exposure. These changes may be involved in the development of the structural abnormalities that predispose to spontaneous pneumothorax. Exposing the lungs to one high or several low energy blasts may precipitate alveolar or ELC rupture. The cumulative effect of repetitive insults to the lung parenchyma or pleura due to these vibrations could lead to injury of the alveolar walls after exposure to high energy impulse noises or blasts.10

A second mechanism may be linked to the presence of a so-called check valve mechanism responsible for a time delay in pressure equilibrium, and for overdistension of distal lung regions. Patients with primary spontaneous pneumothorax may have an inflammatory “bronchiolitis” with distal air trapping.11 Airway inflammation or mucus retention may cause a check valve phenomenon leading to intrapulmonary air pressure differences and possibly chronic anatomical changes (ELC or pleural porosity) and therefore pneumothorax. It is possible that loud music induces changes in atmospheric pressure that are less dramatic than those generated by blasts but which fail to be transmitted immediately to the region distal to this “check valve”. The resulting transpulmonary pressure difference may be sufficient to cause rupture of alveolar or ELC walls. In case 1, weakening of the alveolar surface may have been enhanced by the presence of the underlying Ehlers-Danlos-like connective tissue disorder which is often characterised by poor quality elastic tissue.

A third potential mechanism is related to a particular frequency band of the acoustic pressure wave spectrum. A series of publications has focused on the effects of exposure to low frequency (<500 Hz) high intensity (>90 dB) noise, a range of structural lung changes having been reported mainly in rats12 but also in humans.13 These data suggest that low frequency high intensity noise may lead to structural and functional changes in the airways, pleural mesothelium, and lung parenchyma. With frequencies from commercial loud speakers typically in the range of 30 Hz to 20 kHz, it is the lower frequency band of 30–150 Hz which is usually boosted in big music venues for enhanced effect. These low frequencies could indeed be particularly damaging to the lung parenchyma if they coincide with its natural frequency of around 128 Hz.14 Furthermore, Mahagnah and Gavriely15 showed that, in normal humans, the lung acts as a low pass filter with flat transmitted energy up to 100 Hz or 300 Hz. In view of these experimental results, the most compelling observation in our four patients is that the lower frequency band, which tends to be boosted in the kind of music they listen to, corresponds with those frequencies, thereby ensuring maximal acoustic energy transfer to the lungs.

We conclude that exposure to loud music may be a cause of spontaneous pneumothorax. Possible mechanisms for this observation are suggested. While it may be linked to the mechanical effects of acute transpulmonary pressure differences caused by sudden exposure to sound energy in association with distal air trapping, we speculate that repetitive pressure changes in the high energy-low frequency sound range are more likely to be responsible. Exposure to loud sounds should therefore be included in the list of precipitating factors for primary spontaneous pneumothorax and, as illustrated by case 3, should be asked for specifically when taking the history of a patient presenting with pneumothorax.

REFERENCES

  1. Bense L , Lewander R, Eklund G, et al. Non-smoking, non-alpha-1-antitrypsin deficiency-induced emphysema in non-smokers with healed spontaneous pneumothorax identified by computed tomography of the lungs. Chest1993;103:433–8.

  2. Schramel F , Postmus P, Vanderschueren R. Current aspects of spontaneous pneumothorax. Eur Respir J1997;10:1372–9.

  3. Weissberg D , Refaely Y. Pneumothorax. Experience with 1199 patients. Chest2000;117:1279–85.

  4. Ohata M , Suzuki H. Pathogenesis of spontaneous pneumothorax. With special reference to the ultrastructure of emphysematous bullae. Chest1980;77:771–6.

  5. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl Med J2000;342:868–74.

  6. Noppen M , Alexander P, Driesen P, et al. Manual aspiration versus chest tube drainage in first episodes of primary spontaneous pneumothorax. A multicenter, prospective, randomised pilot study. Am J Respir Crit Care Med2002;165:1240–4.

  7. Pizov R , Oppenheim-Eden A, Matot I, et al. Blast injury from an explosion on a civilian bus. Chest1999;115:165–72.

  8. Zhang J , Wang Z, Leng H, et al. Studies on lung injuries caused by blast under pressure. J Trauma1996;40:S77–80.

  9. Elsayed NM, Tyurina YY, Menshikova EV, et al. Antioxidant depletion, lipid peroxidation, and impairment of calcium transport induced by blast overpressure in rat lungs. Exp Lung Res1996;22:179–200.

  10. Phillips YY. Primary blast injuries. Ann Emerg Med1986;15:1446–50.

  11. Noppen M . Management of primary spontaneous pneumothorax: does cause matter? Monaldi Arch Dis Chest2001;56:344–8.

  12. Grande NR, Aguas AP, De Sousa Pereira A, et al. Morphological changes in rat lung parenchyma exposed to low frequency noise. Aviat Space Environ Med1999;70:A70–7.

  13. Reis Ferreira JM, Couto AR, Jalles-Tavares N, et al. Airway flow limitation in patients with vibroacoustic disease. Aviat Space Environ Med1999;70:A63–9.

  14. Wodicka GR, Shannon DC. Transfer function of sound transmission in subglottal human respiratory system at low frequencies. J Appl Physiol1990;69:2126–30.

  15. Mahagnah M , Gavriely N. Gas density does not affect pulmonary acoustic transmission in normal men. J Appl Physiol1995;78:928–37.

Curious Kids: what happens if you breathe pure oxygen?

The article has been republished from The Conversation under a Creative Commons license. Read the original article.

What happens if you breathe pure oxygen and why? Stephen, age 9, Muntinlupa City, The Philippines

Hi Stephen!

That’s a great question. We can’t live without oxygen. But too much can harm us. Let’s find out why.

Our bodies make the energy we need to run around, play and do schoolwork, by burning the food we eat. Think of this a bit like a candle burning. To burn our food, we need oxygen, which we get from breathing in the air around us.

Oxygen isn’t the only gas in the air. In fact, air’s mostly made of nitrogen. This has a very important job. Nitrogen slows down the burning process so you get enough energy through the day, bit by bit.

If you breathed pure oxygen, the energy from your food would be released all at once. So forget candles. This is more like a firework exploding. Bang! If you breathed pure oxygen, you wouldn’t actually explode. But you would damage your body.

Read more: Curious Kids: when I swipe a matchstick how does it make fire?

Breathing pure oxygen sets off a series of runaway chemical reactions. That’s when some of that oxygen turns into its dangerous, unstable cousin called a “radical”. Oxygen radicals harm the fats, protein and DNA in your body. This damages your eyes so you can’t see properly, and your lungs, so you can’t breathe normally.

So breathing pure oxygen is quite dangerous.

But breathing pure oxygen can sometimes be necessary. Astronauts and deep-sea scuba divers sometimes breathe pure oxygen because they work in very dangerous places.

The length of time they breathe pure oxygen, and how much they breathe, is carefully controlled so they’re not harmed.

Sick people, including premature babies in hospital or people in hospital with the coronavirus, might also need some extra help breathing. They might be given a bit of extra oxygen on top of what’s in the air. It acts like a medicine to help calm and settle their breathing.

Again, too much oxygen can be dangerous. That’s why doctors and nurses keep a close eye to make sure people get just the right amount they need.

So we need oxygen to help us get energy from our food. We might also need a little extra if we’re sick in hospital, or if we’re an astronaut or deep-sea diver. But too much oxygen can harm us.


Breathing pure oxygen sets off a series of runaway chemical reactions.

Effects of Explosion Shock Waves on Lung Injuries in Rabbits

The purpose of this study was to explore the damage effects and injury mechanism of free-field explosion shock waves on rabbit lungs. Six free-field explosion experiments, each with 500 g trinitrotoluene (TNT), were conducted as the shock wave overpressure acting on the rabbits was measured. The peak overpressure of the shock wave was 533, 390, 249, 102, and 69 kPa at the respective test points. Damage to the rabbit lungs caused by shock wave overpressure was investigated through observation, anatomical analysis, and hematoxylin-eosin (HE) staining processing. The shock wave overpressure of 69–102 kPa caused mild-to-moderate injury; the shock wave overpressure of 102–249 kPa caused moderate injury; the shock wave overpressure of 249–390 kPa resulted in moderate-to-severe injury; and the shock wave overpressure of 390–533 kPa caused severe injury to the rabbit. Mild, moderate, and severe injuries destroyed some, most, or all alveolar structures, correspondingly, as well as producing partial cell apoptosis. The overpressure damage mechanism primarily involves the collapse and rupture of pulmonary alveolus in the lung tissue. As a novel attempt, the investigation provided here may serve to improve the current shock wave injury mechanism.

1. Introduction

Explosive weapons may severely injure civilians as well as state officials during military conflicts and terrorist attacks [1–7]. Injury to the lung as induced by the weapons is one of the most dangerous, and even fatal, results of an explosion. The lung, as a gas-containing organ, is highly vulnerable to explosive overpressure and particularly susceptible to barotrauma [8–10]. The incidence of primary blast lung injury (PBLI) in immediate fatalities may be as high as 47% [11]. In a study on explosive injury victims who survived to emergency admission, PBLI was present in 11.2% of 648, 16. 2% of mounted injuries, and 17.1% of dismounted injuries in the same sample developed for PBLI, which is significantly associated with increased mortality [12, 13]. The main physiological characteristics of PBLI are pulmonary hemorrhage, edema, and microcirculation dysfunction, alveolar rupture, pulmonary bullae, and atelectasis; any or all of these may be present at varying extent of severity.

Form literature, previous researchers had explored lung injury effects and explosion shock wave mechanisms. Research showed that the functional and morphological damage to animals is most severe in combined injury groups. A high velocity fragment striking the extremity aggravates blast injury to the lungs. The most commonly injured organ in an explosion is indeed the lungs, which may be unaccompanied by any aggravation to the heart or abdominal organs [14]. Explosive experiments conducted on sheep have shown that the lung is most sensitive to trinitrotoluene (TNT) explosions, whereas the upper respiratory tract is most sensitive to muzzle explosion waves. The injury thresholds of overpressure were 29.0, 29.5, and 41.2 kPa for the upper respiratory tract, lungs, and gastrointestinal tract, respectively, at a single exposure. Repeated exposure (up to 60 explosions) also reduced the injury threshold of the internal organs. Existing safety limits protect 90% of the exposed population against internal organ injuries due to weak explosion shock waves [15].

Lung injury severity increases as the peak pressure and duration of an explosion increases. This relationship can be expressed with linear regression equations; the physical parameters of the underpressure can be used to indicate the severity of the injury to the lungs, as well [8]. Previous researchers had determined the threshold range of damage to animals under the action of two types of complex waves generated by TNT explosions [16]. The damage effects of blast overpressure and underpressure on the lungs of rats and rabbits were investigated with a self-made shock wave segmented simulator, for example, to reveal the mechanism of overtension effects in blast injuries [17].

There is a wealth of extant research on the biological effects of overpressure on the lungs [18–20]. However, the precise mechanism of injury is not known yet. In this study, we examined the damage effects and injury mechanisms of TNT explosion shock waves on the lungs of rabbits to explore the relationship between the physical parameters of the waves and internal organ injury. This analysis may serve to define effective safety limits for weak blast waves as well as safety limits on battle training for military personnel; our results may also be used to design weak blast wave protection devices.

2. Materials and Methods
2.1. Animals

A total of 32 adult male rabbits, each weighing 2.0–2.5 kg, were used in the experiment. Thirty of them were anesthetized using 1.5% pentobarbital sodium in a dose of 30 mg/kg per body weight and morphine (5 mg/kg) was used to relieve their pain. We divided them into six groups of five rabbits each. The remaining two (without anesthesia) were used as a control group. Procedures involving animals and their care were conducted in conformity with NIH guidelines (NIH Pub. No. 85–23, revised 1996) and were approved by Institutional Animal Care and Use Committee of the Navy General Hospital of PLA (People’s Liberation Army), China.

2.2. Overpressure Calculation

As planned, we estimated the peak overpressure of shock wave in a 500 g TNT explosion at different locations based on the empirical formula established by Sadovskyi. The calculated values were used to determine the distances of the rabbits from the center of the explosion. The target shock wave overpressure range was set to 75–550 kPa. Location distances were selected as 1.0, 1.2, 1.5, 2.0, and 2.5 metres (m), accordingly.

Sadovskyi’s empirical formula [21] is expressed as in the two following equations:where is the “contrast distance,” is the TNT equivalence, is the distance from the center of the explosion to the test point, and is the peak overpressure of the blast shock wave. Units are kg, m, and MPa, respectively.

2.3. Experimental Setup

Tests were conducted at the East Garden Experimental Base of Beijing Institute of Technology, which was designed specifically for explosion experiments. The layout of the experimental site is shown in Figure 1 and Supplementary Figure 1.

The explosion test system primarily consists of cylindrical TNT explosives, electric detonators, an initiator, trigger lines, pressure sensors, a multichannel transient recorder, and a high-speed camera. The connections among test parts are shown in Supplementary Figure 2. The distances between rabbits and the explosion center were 1.0, 1.2, 1.5, 2.0, and 2.5 m, individually. The TNT, pressure sensors, and rabbits were all placed 1.5 m above the ground. Free-field pressure sensors were used to measure the overpressure of each explosion shock wave. The TNT explosives were detonated by electric detonators as experimental data were gleaned and recorded by the multichannel transient recorder. The free-field explosion experiments were carried out in six replications each with 500 g TNT. The peak overpressures at the test points in all six explosions were determined by analyzing these data.

Prior to the test, the rabbits were anesthetized and fixed on brackets with ligaments so that their chests and abdomens faced the explosion center. Pressure sensors were properly fixed beside the rabbits. Sensors from the inside to the outside of the explosion center were, respectively, labeled as channels (ch) 1, ch 2, ch 3, ch 4, and ch 5, as shown in Figure 1. The high-speed camera was initiated at the moment the TNT was detonated to record the explosion process. The rabbits were removed from the brackets just after the experiment was completed. Injury to their lungs was judged by preliminary observation; then the rabbits were dissected to further observe the injuries. The lungs were then removed from the thorax, examined, photographed, and immersed in 10% formalin. The fixed lungs were sectioned, embedded with paraffin, and examined microscopically to observe histopathological changes. The animal’s anatomy and naked eye observation in the explosion field and the subsequent section production and treatment were all completed by medical chairs doctors of the Navy PLA at China’s General Hospital, Beijing.

2.4. Statistical Analysis

The explosion experiment was repeated 6 times. SPSS 24.0 software (IBM Corp., Armonk, NY, USA) was used for statistical analysis of experimental data. Comparisons of means among and within groups were performed using one-way repeated-measures analysis of variance (ANOVA). Differences in count data were tested for statistical significance with the Chi-square test. A value < 0.05 was considered statistically significant.

3. Results
3.1. Computational Simulation

A simulation model in ANSYS LS-DYNA was built to determine the relation between the TNT equivalent and distance from the explosion center based on the experimental scenario (Figure 2). The shock wave overpressures at the test points were calculated to glean the results discussed below.

The peak overpressures of the blast shock wave at different test points were obtained according to the empirical calculations and LS-DYNA numerical simulations as listed in Table 1. The empirical calculations and numerical simulation values are in close agreement. The formulas we used thus provided an accurate reference for the selection of experimental TNT equivalents and explosion distances.


TNT quality () Distance (r/m) Contrast distance Peak overpressure (kPa)
LS-DYNA M. A. Sadovskyi’s empirical formula

500 1.0 1.26 559 546
1.2 1.51 379 350
1.5 1.89 226 208
2.0 2.52 114 111
2. 5 3.15 78 71

3.2. Experimental Data on Shock Wave Overpressure

As discussed above, explosion experiments were carried out in six replications. The explosion process (from P1 to P9) was recorded by the high-speed camera as illustrated in Supplementary Figure 3. The interval between P1 and P2 was 1 ms; the interval between P2 and P3 was 9 ms. The interval between the photos shown below was 10 ms. The relations between the shock wave overpressure and time at different positions are delineated in Figure 3.

Figures 3(a)–3(e) are overpressure-time curves of the shock waves at distances of 1.0, 1.2, 1.5, 2.0, and 2.5 m, respectively. The curves measured by corresponding experiments were not as smooth as the curves obtained by numerical simulation. The experimental curves also had multiple peaks; the first peak was the target value of the experiment. The peak appeared earlier when it was closer to the explosion center, while subsequent peaks were formed by shock wave reflection and other interference factors. The shapes of the overpressure-time curves are different at different locations, which reflects the complexity of the interference factors in shock wave overpressure measurement.

The peak overpressure of the blast wave at different propagation distances was obtained according to the information shown in Figure 3. The average values of the six repeated tests were taken as the final measured values, as reported in Table 2.


TNT quality () Distance (r/m) Contrast distance Peak overpressure (kPa)

500 1.0 1.26 533
1.2 1.51 390
1.5 1.89 249
2.0 2.52 102
2. 5 3.15 69

For comparison among the measured, estimated, and simulated values of blast wave peak overpressure, three curves are plotted based on Tables 1 and 2, as also shown in Figure 4. In the beginning and the ending part of the curves, the experimental value was smaller than the empirical formula or numerical simulation values. In the middle part, the experimental value exceeded the other two. Generally speaking, the three curves were close enough to indicate sound agreement among the three sets of data.

3.3. Injury Situation of the Rabbits

The apparent medical damage to the rabbits’ lung anatomies was evaluated after each explosion. The damage was observed with the naked eyes initially and later by HE staining to determine injury to the lung tissue at the cellular level under a scanning electron microscope (SEM). The HE staining images of normal lung tissue are illustrated in Figure 5 and those of blast-injured tissue are demonstrated in Figure 6.

The normal lung tissue is clear: The cell membrane was well connected and the space tissue was intact. There was neither obvious hyperemia or edema nor inflammatory cell infiltration or fibrosis. No obvious exudate was observed in the alveolar space. The alveolar structure was normal and without any obvious rupture.

The alveolar structure was destroyed and inflammatory cell infiltration occurred in all blast groups regardless of distance to the explosion. A large number of inflammatory cells exuded (black arrows) and filled the surrounding alveoli. The alveolar structure broke, expanded, and fused to form bullae of lung (red arrows) with marked bleeding and localized atelectasis. Injury to the lung was more severe, however, when nearer the explosive center. The 10X microscopy showed near-complete destruction of the alveoli structure at 1.0 and 1.2 m with only a few normal structural alveoli. The cells were compressed and there was considerable bleeding in this sample as well. An abundance of inflammatory cells were present in the 40X microscopy with some apoptotic cells at the 1.0 m distance. Alveolar damage and the extent of hemorrhaging decreased as distance to the blast increased. The 10X microscopy showed normal partial alveolar structures at 1.5, 2.0, and 2.5 m, with relatively little bleeding. The 40X microscopy showed fewer inflammatory cells and no apoptotic cells at greater distance from the explosion center.

4. Discussion
4.1. Comparative Analysis of Shock Wave Overpressure

As shown in Figures 2 and 3, the overpressure-time curves obtained by the experiments are not as smooth as the typical shock wave overpressure-time curves; there were numerous interruption signals which affected the accuracy in the actual test process. Blast shock wave tests are usually carried out with multifragmentation, strong vibration shock, transient high temperature, and other parameters. The test process is typically influenced by several factors. For example, the signal produces a spike in interference when the ballistic wave produced by the fragment passes through the sensor surface. The explosive test is usually accompanied by strong mechanical shocks, such as seismic waves or the mechanical impact of the sensor mounting plate. In addition, high-temperature effects cause the measured overpressure shock curve to drift. The explosion also produced high-speed charged ions which form electromagnetic waves acting on sensors and connecting cables to produce interference signals in the pressure test channels. There was also drift on the test signal due to the low detection frequency of the test system. In short, the entire test system was multiple-input and single-output. The signals of shock wave overpressure were mixed with plenty of complex interference signals. Accordingly, it was essential to filter the shock wave to secure accurate results.

As shown in Figure 4, the measured peak overpressure of the blast shock wave diverged from the empirical and simulated values; however, the differences were fairly slight. In effect, previously published empirical formulas did have reference significance for estimating explosion shock wave overpressure. The numerical simulation method we used was also applicable in the early stages of prediction. Differences between the measured and estimated values were attributable to the disturbances in the testing process. Further, the estimated value can only be used as a reference; the actual value must be based on a physical experiment. The working condition of the empirical formula was the explosion of TNT spherical charges in an infinite air medium, which was not fully replicable in an actual experiment. Generally speaking, however, the overpressure test results were in line with the calculations.

4.2. Analysis between Damage Criterion and Experimental Results

We divided the level of injury across our sample into four levels according to the degree of destruction of the alveolar structure: mild, moderate, severe, and fatal (Table 3).


No. Distance (r/m) Peak overpressure (kPa) Injury level Injury situation

1 1. 0 533 Severe Alveolar structure completely destroyed; partial cell apoptosis
2 1.2 390 Severe
3 1.5 249 Moderate Most alveolar structures destroyed
4 2.0 102 Moderate
5 2.5 69 Mild A small number of alveolar structures destroyed

As shown in Table 3, the shock wave overpressure in 69–102 kPa caused mild-to-moderate injury to the rabbit; the shock wave overpressure in 102–249 kPa caused moderate injury; the shock wave overpressure in 249–390 kPa resulted in moderate-to-severe injury; and the shock wave overpressure in 390–533 kPa caused severe injury to the rabbit. The mild, moderate, and severe injuries, respectively, represented a small number of alveolar structures destroyed, most alveolar structures destroyed, and the alveolar structure completely destroyed accompanied by partial cell apoptosis.

Table 4 presents the traditional damage criteria of shock wave overpressure to the human body. The relationship between the shock wave overpressure and injury to rabbit lungs was far different from the data given by the traditional damage criterion, which was related to the posture of the rabbit in the experiment [22–24]. The rabbit’s chest and abdomen faced the explosion center in our experiment and the lung was the target organ of the explosion shock wave. Therefore, the injury to our rabbits was rather severe. It was crucial to rely on not only extant blast wave damage criteria but also experimental data as a primary evaluation criterion when evaluating the effects of shock wave overpressure. In addition, the characteristics of the experimental scene and experimental conditions must also be properly considered. The existing shock wave damage criteria did not account for any experimental conditions and were not supported by clear-cut test parameters or methodology. Objectives and comprehensive evaluations should be defined according to the specific situation (e. g., target object and target scene were explosion mode) to accurately assess the damage effects of blast shock waves. The damage criteria of shock wave should not be referenced unilaterally; impulse criteria of shock waves should also be considered.


Data sources Injury level
Mild Moderate Severe Fatal

American scholar 15.7 23.5 53.9 186.34
Former soviet scholar 19.6–39.2 39.2–98.0 235.4
Case statistics of explosion accident 10.8–27.5 27.5–49.0 49.0–127.5 127.5

4.3. Mechanism of Lung Injury in Rabbits

As shown in Table 3, the rabbits suffered varying degrees of damage under the action of different blast shock wave overpressures. The mechanism of lung injury related to hemodynamics theory and to the pressure difference between the fluid and gas phases in the lung. When the air blast wave acted directly on the chest wall, the volume of gas in the thoracic cavity decreased sharply and swiftly spiked the local pressure in the thoracic cavity (tens-fold or even hundreds-fold). The negative pressure led to a prompt expansion on the compressed air bubbles in the lung, which teared the surrounding capillaries and venules, causing bleeding and allowing blood to enter the trachea. The mixture of edema fluid and blood formed a pulmonary edema. Injuries to rabbits, from mild to fatal, were characterized by the amount of bleeding and severity of arterial air embolism.

4.4. Injury Effects of Shock Wave Overpressure on Rabbits

The shock wave can be divided into three stages according to the damage caused. The first damage effect originated in the peak overpressure of the blast shock wave. The second damage effect involved driving penetration or nonpenetration of rock fragments and other explosion fragments. The third damage effect was caused by the entire displacement of the target due to the shock wave and pneumatic pressure. The influence of all three factors must be considered when evaluating the damage effects of blast waves on rabbits as opposed to simply the overpressure; the duration of the positive pressure zone also merited careful consideration, as well as the specific impulse of the shock wave.

5. Conclusions

Six repeated experiments were conducted in this study to delve into the effects of blast shock waves on rabbit lungs. We compared theoretical calculations and experimental data including preliminary observations of injuries, medical anatomy assessment, and postprocessing of HE staining. The conclusions can be summarized as follows:(1)The blast shock wave overpressures estimated by numerical simulation and empirical formula were deemed accurate by comparison against the overpressure determined in the experiment.(2)The shock wave created complex injuries in the rabbits characterized by interactions among multiple factors (e. g., dominant overpressure, fragments, and posture). The shock wave overpressure defined in this study was 69–533 kPa, which caused mild-to-severe injury to the rabbits. Mild, moderate, and severe injuries were defined, respectively, by a minute number of alveolar structures destroyed, most alveolar structures destroyed, and alveolar structure completely destroyed accompanied by partial cell apoptosis. Our results diverged considerably from those in the extant criteria for shock wave overpressure. To this effect, the results may be used to modify, complement, and perfect the criteria to enhance their precision and efficacy.(3)The mechanism of lung injury was highly complicated and not yet exceptionally clear. Our results indicated that lung injury in rabbits was caused by pulmonary hemorrhage and pulmonary edema.

Data Availability

The data used to support the findings of this study are included within the article.

Conflicts of Interest

The authors declare that there are no conflicts of interest regarding the publication of this paper.

Acknowledgments

This work was financially supported by the National Key Research and Development Program of China (Grant no. 2017YFC0804700).

Supplementary Materials

Supplementary Figure 1: experimental site layout. Supplementary Figure 2: schematic diagram of test equipment connection. Supplementary Figure 3: pictures (P1 to P9) on explosion of 500 g TNT. (Supplementary Materials)

Can lungs explode? – AnswersToAll

Can lungs explode?

Lungs: There is a risk of pneumothorax, arterial gas embolism, and mediastinal and subcutaneous emphysema during ascent, which are commonly called burst lung or lung overpressure injury by divers. To equalise the lungs, all that is necessary is not to hold the breath during ascent.

Can you breathe in too deep?

Controlled, deliberate deep breathing should not be confused with ‘big breathing,’ which is taking in bigger-than-necessary volume breaths. This leads to over-breathing and can seriously mess with the delicate balance of the oxygen-carbon dioxide exchange taking place inside your body.

What happens if you have too much air in your lungs?

The result is that you have too much air in your lungs—a process called hyperinflation—which makes it harder for you to breathe. The damage to the air sacs in your lungs makes it harder for oxygen to pass into the blood vessels in your lungs, meaning less oxygen in your body.

Can you breathe in too much?

Excessive breathing creates a low level of carbon dioxide in your blood. This causes many of the symptoms of hyperventilation. You may hyperventilate from an emotional cause such as during a panic attack. Or, it can be due to a medical problem, such as bleeding or infection.

Why do I occasionally gasp for air?

The desperate gasping for air is usually a symptom of the heart no longer circulating oxygenated blood, or there’s an interruption of lung activity that’s reducing oxygen intake. It can often signal that death is imminent. If you see someone struggling to breathe, call your local emergency medical services immediately.

Why am I forgetting to breathe when falling asleep?

Central sleep apnea is a sleep disorder in which you briefly stop breathing during sleep. Moments of apnea can occur repeatedly throughout the night as you sleep. The interruption of your breathing may indicate a problem with your brain’s signaling. Your brain momentarily “forgets” to tell your muscles to breathe.

90,000 Check your lungs easy | Articles of the clinic Medservice

No breath means no life. To be healthy and energetic, you need to have even and easy breathing. What is your breathing? Maybe you don’t know something about yourself? This test should help determine if you have respiratory problems. Learn about your breathing quality by answering the following questions.

1. When calm, do you breathe through your nose or sometimes through your mouth?
Inhalation should always be done through the nose, except when pronouncing long phrases (speech breathing), exhalation is also possible through the mouth.

2. How many breaths and breaths do you take per minute while at rest?
If you are in good health, you should have 8 to 12 breaths per minute at rest.

3. Do you have breaks between inhalation and exhalation, between exhalation and next inhalation?
In a calm state, your breathing should be continuous, that is, there should be no breaks between inhalation and exhalation.

4. Lean your back against the wall or the back of a chair – in which part of your back do you feel movement when you inhale and exhale ?
It is normal if during inhalation you can feel the pressure of the back on the support in any of its areas.Most of the time, it is better to breathe with the lower part of the lungs, pushing forward the belly and lower back. This is the lightest breath.

5. Can you continuously pronounce the sound “ah” for 20 seconds?
If the longest exhalation is noticeably shorter, your breathing is too shallow, then all your internal organs experience oxygen starvation.

6. Does it happen that they say to you: you snore? Or maybe your voice sits down in the morning?
Being healthy means no such symptoms.

Respiratory disorders are most often associated with illness or poor physical fitness. To be healthy, to maintain ease of breathing, undergo spirography, learn everything about the functional state of the respiratory system.

If you are interested in the health of the respiratory tract, often have a cough or runny nose, you smoke, often work in the open air, go in for sports, come to the Medservice clinic and undergo a respiratory function test (spirography). The procedure is painless, safe and informative.

Breathe easily and freely and be healthy!

Dark Business: Strange Things We Do in Sleep

Recently, more and more people turn to doctors with complaints of sleep disorders, while some of them do quite extravagant things in their sleep actions.

Clinics specializing in such disorders are experiencing an unprecedented influx of patients.

This should not be surprising. In Britain alone, more than 30% of the population currently suffers from insomnia or other sleep disorders, according to the UK Mental Health Organization. This can have quite serious psychological and physiological consequences.

According to information from clinics, every week up to 50 new patients come to them on referrals – five times more than a decade ago. This solid increase is associated with increased awareness of the population about sleep disorders and the fact that more people began to talk about their problems to doctors.

In addition, clinics today are increasingly dealing with various oddities that people do in their sleep. However, some eccentricities are becoming more widespread. What is this oddity?

Blind dialing

Photo caption,

What happens in the head of a sleeping person remains a mystery to science

Technologies occupy a significant place in our life, so there is nothing incredible in the fact that we observe new forms of behavior in a dream related to them.

More and more people are complaining about sending text messages in their sleep, says Dr. Kirsty Anderson, head of sleep neurology at the National Health Service in Newcastle. With 92% of Britons owning a mobile phone today, this should come as no surprise. Many, falling asleep, put their cell phone next to them.

“It’s okay for people to do things in their sleep that they do regularly throughout the day,” says Anderson.

This behavior belongs to a group of disorders called parasomnia.These involuntary, undesirable actions performed in a dream can be either completely harmless, such as spontaneous opening of the eyes without awakening, or very dangerous: there are cases when people drove a car in a somnambulistic state. Anderson once had a patient who, in his sleep, could neatly take apart his grandfather’s clock.

What happens in our brain during such episodes is still a mystery. Very little research has been done on this topic, mainly due to the great difficulty in collecting data.

“The problem is that people rarely do this in a controlled setting,” laments Dr. Chris Idzikowski, director of the Edinburgh Sleep Clinic. equipment for capturing the behavior of people in their own beds. ”

The consolation is that SMS messages sent by people in a dream are often meaningless. Despite the fact that people in a dream repeat the same actions as during the day, it turns out, as a rule, more awkwardly.

Night gluttony

Photo caption,

Night gluttony can be experienced by those who have exhausted themselves with hunger or had a diet. The desire to eat something in your sleep is not too much of a problem, however, in more severe cases, it is already classified as a night meal syndrome, which must be treated.

Sufferers of this ailment can raid the kitchen several times a night, however, upon waking up, they do not remember anything about it.Often this leads to overweight, which entails a whole range of relevant problems – both physiological and mental. In addition, there is a risk of choking on food during sleep.

Like other strange sleep habits, nighttime gluttony often occurs against the background of various parasomnias, which, according to doctors, are regularly experienced by half a million people in Britain. Eating while sleeping is often related to what people did before going to bed.

“Sleepwalkers often do simple things that make sense to some extent, like going out to eat, going to bed hungry, or dieting all day,” says Anderson.

In more difficult cases – for example, when someone is engaged in cooking in a dream – in fact, the person is awake, but the next morning he does not remember anything about it. It’s a kind of amnesia, says Professor Jim Horn of the Sleep Research Center at Loughborough University.

“As a rule, they experience a state of confused awakening. In these, more extreme cases, this problem cannot be attributed to sleep itself. Often it can be, for example, a stressful condition that affects the quality of sleep,” explains Professor Horn.

Unbreakable sex

Photo caption,

A spouse who begins to molest in the middle of the night may not be aware of his actions.

Sexomnia, a disorder in which sleepers have sex, has only come into the public eye in recent years. According to experts, very little research has been carried out on this topic so far, but the number of applications with such complaints is growing.

The frequency of these abnormalities is influenced by stress, alcohol or medication.The disorder can manifest itself in different ways, ranging from small deviations that do not cause much concern to others, to full-fledged intercourse, sometimes with serious consequences.

Idzikowski acts as an expert in litigation, where in particular cases of rape and other sexual crimes are heard.

According to him, sexomnia is a manifestation of parasomnia. It most often occurs during deep sleep, when areas of the brain that are responsible for intelligent activity and control of the environment are turned off, but areas that regulate basic needs, including libido, remain active.

“This is an instinctive behavior. People at this time are not aware of their actions,” says Idzikowski. “In a state of deep sleep, people are not capable of making rational decisions or moral assessment of their actions.” According to the doctor, he is never tired of being amazed at what sleep disorders people can live with over the years, often without even realizing that they can be helped.

If a sleeping person stops breathing, it is often caused by a disorder known as obstructive sleep apnea syndrome.Although it is not something new, more and more patients are referred to specialized clinics with this diagnosis. Since obesity is one of the risk factors, experts predict that the number of visits will continue to rise.

With usually very loud snoring, sleep apnea occurs when the relaxed pharyngeal muscles collapse, blocking the upper airways. Cessation of breathing usually lasts a couple of tens of seconds, although in severe cases it can reach 2-3 minutes.To start breathing again, the sleeper needs to wake up for a short time, as a result the sleep becomes exhausting and does not bring rest.

“I was wildly scared when the doctors said that my breathing stopped for almost half a minute,” says one patient. I have a snoring problem but didn’t know it was that serious. ”

Dr. Idzikowski spoke about a 47-year-old truck driver who, due to respiratory arrest, was forced to wake up at night up to 50 times an hour.In extreme cases, this went up to 80 times.

“A person suffering from this ailment often does not remember their awakenings. Due to the lack of proper connection between the brain and the body, a person is awake, but is not aware of it. It can take about a minute for the brain to establish a connection with the body before a person is aware of himself woke up, – says the expert. – As a result, the patient is not able to fall asleep deep sleep, which is necessary for recovery. Waking up in the morning, such a person feels extremely overwhelmed. “

If a chauffeur, train driver, complex machine operator or air traffic controller experiences this kind of frustration, it can lead to great disaster.

“Brain Explosion”

Imagine: you are peacefully falling asleep in bed, and suddenly, like a bomb explodes in your head. This is called the “exploding head” syndrome – when a sharp deafening rumble is heard inside the cranium.

This is another case of parasomnia. Those who have experienced it describe it as a bursting of a shell, a thunderclap, a blow to the timpani, or a gun salvo emanating from the inside of the head while falling asleep.It doesn’t hurt, but it can be quite unpleasant. There are cases when people were in a hurry to look out the window, as they believed that somewhere nearby a bomb had exploded.

Photo caption,

Exploding head syndrome is painless and harmless, but it can seriously frighten complaints. She calls it the sensory equivalent of the sudden, sudden jolt or fall that many experience when falling asleep.

“People hear a really loud bang or bang the moment they fall asleep, and then it turns out that it couldn’t have happened outside because no one else heard it. Sometimes people see bright flashes of light,” says Anderson “This effect is not dangerous at all, but it can instill anxiety, so we just try to calm down those who come to us with complaints.”

However, in some cases, those suffering from exploding head syndrome have to prescribe medications: when people are so anxious that they are afraid to go to bed.

In most cases, such outbreaks occur haphazardly and it is impossible to establish any patterns. They can last for years and seriously affect the quality of life.

Film Without Brakes (2016) watch online for free in good HD 1080/720 quality

Paris. Plastic surgeon Tom Cox is on vacation for the first time. He wakes up his family: wife Julia, daughter Lizon and son Noah. They go to the sea. Julia is in her last month of pregnancy. The bell rings.This is Tom’s father Ben. He is going on vacation with his son’s family. Julia is unhappy. She demands that her husband not take Ben with them. But that was recently abandoned by his girlfriend, he needs to unwind. The family plunges into their newly purchased car, a bright red minivan. Tom is about to get under way, but Noah remembers that he forgot his spear gun at home. Tom says that they will buy exactly the same at sea. But then Ben asks to go to the toilet. Tom and Ben return to the apartment, Tom is looking for a gun. Ben in the toilet drops several rolls of toilet paper into the toilet, a blockage occurs, Ben quietly leaves the toilet and tells his son that he will wait for him outside.Tom finds a harpoon gun, hears some sounds in the kitchen, sneaks up, shoots. The spear flies past Ben’s face as he was eating cornflakes. Tom’s phone rings. His patient complains that her body rejects botox, her face is swollen. Tom says that nothing terrible is happening, this is not the first such operation for Madame.

Finally, the family hit the road. Tom stops at a gas station. Ben meets a girl whose hair is dyed purple. Her mother forgot her at the gas station, the girl (her name is Melody) did not take the phone, she does not remember her mother’s number.Ben hides it in Tom’s car. While wiping the windshield, Ben breaks the wiper. The car starts to move. Tom turns on cruise control, setting the speed at around 130 kilometers per hour. Ben asks his daughter-in-law about the unborn child: gender, name? She doesn’t want to answer, it’s their secret with Tom. But then it turns out that Tom told his father that they will have a boy, who will be named Gaspar. Julia is angry. She demands that Tom take her and the children back to Paris, while he and his father go to sea. Tom discovers that the cruise control system is out of order.The car does not want to slow down, the brakes do not work. Julia reads the instructions for the car, she does not find a solution to the problem. Melody discovers her presence in the car. Julia is outraged. The girl asks to drop her off at the nearest gas station. Tom calls the dealer who sold him the car. He is busy selling the same car, he does not give Tom any intelligible recommendations. Melody takes aim at Tom’s harpoon gun and demands that he stop the car. Noah and Lison shout at the girl. Tom tells his father that the gun is not loaded.He tries to disarm Melody, she shoots, the harpoon pierces the interior trim a few centimeters from Tom’s head. Tom’s car hits a yellow BMW on the side of the road and breaks its door. An enraged driver rushes in pursuit.

A couple of road police officers (man and woman) have sex in the roadside bushes. They see two cars, red and yellow, flying past at great speed. They get on their motorcycles and give chase. The gendarme catches up with Tom’s car, demands from the driver to stop.Passengers of the minivan write on the back of the SOS card, take the card out of the passenger compartment, it hits the gendarme’s face, he discards it, it sticks to the windshield of the BMW. Tom’s pursuer slows down, a police woman catches up with him, demands to show documents. The intruder disobeys and tries to hide. Ben invites Tom to step on the gas and then remove his foot. This leads to the fact that the cruise control now maintains a speed of 160 kilometers per hour.

Toll road ahead.The policeman asks Tom if he has a lot of gasoline. Enough for 850 kilometers. The gendarme calls his superiors. It is necessary to raise the barriers at the payment point and clear the way for Tom. Before approaching the toll booth, Tom discovers that the wrong side of the road has been cleared, he drives into the oncoming lane and passes through the toll booth. The same maneuver is repeated by the BMW driver. Patient Tom’s husband is calling. Her face was swollen even more. Tom tries to turn on the janitor, and as a result the glass is covered with foam. Ben gets out through the hatch and wipes the glass.Under the driver’s seat, the heating turned on, Tom’s body was cramped, he asks Ben to replace him. BMW catches up with them. The driver threatens Tom with violence, tries to push the minivan to the side of the road. Noah shoots the brute with a gun, the harpoon hits him in the thigh. Tom calls the car dealership again. The dealer has his own problems: a family of buyers was blocked in the salon of a new car, they feel sick, the car has to be opened with a grinder. No help for Tom again. A wasp appears in the cabin of a car rushing at great speed.Julia drives her out of the car with a newspaper. The wasp flies into a BMW, bites the driver, who crashes into a car standing by the side of the road. In a rage, he knocks out the cracked windshield and continues in pursuit. The gendarme accompanying Tom’s car is informed that a few days ago the same car showed a speed of 190 kilometers per hour. There was a girl there. The gendarme accused Julia of false pregnancy. She shows him her naked belly.

A giant traffic jam awaits Tom’s car 60 kilometers away.Julia’s phone rings. Their downstairs neighbor, artist Juan, complains about the flood. Tom is surprised at the close acquaintance of his wife with a neighbor, grabs her phone and hears Juan’s frank wishes addressed to Julia. Tom throws away the phone, gives his wife a jealousy scene. There is very little left before the cork. Children and Melody manage to be transplanted into the car on which the police are traveling. A helicopter comes to the aid of the rest of the passengers of the minivan. Julia is pulled out through the hatch. Then the car is hooked up with a cable, the helicopter carries the car through the traffic jam, while the roof of the car comes off, but Tom and Ben were not injured.Julia starts contractions right in the helicopter, she is taken to the hospital. A boy is born. They call him Gaspar. The family goes home. The elevator car suddenly stops. The light goes out.

Recommendations to the population on methods and techniques of behavior in case of fire

Practice shows that fires in residential buildings occur mainly due to ignorance and non-observance by the population of fire safety rules in everyday life. That is why the main causes of fires in the residential sector for a long time remain careless handling of fire, careless use of heating devices and household chemicals, violation of the rules for the operation of electrical wiring, various current collectors and gas stoves, children’s prank with fire.At the same time, fires in residential buildings are more often than others accompanied by the death and injury of people.

Fire brigade call:

Immediately report a fire to the fire department by phone “01” or by mobile phone “112”. When calling firefighters, you need to clearly state the name of the settlement or region, street name, house number, floor where the fire occurred. It is necessary to sensibly explain what is burning: an apartment, an attic, a basement, a corridor, a warehouse, or something else. Explain who is calling, give a phone number.

If you do not have a telephone in your house, and you cannot leave your house or apartment, open a window and call for help by shouting “Fire”, attract the attention of passers-by.

Fire extinguishing:

If the hearth of ignition is small, then it can be extinguished with clear and confident actions. Remember: the house always has the means to extinguish the fire – blankets, rough cloth, buckets and other containers for water.

In this case:

– Do not open windows and doors, or break window panes.It is necessary to avoid the creation of drafts and a strong flow of air into the room where the fire has occurred, because an inflow of fresh air will support the combustion and the fire will spread strongly. Therefore, it is necessary to limit the opening of windows and doors;

– Do not extinguish electrical appliances connected to the network with water. First of all, an electrical appliance that has caught fire must be disconnected from the mains, i.e. remove the plug from the socket and then fill with water. If there is no water nearby, then you can cover it with a thick blanket. On a burning TV, you can pour water on the back side, standing to the side of the screen, i.e.The heated picture tube may explode and injure you.

Evacuation of people:

If you see that you cannot cope with the fire, and the fire is rampant, then you need to urgently leave the premises and help people leave the premises.

First of all, it is necessary to remove the people who are there from the fire zone. At the same time, people are taken out of those rooms where the danger of their lives is most threatened in a fire, as well as from the upper floors of the building, and, first of all, young children, the elderly and the disabled are taken out.It is very important in winter with severe frosts to take warm clothes with you and warmly dress the children or wrap them in blankets. When leaving the premises, it is necessary to turn off, as far as possible, electricity and gas.

In case of fire, smoke accumulates in the upper part of the room, therefore, in case of strong smoke, you must bend over or lie on the floor, because toxic products of combustion with warm air rise up, covering the nose and mouth with a wet handkerchief or towel, and move on all fours or crawl towards the exit along the wall so as not to lose direction.

If the staircase in a multi-storey building is smoggy, you need to quickly open the windows on the staircase, or knock out the glass in order to release the smoke and provide an influx of fresh air, and close the doors of the rooms from where the smoke enters the staircase.

Do not try to get out through a smoky hallway or staircase (the smoke is very toxic), the hot gases can burn your lungs.

If the stairs are cut off by fire or heavily smoked, it is better to stay in the apartment and wait for the arrival of the firefighters.In this case, you should go to the balcony or go to the window and attract the attention of passers-by. Seal the door through which smoke can penetrate: wet rags, towels, sheets and, closing the doors tightly, try to plug the cracks between the door and the jamb as carefully as possible.

Rescue should be carried out on balconies, external stationary, attached and retractable stairs. Going down drainpipes and risers and using tied sheets is extremely dangerous, and these techniques are only possible in exceptional cases.It is unacceptable to jump from the windows of the building, because injuries are inevitable.

In case of burns:

When clothes catch fire, it is necessary to wrap the victim with a dense cloth or coat, a blanket, preferably wet, or douse with water. The flames can also be knocked down by rolling on the ground while protecting the head first. Do not let the injured run, try to rip off their clothes.

It is necessary to prevent the movement of a person, up to the use of a footrest. To completely extinguish the flame, eliminate any air flow under the protective cover.

An ambulance should be called to a victim in the fire by phone “03”, and while she is traveling – take the person out into the fresh air, freeing him from embarrassing clothing, do artificial respiration and rubbing the body. In case of burns, do not bandage the victim, but, on the contrary, take off his clothes. Do not touch anything that is stuck to the burns. You can apply a damp cloth to burns. Do not lubricate burns.

If you smell gas:

A strong smell of gas in the room is considered to be no less dangerous situation.Doors and windows must be opened immediately. You must not light matches and turn on the electric light, because the slightest spark can cause an explosion and fire. It is necessary to turn off the gas valve and call the emergency service by calling “04”.

If there is a gas network in burning rooms, it is necessary to turn it off as soon as possible. If you smell gas, avoid any activity that could cause sparks and increase the temperature in the room.

Remember:

1.If a fire started in your apartment, then first of all call the firemen, as a precaution, duplicate the call from another phone. If you cannot cope with the fire and you see that the fire is taking on threatening proportions, then remove everyone from your floor using the spare stairs on the balcony to the lower floors, or, if this is possible and provided for during the construction of your house, break the partition. separating your balcony from the adjacent section, and go to the adjacent balcony.

2.If the corridors and stairs are not too full of smoke, turn off the gas supply tap, turn off the electricity. Close all doors in your apartment (room, office, etc.) to avoid air inflow and fire spread. Leave on the safest route in this situation (you must study it in advance). Meet the fire brigade, indicate the place of the fire. Do not enter a building without permission from the firefighters.

3. If it is impossible to evacuate to the street on your own and if smoke has filled the corridors and staircase, then, in order to prevent the spread of fire and smoke, tightly close the front door of your apartment (office, office, etc.)and fill up all the cracks with wet rags. By pouring water on the door leaf, you can increase the time of its resistance to fire for a long time. If smoke has entered the room, try to crawl around. there is fresh air near the floor. Do not panic and do not try to get out on your own through the windows or balcony onto the street, firefighters will arrive in a few minutes, because the arrival time of fire departments in urban environments takes several minutes.

4. Do not try to take the elevator down.because in the event of a fire, all elevators are automatically turned off and the elevator shafts can be filled with smoke.

5. Regardless of whether the fire started in your apartment or in another part of your house, warn the firefighters by phone, do not assume that others have already done so.

6. Know how to use a fire extinguisher if available in the room. Before the firefighters arrive, help each other to save people and put out the fire.

7. Don’t panic. Panic is always the loss of the ability to find a reasonable way out.Avoiding danger is easier if you act calmly and intelligently.

Fire and rescue squad of the Admiralteisky region.

90,000 The doctor spoke about the increase in the number of patients with “lung rupture” due to coronavirus: Society: Russia: Lenta.ru

The number of patients with COVID-19 who have spontaneous “lung rupture” has increased. Oksana Stanevich, an infectious disease specialist at the First St. Petersburg Medical University named after Pavlov, an expert of the Just Ask service of the non-profit foundation of medical decisions “Not in vain”, spoke about this in a conversation with Lenta.ru.

“With this complication, air accumulates between the pleural layers (serous membrane of the lungs – ” Lenta.ru “), collapse occurs (decrease in volume and loss from the breathing process – ” Lenta.ru “) of the lung, it collapses and grows respiratory failure. This is already an acute surgical situation, it is necessary to drain the lung, let the air out, ”explained Stanevich.

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She added that ruptures most often occur in the most inflamed area of ​​the lung.However, sometimes even a small number of “frosted glass” areas are sufficient for this. Smoking and other chronic illnesses that damaged the lungs prior to COVID-19 could also affect the rupture.

According to Stanevich, a rupture can occur in any phase of the disease, but most often occurs during the second phase – on the 10-12th day of illness, when a person’s pulmonary symptoms worsen, as well as in the last third phase – after 12 days of illness, when inflammation in the lungs increases.

“At the very beginning of the pandemic, in the first wave, this was not the case. And already in the second wave, we began to notice such phenomena. There is a hypothesis that the coronavirus has acquired mutations that cause a stronger inflammatory response. Perhaps some genetic characteristics are involved, ”she summed up.

Earlier, the doctor Alexander Karabinenko estimated the likelihood of complete recovery of the lungs after coronavirus. According to him, the human lungs themselves are able to recover from the disease. However, the transferred pneumonia can lead to fibrotic changes, including shortness of breath and cough.

90,000 Read “Beyond the Dark Portal” – Rosenberg Iron S. – Page 56

Fortunately, Gruul kept all the dragon’s attention on himself, and none of the giants noticed the little man who was crawling towards them and was already ten steps from Deathwing’s head. Gruul struggled to wriggle out of the heavy, clawed paw that the dragon had gripped tightly with, and the dragon bent over to bite the gronn as Khadgar raised his arms and cast a spell.

Sensing the magic, Deathwing looked around and, watching Khadgar, laughed at the sorcerer.

– Again your tricks? – teased the dragon, narrowing his eyes like a cat. – How curious. Haven’t you realized yet that your strongest spells will not harm me? – but when Khadgar began to speak the words of the spell, the dragon’s eyes widened in alarm. – What the? … You pathetic bastard, I will silence you! Forgetting about Gruul, he turned and glared at Khadgar.

This look so horrified the magician that he almost forgot the end of the spell. Shaking his head, he pulled himself together and finished the mantra in a trembling voice.

A loud creak was heard from the dragon. Deathwing screamed, writhing in pain as the iron plates covering his body began to shift and slide off his body. Previously connected, they broke off and several of them completely fell off – and from those places, like from a volcano, lava erupted, flooding the ground of the valley. The armor really held Deathwing’s body together, and after Khadgar’s spell he began to crumble before our eyes.

– No! “Deathwing, if that was possible, was truly frightened.He stared at his wounds, then turned his glowing gaze directly to Khadgar. “You may have won the battle, but I will not forgive that. Cut it on my nose that I saw you, magician.

Khadgar swallowed, unable to tear himself away from the dragon’s gaze.

– With fire I have engraved your face in my memory! Deathwing continued, his voice trembling inside Khadgar. – I will come to you in dreams and in reality. Remember, I will return, and the last thing you ask me to do is to rid you of fear by death.

He unfolded his powerful wings and spread his claws, releasing Gruul and the skull, while he soared into the air and with one flap of his wings disappeared behind the mountains. Khadgar’s trembling legs finally gave up, buckled, and he collapsed to the ground and for a while just lay there, breathing heavily and repeating to himself that he was damn, damn lucky.

Without their father and ruler, the black dragons lost heart and lost confidence. One of the huge creatures, wounded and with a torn wing, immediately stopped fighting.

– Father! the dragon shouted, turning one last time to free its tail from the lesser gronn’s stranglehold. – Father, wait!

Spitting lava, the dragon burned the gronn’s hands, and when he cried out in pain and let him go, he rushed after Deathwing.

From the horror that Deathwing inspired, the ogres and gronn seemed to have gone mad. They threw themselves at the dragons that did not have time to escape, tearing them apart with fists and teeth, gnawing into their throats, throwing their bodies into the sky, where they bumped into rocky spiers.

Khadgar, taking advantage of the unrest that reigned around, lifted the skull thrown by Deathwing from the ground.

“Human … but strong. I feel a lot of potential! Oh yes, this is a young apprentice of Medivh? You can become even stronger if you have the courage to change your destiny. Why don’t you learn from me? I will show you, that blood and carnage are the keys to the truth … “

– Ah! Khadgar gasped, nearly dropping his skull. Gul’dan! He gritted his teeth and closed his mind.Even dead, Gul’dan was dangerous. He quickly hid the skull in a pouch and hurried to where Turalyon was still fighting.

“I have the skull,” he said to Turalyon, finding his friend at the writhing body of the dragon.

– Well done! Turalyon said. – Now we need to get out. Let’s retreat! Now! His squad quickly gathered, and soon Alleria and her rangers came up. The ogres and gronn were too busy slaughtering the dragons to notice their departure.

Turalyon quickly led them out of the valley.

“Your ploy was one hundred percent successful, Khadgar,” he remarked to a friend as soon as they left the battlefield. “We have the skull, and the dragons will no longer disturb us – they will no longer help the Horde.

Khadgar remembered Deathwing’s last words, and he couldn’t help shivering. He did not share Turalyon’s optimism, but nevertheless nodded in agreement.

– All that’s left is to deal with Ner’zhul. As soon as the book is in my hands, I can close the Portal.

All that remains is to stop the powerful shaman, who possesses the power of heaven and earth, from opening portals to countless worlds.On the other hand, they just forced the greatest dragon to retreat. Who knows, maybe they can cope with this task. One thing he knew for sure – if they did not stop the orcs now, on Draenor … they would never stop them.

Chapter 23

– Village Ahead! – Ba’rak reported, putting his hands on his knees and trying to catch his breath. Traces of caked blood could still be seen on his bandages, which were applied shortly after the Shattered Hand had left Hellfire Citadel on Kargath’s orders.But among their small squad, Ba’rak was probably the least affected.

And that’s why they were here.

“I’ll go there myself,” Kargat said to Ba’rak and others. “It’ll be faster this way.” He looked around at the other orcs. – Try to bounce back. When I return, we will continue on to the Black Temple.

Along the way, Kargath wondered how they had come to this. When Ner’zhul ordered them to contain the Alliance in Hellfire Citadel, it was obvious that he was sending them to certain death.No, neither he nor his warriors of the Shattered Hand feared death in battle, but to fall with honor is one thing, and to die uselessly is quite another. Leaving Ner’Zul and the others to be torn apart by the forces of the Alliance would be a shame for him and his entire clan, even if they fell in this battle. And that’s why, when Kargath saw that the Alliance broke into the citadel and broke the defenses, he gathered all the surviving warriors and went to his leader in the Black Temple. But the survivors were too few, and many were so wounded that they did not survive the first night.Now he had only a handful of warriors weakened from wounds.

Quietly striding forward, he noted significant changes in the surrounding nature. Much of Draenor was like Hellfire Peninsula – red soil, bare rocks. But why was the land he was walking on now was blossoming and green? He walked soundlessly through the dense grass, past bushes and lonely trees. Nagrand was unaffected by the corruption that had plagued their world. But why?

There was an irony in this – the greenest and healthiest part of Draenor was a home for the sick and weak orcs.Climbing a low hill, Kargath saw a small village at its foot. Dense walls, domed roofs near houses, wooden flooring – she looked like many Orc villages, including his native one. In a second, Kargath figured out how to capture the village and deploy his warriors here. They could not let the war break them down – Ner’Zul does not hope to see them again and will not be very upset if they do not come.