This article refers to the workings of Smith’s Medical Pneupac ParaPac and the newer ParaPac Plus. Other transport ventilators may vary in their settings and processes. Please check what unit your ambulance trust has before following the information here.
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The pressure of air inside our lungs is normally just right to not only ensure that negative pressure breathing occurs but also to prevent a shunt (where blood bypasses the lungs) (Hess & Kackmarek, 2014: 431), the oesophageal spinchter from opening, causing air to enter the stomach (Baker, 2012: 1), and a host of other potential problems. Any means of supported ventilation where the patient is not breathing for themselves produces positive pressure ventilation. Not only does this change the way air enters the patient’s lungs while they are ventilated, but it also comes with all of the above risks if any of the settings are incorrect, and more.
Many of the effects ‘are related to mean airway pressure [which is] […] the average pressure applied to the airway during the ventilatory cycle’ (Hess & Kackmarek, 2014: 420) With too ⇑ pressure comes ⇓ venous return (Hess & Kackmarek, 2014: 420) and ⇑ chance of barotrauma (Baker, 2016: 75).
To summarise, the potential negative effects are:
Blood bypassing the lungs (a shunt) (Hess & Kackmarek, 2014: 431)
Because modern ventilators are volume-controlled, preventing a different problem that occurs during pressure-controlled ventilation, there is a set tidal volume which the ventilator will always provide to the patient. To provide this volume, the pressure will constantly increase until the volume is reached (Baker, 2016: 132).
The Means of Avoiding These Problems
In ventilators, the pressure of an oxygen cylinder ‘is lowered through a reducing valve down to 30-90psi’ from 2000psi. It’s then delivered to the patient ‘to a maximum of 40cmh20 or 60cmh20’, (Baker, 2012: 18)*, depending on whether you’re in the UK or the US.
*cmh20 = centimetres of water pressure (SensorsONE, 2017)
Since we can’t have too much pressure there needs to be a way of stopping the ventilator if things get awry. The relief pressure is what this refers to. Via a safety valve (Baker, 2012), otherwise known as ‘exhaust valves’ the supply is cut and excess peak inspiratory pressure (PIP) is released into the atmosphere (Zaconeta et al, 2010), ‘prevent[ing] over-ventilation of the lungs’ (Baker, 2016: 145)
Why would the pressure get this high anyway?
‘The patient circuit […] [could be] blocked or kinked’ (Baker, 2016: 142). Best to check it.
‘If the lung compliance[*] is low and the airway resistance is high the pressure can rise to high levels’ because, as above, the pressure will keep rising until the set tidal volume is delivered (Baker, 2016: 142).
The wrong relief pressure settings.
*Compliance ‘refers to the ease of expansion of the lungs and the walls of the thorax’ (Baker, 2012: 8). Ordinarily, according to Baker (2012: 8), the value is 100 cmh20 but when ventilated it’s 40-50cmh20. Physical injuries and medical conditions may further alter this figure.
Which dial are you talking about?
This one
The Pneupac ParaPac (Smiths Medical). Photo highlights the Relief Pressure dial.
What should I set it to?
40cmh20 if you’re in the UK (Baker, 2012)
Why is the relief pressure set at 40cmh20 in the UK? Why is it 60cmh20 in the US?
Article 999 is struggling to find the answers to these questions. If you know the answers, please get it touch. It would be great to add the information to this resource.
This post is yet to be peer reviewed. Please get in touch if you have any comments.
[tabby title=”Super Summary”]
Article 999 previously posted an article on positive pressure ventilation, including its risks. The aim of positive pressure ventilation is to ‘maximise the potential benefit of mechanical ventilation while minimizing the potential for harm’ (Hess & Kackmarek, 2014: 407). The relief pressure dial on the ventilator ensures that the pressure of ventilation is not so high as to cause blood bypassing the lungs (Hess & Kackmarek, 2014: 407), the oesophageal spinchter opening (Baker, 2012: 1), barotrauma (Baker, 2016: 75; Hess & Kackmarek, 2014) and more. The ventilator’s other settings ensure that the patient actually receives ventilation, but the relief pressure setting ensures that a valve drains excess air when settings, poor setup, or the patient’s lung compliance (Baker, 2016: 43) have caused the pressure to get to high.
What should I set it to?
40cmh20 (Baker, 2012)
What should I look out for if the pressure is too high?
Kinked tubing (Baker, 2016: 142) & your settings
Read more in the Detail tab.
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References
Baker, D. 2012. Emergency and Transport Ventilation, an introductory guide, Smiths Medical International Limited: Luton
Hess, D.R. & Kacmarek, R.M. 2014. Essentials of Mechanical Ventilation. McGraw Hill Education: New York
SensorsONE, 2017. cmh20 – Centimetres of Water Column at 4 deg C Pressure Unit, Available Online: https://www.sensorsone.com/cmh2o-centimetres-water-column-4-deg-c-pressure-unit/ (Accessed 16/11/17)
Zaconeta, C.A.M. et al, 2010. ‘Evaluation of peak inspiratory pressure and respiratory rate during ventilation of a preterm infant lung model with a self-inflating bag by paramedics of the Fire Department’, Revista Paulista de Pediatria, vol. 28. No. 1.
Not endorsed by but with thanks to Smiths Medical for providing information.
Positive pressure refers to the way artificial ventilation ‘inflate[s] the lungs’ (Hess & Kacmarek, 2014). ‘Normal breathing depends on drawing in air to the lungs by creating a partial vacuum inside the chest cavity’ (Baker, 2016: vi). The mean airway pressure, an average combined of ‘the amount and duration of pressure applied during’ expiratory and inspiratory phases in normal breathing is negative (Hess & Kacmarek, 2014: 420 ebook). See the article on negative pressure breathing for more information. Intermittent positive pressure ventilation, on the other hand, is for inspiration the ‘exact reverse of this process with air being forced into the lungs’ (Baker, 2016: vi).
Positive pressure ventilation includes the use of bag-valve-masks, but the majority of this article will focus on the ventilator.
Upcoming articles will discuss the specific settings and how-tos relating to the Pneupac ParaPac ventilator. Current links:
Ventilators have 4 phases of operation:
1. ‘The inspiratory phase’
2. ‘Cycling between the inspiratory (I) and expiratory (E) phase’
3. ‘The expiratory phase’
4. ‘Cycling between the E and I phase’
(Baker, 2016: 117)
The majority of ventilators are set to an I (Inspiratory) to E (Expiratory) ratio of 1:2, i.e. the expiratory phase is twice as long as the inspiratory phase, ‘which mirrors normal breathing’ (Baker, 2016: 108). If required, some ventilators allow this setting to ‘be altered to assist with restrictive lung diseases’ (Baker, 2016: 108). ICU ventilators contain additional settings that alter this ratio, including a ‘respiratory pause’ between the I and E phases ‘to allow distribution of gas within the lungs’ (Baker, 2016: 108).
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Mechanics
So, inspiration occurs when air is ‘forced into the lungs’ (Baker, 2016: vi). Expiration, however, occurs when ‘the ventilator stops delivering a positive pressure and the patient breaths out passively, as in normal breathing. This passive expiration (E) is ensured by the elastic recoil of the lungs and the chest wall’ (Baker, 2016: 108). The timing is aided by a ‘pneumatic oscillator’ (Baker, 2016: 22).
The gas is delivered by the ‘patient circuit’, which also ‘evacuate[s] expired CO2’ (Baker, 2016: 109). This is delivered ‘as close as possible to the airway device being used’ by a valve (Baker, 2016: 109). There are also filters to prevent contamination of the ventilator from the patient.
Early ventilators had a ‘lack of interactivity with the patient’s own breathing efforts if there was only partial respiratory failure’ (Baker, 2016: 22) but modern ventilators tend to have different modes to account for this and additional settings beyond a simple tidal volume dial. In particular, ventilators feature a ‘demand valve’ which detects when a patient takes a breath (Baker, 2016: 22). There are also settings for tidal volume and ventilation frequency. These settings will be discussed in upcoming articles.
The main positive effect of artificial ventilation is fairly obvious: it assists with the ventilation of a patient who is completely or partially unable to breathe normally. There are however a number of negative effects created by positive pressure ventilation. Related to these is the fact that mechanical ventilation can cause ‘heterogeneity’ of the lungs, meaning that ‘some lung units are prone to overdistension and others are prone to collapse’ (Hess & Kacmarek, 2014: 493). These are part of the reason most ventilators have relief pressure settings. This setting will be discussed in an upcoming article. You can check back here for the link.
Positive pressure ventilation can cause or effect the following:
The following are unavoidable results of ventilator use:
Decreased cardiac output
…Leading to ‘hypotension and potential tissue hypoxia. This effect is greatest with high mean airway pressure, high lung compliance, and low circulating blood volume’ (Hess & Kacmarek, 2014: 513). The high pressure ‘decreases venous return and right heart filling, which may reduce cardiac output’ (Hess & Kacmarek, 2014: 513).
This pressure is normally lowest ‘during inhalation’, so venous return would be highest. But with positive pressure ventilation, ‘venous return is greatest during exhalation’ as opposed to inhalation (Hess & Kacmarek, 2014: 513-520).
Renal and gastric effects
Mechanical ventilation reduces urine output due to ‘decreased renal perfusion’ which results from ‘decreased cardiac output’ (Hess & Kacmarek, 2014: 527). Unfortunately this can cause many of the issues common with fluid retention. Similarly, gastric distension can result, along with gastrointestinal bleeding’ (Hess & Kacmarek, 2014: 533).
Increased intracranial pressure
…in head injury patients, due to ‘a decrease in venous return, which increases intracranial blood volume and pressure’ (Hess & Kacmarek, 2014: 540).
Pneumonia may occur, especially due to invasive ventilation which is the form in emergency practice (non-invasive refers to ventilatory support such as CPAP). It ‘results from aspiration of oropharnygeal secretions around the cuff of the endotracheal tube’ (Hess & Kacmarek, 2014: 499).
The following can occur as a result of ventilator settings:
Hyperventilation and hypoventilation
These risk effecting the pH, and causing respiratory alkalosis (Hess & Kacmarek, 2014: 499)
Oxygen Toxicity due to high oxygen levels (Hess, 2014: 506)
A Shunt is usually partly decreased but settings can change this:
A shunt is ‘perfusion (blood flow) without ventilation’, which happens ‘when blood flows from the right heart to the left heart without participating in gas exchange’ (Hess & Kacmarek, 2014: 427). There are two different types of shunts: capillary and anatomic. The first occurs when the alveoli are not ventilated. One example of this is pneumonia (Hess & Kacmarek, 2014: 427). The latter type of shunt occurs when blood flow ‘completely bypasses the lungs’, which can sometimes happen with ‘congenital cardiac defects’ (Hess & Kacmarek, 2014: 427).
Positive Pressure Ventilation’s typical effect is to decrease capillary shunt by improving ‘the distribution of ventilation, particularly by improving the ventilation of previously underventilated areas of the lungs’ (Hess & Kacmarek, 2014: 427-446)
Despite the above improvements, if the settings are not ideal hypoxemia can result. This is the same outcome as a shunt but would in this case be caused by ‘redistribution of pulmonary blood flow to unventilated regions’ due to ‘overdistension of some lung units’ (Hess & Kacmarek, 2014: 324). Positive pressure ventilation can also increase anatomic shunt (Hess & Kacmarek, 2014: 441)
Also due to incorrect settings, the following can occur as a lack of pressure or volume:
Atelectasis occurs when the pressure or volume during or after artificial ventilation isn’t enough to inflate the lungs –> complete or partial collapse.
Atelectasis ‘is larger with obese patients and when a higher fraction of inspired oxygen (FI02) is used […]. During mechanical ventilation […] atelectasis may occur when lungs are underinflated due to low tidal volumes, or when compression occurs (such as patient position or obesity)’ (Open Anesthesia, 2017). If the volume or pressure isn’t enough to ‘prevent the alveoli from collapsing’ (Open Anesthesia, 2017) then regardless of ventilator type (pressure vs volume controlled) atelectasis may result.
The following can occur as a result of apparatus setup:
Dead Space can be increased by mechanical ventilation (Hess & Kacmarek, 2014: 471). It may be ‘reduced by an artificial airway (ETT) but is increased by increasing distance from the end of the ETT to the means of evacuating CO2 in mechanical ventilation’ (Baker, 2016: 111). Size, age, upright postures and neck extension also increase it (Baker, 2016: 111).
The following can occur due to overdistension:
Barotrauma = ‘alveolar rupture due to overdistension’, which can cause numerous problems including pneumothorax (Hess, 2014: 480). Volume generators have a ‘safety valve which activates at a preset pressure’ to avoid barotrauma’ (Baker, 2016: 118). This will be discussed in an upcoming article.
Ventilator-Induced lung injury caused by overdistension. Massively effected by ventilator settings for tidal volume and relief pressure (Hess, 2014: 493)
There are additional risks of positive pressure ventilation, particularly mechanical ventilation. Some of these are related to the use of airway adjuncts. Others are related to the removal of the ventilator. To read more, check out the references below.
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Types of Positive Pressure Ventilation
‘A spectrum of modes exist between total artificial ventilation and a patient who is still breathing spontaneously but with reduced efforts’ (Baker, 2016: 105).
There are two main types of ventilators:
– Pressure generated
– Volume generated
Pressure generators ‘provide a constant pressure during the inspiratory phase’ (Baker, 2016: 118). Volume generators release gas once a set volume has been reached. In each one, only the pressure or the volume is a constant. Everything else is relative and will adjust until the preset parameter of volume or pressure has been reached (Baker, 2016; Hess, 2014).
Issues
‘The problem of pressure generation is that it cannot guarantee an adequate Vt [volume] in situations where the lung mechanics are abnormal or where a guaranteed Vt is required due to life-threatening hypoxia. They are therefore not suitable for most emergency ventilation, with the notable exception of neonatal and infant ventilation where flow generators are contraindicated due to the fragility of the lung tissue’ (Baker, 2016: 118).
Additional Types
Most ventilators switch from inspiration to expiration by ‘time cycling’ (Baker, 2016: 119). However, this can also be due to volume or pressure cycling. The time cycling ratio is usually 1:2 for I:E, in other words the expiration time is twice as long as the inhalation time. ‘Ventilation modes can best be understood as a spectrum describing the work of breathing done by the ventilator and by the patient’ (Baker, 2016: 122.
The modes are: Controlled Mandatory Ventilation, in which ‘ventilation is provided entirely by the ventilator’ (Baker, 2016: 122), Assisted Controlled Ventilation which is fairly self-explanatory, and Synchronised Mandatory Ventilation, in which ‘the patient’s respiratory efforts in initiating a ventilation are synchronised with ventilations provided automatically by the ventilator.’ This is best used to supplement the patient’s efforts. It’s otherwise known as ‘assist-control’ and is typically found in ICU. (Baker, 2016: 123).
In portable ventilators the modes are:
Intermittent Mandatory Ventilation, Synchronised intermittent mandatory ventilation, and synchronised mandatory minute volume but only the latter two are still in use. The second overcomes the problems of the first, ensuring that breaths are supplemented by the ventilator and that supplemented breaths are activated only when there is a certain trigger e.g. low pressure. There is a modern, more complex version of this now in use in hospitals but this may exist in emergency ventilation practice to assist a patient who is ‘in partial respiratory failure’ (Baker, 2016: 124).
The first two divide minute volume between the ventilator and the second. The latter is based on time, which is compared with a ‘set minute volume. If there is a discrepancy between the actual minute volume and the set delivered minute volume, an automatic ventilation is delivered which corrects the difference’ (Baker, 2016: 124).
Because there is an issue of the ventilator being unable to tell the difference between dead space ventilation and alveolar ventilation, Pneupac have modified the above with a series of Ifs (if the patient takes a breath, if there is no further breath, if the tidal volume is too low, etc) that adjusts settings accordingly (Baker, 2016: 124). There are more modes that exist for ICU ventilators, which tend to be a lot more complex in design (Baker, 2016).
CPAP is also a form of positive pressure breathing and is designed ‘to improve oxygenation in lungs that may not be exchanging oxygen with the blood adequately’ (Baker, 2016: 126). There is a constant pressure in CPAP, versus ‘different pressures during inspiration and expiration’ in BIPAP’ but both are designed to allow the patient to do all the work of breathing. They merely increase oxygen and make inspiration easier while increasing the work of expiration. ‘Breathing with CPAP has been compared to the sensation of breathing against a very strong wind’ (Baker, 2016: 128). They ‘open up (recruit) alveoli in the lungs that may be non-ventilated.’ (Baker, 2016: 127). Both push back fluid ‘into the circulation via lymphatic drainage of the lung interstitial space’ and increase ‘the diffusion of oxygen into the pulmonary capillaries’ (Baker, 2016: 127).
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PEEP
Positive End Expiratory Ventilation applies ‘a positive pressure to the patient during the expiratory phase’ to ‘increase the functional residual capacity of the lungs and thus the efficiency of oxygenation of the blood’ (Baker, 2016: 126). ‘In order to be able to deliver a set tidal volume against variable lung compliance and airway resistance, resuscitation ventilators should be time-cycled, volume preset flow generators’ (Baker, 2016: 132).
There is a common misconception that if someone experiences heart burn it is because they have too much stomach acid that is passing up the lower esophageal sphincter (LES). The LES is the valve which, in a healthy person, prevents this from happening. Interestingly, many patients presenting with heart burn actually have LOW stomach acid, which results in the same symptoms.
[tabby title=”Super Summary”]
• Low stomach acid is more likely to be the cause of heartburn
• Bloating and food intolerances may be heightened by low stomach acid
• Anti acid medications can make the problem worse
• Getting into a decent sleep pattern can make all the difference.
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The Stomach’s locationThe stomach in relation to other organs
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Low stomach acid is the result of many factors that come into play at the same time. These factors, or causes are common in our modern day lifestyle, far more common than the causes of potentially high stomach acid. Their prevalence means that in the majority of cases you can be pretty sure that the cause of heart burn is not high but low stomach acid.
Attributing causes are:
• Poor sleep
• Under eating (e.g on a diet)
• Stress
• Too much exercise in a calorie deprived state
• Over use of antibiotics
• Regular use of NSAIDs
• H Pylori
• Eating too quickly
• Small intestinal bacteria overgrowth
• Yeast infections
• Food sensitivities
• Age
• Alcohol
Now if you look through the list above you probably know a few people (if not many) who fit into at least 3 or 4 of those categories. If nothing else most people are sleep deprived and even if they do actually get to bed, the quality of their sleep is poor and broken. A high number of people have been on some kind of diet (which usually means calorie restriction) for many years. They are likely stressed and probably have a drink now and then.
As you can see, it’s easy to live what is considered an apparently ‘normal’ lifestyle nowadays, a lifestyle that causes low stomach acid.
[tabby title=”What is Stomach Acid & Why Is It Important?”]
Stomach acid is also called hydrochloric acid due to its chemical structure of one hydrogen ion combined to one chlorine ion, making HCL. It is responsible for sterilizing any food that wishes to make it into your gut. It assists with killing off viruses, yeast, parasites and breaking down protein.
Its most important role is the breakdown of protein in to its constituent amino acid parts, ready for absorption later in the digestive process.
So, without adequate levels of stomach acid, there is a vicious cycle of poor digestion, chronic gut inflammation, microbial overgrowth, leaky gut, elevated stress hormones and lowered nutrient absorption. The only things that will break this loop are to reduce stress in all its forms and support adequate stomach acid production.
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[tabby title=”So What’s Wrong With Omeprazole?”]
This is the problem with mistaking low stomach acid symptoms for high stomach acid:
The GP will recommend any one of a number of anti-acid medications such as Omeprazole, or the patient will self medicate with over the counter remedies such as Rennies or Gaviscon.
If this is the case it will stop the feeling of heartburn BUT it will actually push the stomach acid down even further. Once this happens the health of the patient will decline over time due to even poorer absorption of nutrients, higher chances of bacterial infections and higher elevation of stress hormones.
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So what’s the answer?
Its pretty simple really. The first thing to do is manage the lifestyle factors causing the issue in the first place. Better sleep, manage stress, less alcohol, etc.
From a support point of view a good digestive enzyme that includes HCL with each meal would be all you really need to stop the pain immediately. For good measure, a 30 day course of probitiocs to improve the good bacteria in the gut would be a positive step.
[tabby title=”Questions To Be Answered Soon”]
Should we continue encouraging patients to try their own gaviscon in non-cardiac sounding chest pain as a one-off measure to see if it resolves the pain?
If the gaviscon does resolve the pain, what does this tell us about the likely cause of the chest pain? (Remember, trop-t levels may still be necessary).
Do acidic or alkaline foods affect the reflux much?
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This was the first of Article 999’s Guest Posts, posts that have been written by other professionals. These posts, unlike the remainder of Article 999’s, are not referenced to academic sources as they are the expert opinion of the author. These posts are additions to the category of ‘nice to know’. Please remember to check your local guidelines and read our full disclaimer before putting into practice anything you see here.
Comments? Questions? Let us know what you think by adding your comments below.
This post is yet to be peer reviewed. Please get in touch if you have any comments.
Negative pressure breathing is how we breathe normally, without the aid of bag-valve-masks or mechanical ventilators.
Inspiration – Normally
Breathing in is produced by ‘contraction and downward motion of the diaphragm [which] causes a negative pressure in the chest’ —–> inspiration. (Goldberg, 2014: 51, emphasis added)
Inspiration is therefore a muscular process (the diaphragm is a muscle) which is normally mainly reliant on the diaphragm. However, accessory muscles including the ‘pectoralis major and minor’ may also be used and are ‘vital to survive in certain pulmonary conditions’ (Goldberg, 2014: 51).
Let’s explain this by breaking it down:
Why does a contracting diaphragm cause negative chest pressure?
Because the volume has increased. This process is represented in Boyle’s Law (Rice University, 2016). Put simply, more space = more volume. When there’s more space in the chest, as with the contracting diaphragm, there is more room for air particles to move. They’re not crammed in any more, so there’s not much pressure.
On the other hand, when those air particles are tightly squeezed in a smaller space, there is less pressure.
To summarise:
more space = more volume
less space = less volume
more volume = less pressure
less volume = more pressure
Tightly squeezed particles in little volume cause a lot of pressure
Free moving particles in a lot of volume cause less pressure
Why does negative pressure cause inspiration?
This has to do with the laws of thermodynamics. ‘For anything to happen, energy has to move or flow or change’ and ‘energy has an absolute unfailing tendency to go from “more concentrated” to “less concentrated”‘ (Watson, 2014).
So, it’s not so much because there is a negative pressure that we inhale. It’s because there is a change in pressure. When the diaphragm contracts, the pressure changes from high to low. Now there is no equilibrium. One of the laws of the universe (which is called a law because it’s been observed over and over again in different ways) occurs as a result: energy attempts to shift toward equilibrium. And the way it does that is by moving from an area of high pressure (outside the body) to one of low pressure (inside us).
This is ‘largely passive’, frequently happening ‘without any muscle action’ when relaxed. The contracted diaphragm simply ‘springs back into shape’ (Goldberg, 2014: 51). However, using the ‘external and internal intercostal muscles’ amongst others, you can ‘voluntarily exhale forcefully’ (Goldberg, 2014: 51).
Either way, this process creates more pressure because there is now less volume (less space) for air particles to move around. Following the laws described above, air moves from an area of high pressure (the lungs) to an area of low pressure (outside) (Collison et al, 2002: 57; Watson, 2014).
It’s intuitive that this change in pressure and lack of equilibrium (Watson, 2014) will ensure that the process repeats itself. Each time the diaphragm contracts, the volume changes so the pressure changes. Air flows inside. Then there’s too much pressure and less volume as the diaphragm is returning to shape (Goldberg, 2014). So air flows out. Then the diaphragm contracts again…
References
Baker, D. n.d. Emergency and Transport Ventilation: an introductory guide, Smiths Medical International Limited: Bedfordshire
Collison, P. et al, 2002. Nelson Modular Science: 2, Nelson Thornes Ltd: Cheltenham.
Goldberg, S. 2014. Clinical Physiology made ridiculously simple, MedMaster: Miami.
Rice University, 2016. The Process of Breathing, Available Online: https://opentextbc.ca/anatomyandphysiology/chapter/22-3-the-process-of-breathing/ (Accessed 01/11/2017)
Watson, D. 2010. The Second Law of Thermodynamics, Available Online: http://www.ftexploring.com/energy/2nd_Law.html (Accessed 01/11/2017)
This article has not been endorsed by any company.
With thanks to Smiths Medical for providing information.
This post is yet to be peer reviewed. Please get in touch if you have any comments.
This post is due to be peer reviewed. All of Article 999’s posts will soon be updated with this image, or with an image that shows 1 or more, or 10 or more individuals have peer reviewed that post.
Over the coming weeks and months, Article 999 aims to build a video library of skills and equipment, and in the future, scenarios. The aims are to make it easier for all operational staff to access refreshers or aid their training, while also enabling students to learn how to find and use equipment.
These videos should add to a resource that provides information that is easy to find and quick to learn from. Importantly, all of our videos have been produced based on publicly available information that is referenced, and all of them have been created by and for operational staff in the UK.
Feedback is welcome. As with all of our content, please remember to check local guidelines and read our full disclaimer before putting into place anything you see or read here.
Presenting one of our videos, I Gel: Why, What, When, How?
This video has been reviewed by one or more individuals. No drastic changes have been suggested but improvements will be made to future videos. Let us know if you have any feedback in the comments below.
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Section 2 – Purpose: Admission for patient assessment.
Duration of section: 28 days
Section 3 – Purpose: Admission for treatment of a patient.
Duration of section: up to 6 months
Section 4 – Purpose: Urgent admission for patient assessment from the community, usually enforced when a section 2 would take to long to enact.
Duration of section: 72 hours (may be converted to section 2 to extend assessment period to 28 days)
Section 5(2) – Purpose: Urgent detention of inpatient
Duration of section: 72 hours
Section 5(4) – Purpose: Urgent detention of an inpatient by a nurse were a doctor is absent
Duration of section: 6 hours
Section 135 – Purpose: Removal of person from home to place of safety. This requires a court order to enact and remove someone from a private property.
Duration of section: 72 hours
Section 136 – Purpose: Removal of a person from a public place to a place of safety. This does not require a court order.
Duration of section: 72 hours
Community Treatment Order – Purpose: An order that a patient is placed upon after discharge from hospital for psychiatric treatment that allows continued treatment within the community setting.
Duration of section: up to 6 months.
References
Crown Copyright (1983) Mental Health Act 1983 [online]. Available at: http://www.legislation.gov.uk/ukpga/1983/20/contents (Accessed 21/07/17) (amended by the Mental Health Act 2007)
J. Collier, M. Longmore, T. Turmezel and A. R. Mafi. Oxford Handbook of Clinical Specialties, 8th edition, Oxford University press, 2008, pp: 398-401
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A sectioning order is legislation powers given to health care professionals and police officers under the Mental Health Act’s of 1983 and 2007 that allow for compulsory admission of an individual to hospital or a place of safety. These are enacted if a patient is judged to have a mental disorder that is sufficiently severe to require treatment for said disorder or to remove a person to a place of safety who could be at risk of being a danger to themselves or the public.
References:
Crown Copyright (1983) Mental Health Act 1983 [online]. Available at: http://www.legislation.gov.uk/ukpga/1983/20/contents (Accessed 21/07/17) (amended by the Mental Health Act 2007)
J. Collier, M. Longmore, T. Turmezel and A. R. Mafi. Oxford Handbook of Clinical Specialties, 8th edition, Oxford University press, 2008, pp: 398-401
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There are several different types of sectioning orders as listed in the relevant tabs. Each one is used for different purposes, lasts for different lengths of time and can be used by a variety of different health care professionals and police officers. However, not everyone may use every type of order. The following are the sectioning powers available to the following professions:
Nurses: Section 5 (4)
Doctors: Section 5 (2)
Police Officers: Sections 135 and 136
A mental health professional and doctor:
Approved mental health professionals (social workers, nurses, psychologists or occupational therapists) and rarely relatives may also put an application in for sections 2, 3 and 4. These all require approval by 1 or more doctors to be carried out.
References
Crown Copyright (1983) Mental Health Act 1983 [online]. Available at: http://www.legislation.gov.uk/ukpga/1983/20/contents (Accessed 21/07/17) (amended by the Mental Health Act 2007)
J. Collier, M. Longmore, T. Turmezel and A. R. Mafi. Oxford Handbook of Clinical Specialties, 8th edition, Oxford University press, 2008, pp: 398-401
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An summary of a Krausz et al (2009) article discussing the importance of effective airway management in the maxillofacial trauma patient and the complexities that such an injury presents. Only points relevant to UK paramedics have been included. For more details, please read the original article. Any additions made by Article 999 are in square brackets [].
Remember to follow ATLS protocol [and/or your local guidance and JRCALC guidelines]
Use cervical spine control along with effective airway management
‘The most common critical care errors are related to airway and respiratory management. Gruen et al studied 25 trauma mortality patients […] [and] found that failure to intubate, secure or protect the airway was […] responsible for 16% of inpatient deaths’ [and that was in a trauma centre, albeit in 1996-2004!] (Gruen et al, 2006)
Hutchinson et al (1990) (in Krausz et al, 2009) found 6 potential ways maxillofacial trauma might prevent effective airway management.
These, from the top of the head downwards, can be summarised as:
Head and soft tissue trauma
– These risk ‘delayed airway compromise’
Nasal bleeding/open wounds causing obstruction
Mandible fractures
– Leading to the tongue to drop back, blocking the oropharnyx
– Leading to blockage of the nasopharnygeal airway
Mouth obstructions
– From loose items & bodily fluids
Tracheal trauma
– Leading to swelling and displacement of essential airway structures behind them.
C-spine injury
– Leading to the need for “in-line stablization”. This can cause a reduced view during intubation
– The act of intubating might increase neck movements, potentially worsening this injury
Stomach
– [All patients ambulance personnel intubate in the prehospital environment might realistically have a full stomach]
– Note the risk of regurgitation
– Consider cricoid pressure – but also consider that this might ‘worsen the larnygeal view’
– Other tips noted in this section are not relevant to UK paramedics. Please read the full article for more information
These cause:
– Difficulties fitting a mask
– Less ‘efficient air transferring from the mask to the lungs’
– A ‘difficulty in visualizing the vocal cords’ when intubating due to fluids & obstructions
Final points
Consider all of the above and ‘avoid future complications’. Then address other injuries.
Emergency intubation is fraught with risks
Consider your expertise and experience. Ensure the trauma patient can access ‘the most experienced personnel’ where possible. This would reduce one of the risks.
Ensure prompt treatment
Consider the patient’s GCS, breathing level & risk to aid your decision making about transport
Check the ‘extent, the composition and the anatomy of the injury’. Is it possible to ventilate with a mask?
‘Is there a limitation in mouth opening? Is that limitation the result of pain’ only? [In a prehospital environment, this may be difficult to ascertain]
An LMA may ‘not be suitable for managing trauma patients. However, it could enable ventilating the patient until definitive airway is achieved’
References
Gruen, R.L. et al. 2006. Patterns of Errors Contributing to Trauma Mortality: Lessons Learned from 2594 Deaths, Annals of Surgery, 244 (3): 371-380, Available Online:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856538/
Krausz, A. et al. 2009. Maxillofacial trauma patient: coping with the difficult airway, World Journal of Emergency Surgery, 4: 21, Available Online: https://wjes.biomedcentral.com/articles/10.1186/1749-7922-4-21
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[restab title=”Article 999 Super Summary”]
Remember to follow ATLS protocol [and your local guidelines], use cervical spine control and focus on airway management.
Head and soft tissue trauma, nasal bleeding or open wounds, mandible fractures, mouth obstructions, tracheal trauma, c-spine injury and the patient’s stomach contents can all make airway management more challenging (Hutchinson et al, 1990 in Krausz et al, 2009).
Top tips?
Consider cricoid pressure but bear in mind it may actually worsen your view during intubation.
Ensure rapid transport and treatment of the patient and consider your own expertise.
What level of experience do you really need to deal with this patient, who has it, and where are they?
The patient’s GCS, breathing level and risk should all support this decision.
You can use an LMA, but it’s a time-stop measure [Article 999 interpretation; see full summary].
Consider the ‘extent’ of the patient’s injuries and how they are going to make it difficult to use a mask and intubate if required.