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    Our latest podcast is out and can be streamed here!

    Pain. The most common presenting complaint in emergency departments.1 Considered the 5th vital sign, it’s the bread and butter of all clinical assessments. Whether in the ED, ICU, or the prehospital environment, pain management falls under all practitioners’ scope of practice and should be treated accordingly.

    Long Story Short (LSS) at the bottom

    Definition:

    Pain is a complex interaction of sensory, emotional and behavioural factors. Pain is an unpleasant sensory and emotional experience, associated with actual or potential tissue damage or described in terms of such damage.2

    Pathophysiology

    So how do we perceive pain? How do our brains interpret pain, and how does it affect our bodies?

    An easy way to think about how pain works is to think of it like an electrical system. The Nociceptors (pain receptors) respond to changes in pressure, temperature, and chemicals. The picture below gives a good description of the pathway that pain takes, from translation, transmission, and modulation to perception.

    Acute vs chronic

    Time is an important factor when it comes to pain. We often see patients in the acute phase of their pain. Acute pain is usually short and limited in duration, with an identifiable cause (trauma, surgery, or inflammation).2

    Chronic pain occurs when acute pain is inadequately treated.

    Emotional vs sensational pain

    Often, we forget about the emotional pain that a patient may be experiencing. We can measure a patient’s pain using scales, but we often forget about the emotional aspect of pain and the often traumatic experiences that go along with it. Pain management also includes effective splinting, patient comfort, keeping the patient warm and talking to the patient. Do not underestimate the power of compassion.

    How to accurately measure pain

    Pain is a subjective sign that will differ from patient to patient. Previous painful experiences and expectations will often cause different pain scores between patients. There are several ways to assess pain, using visual and analog scales. Most often, a verbal numerical pain scale is used. The patient is asked to rate their pain on a scale of 1 – 10, with 1 being little/no pain and 10 being the most severe/excruciating pain. The Wong-Baker faces can be used as they are a visual tool that is easily understood. It is validated to be used on children as young as 5 years old. Regardless of the tool you use, pain should be measured to determine the effectiveness of your treatment.

    Choices of drugs

    We have a plethora of medication that we can use to treat pain. It is important to know when to use which medication and what dose to use.

    • Entonox
    • Penthrox
    • NSAIDS
    • Paracetamol
    • Morphine
    • Ketamine
    • Fentanyl

    Multimodal Pain Management 

    Opioid free ED?

    The term “opioid free” seems like an unachievable target within the current EM spaces. Morphine, Fentanyl, Pethidine are all medications that we are used to using and are comfortable with. There are, however, problems associated with the use of opioids. There can be severe side effects (particularly in the elderly population), addiction/misuse, poor titration practices and there is no consensus on the optimum dose.3

    More information and some really awesome podcasts on the topic can be found here.

    LSS:

    • Patients experience pain differently
    • Assess the pain using a validated scale
    • Know your medication and dose ranges
    • Opioids might not be the best choices – consider other medication!

    References:

    1. Abdolrazaghnejd A, Banaie M, Tavakoli N, Safdari M, Rajabpour-Sanati A. Pain Management in the Emergency Department: a Review Article on Options and Methods. Adv J Emerg Med. 2018;2(4): e45
    2. South African Society of Anaesthesiologists. South African Acute Pain Guidelines (2017) Available from: https://www.sajaa.co.za/index.php/sajaa/article/view/1960
    3. O’Connor, A. B., Zwemer, F. L., Hays, D. P., & Feng, C. (2010). Intravenous opioid dosing and outcomes in emergency patients: a prospective cohort analysis. The American journal of emergency medicine28(9), 1041–1050.e6. https://doi.org/10.1016/j.ajem.2009.06.009

    Spinal Motion Restriction

    28-year-old PVA patient complaining of neck pain…

    The typical trauma patient. South Africa has a huge trauma population that only seems to be getting larger! Spinal motion restriction is used every day, often with patients who don’t need it, or applied in a way that may result in more harm than good. This post and podcast covers a broad spectrum of information for the application of Spinal Motion Restriction specific to the South African Environment.

    LSS: for the Long Story Short summary scroll to the bottom

    SMR – What is it?

    Spinal motion restriction refers to restricting a patient spine to prevent injuries from getting worse. We can use a bunch of different devices and methods to “hold c-spine”. Which ones are good, and which should we get rid of?

     

    What devices can be used?

    There are a variety of ways that we can ensure that spinal motion restriction can be applied. Starting from the most basic, we have self-immobilisation. Asking an awake patient to hold their own head and neck still is a great way to keep a patient’s spine still. If a patient has true pain on their C-spine, they will instinctively hold their own neck still 2.

    Hard/soft collars have fallen out of favor and for good reason. There is currently no evidence that they are beneficial to patients, and there is a some evidence showing that they cause more harm than good1. For some reason, they are still used and can be found on most ambulances. We discuss the possible use of these devices only for the movement/extrication of a patient out of a space, if they are unable to maintain their own C-spine due to level of consciousness.

    Spine (trauma) boards. These boards were designed as an extrication device only, to assist with the removal of patients from vehicles and in rescue situations. They are NOT immobilisation devices. There is lots of evidence that has shown that prolonged periods on a spine board can cause respiratory compromise, pressure wounds, pain, and claustrophobia2. Standing takedowns are worthless – we’re not going to waste our time with this. More information can be found in the ITLS Position Statement on the use of these devices.

    Scoop stretchers are a level up from spine boards, as they are rounded to allow for more comfort. Ideally, patients should still not be kept on one for a long time, as it can still cause pressure wounds. Scoop stretchers are also poor insulators, and a risk of hypothermia is present2.

    So what is the gold standard for spinal motion restriction? We want a device that doesn’t cause pain, prevents pressure wounds and is comfortable for the patient.

    Vacuum mattresses are currently the best device used to apply spinal motion restriction from a comfort and patient safety point of view.  Be careful to ensure that temperature management is a concern as long periods of time in hot environments can result in patients overheating easily.

    In hospital, you have better options in terms of patient comfort. Lying a patient supine on a hospital bed with head-blocks can be an effective way to keep SMR.

    When do we apply SMR?

    “Not all trauma patients are created equal “– South African Proverb

    We see a lot of trauma patients in SA. It becomes difficult to identify a true spinal injury, but a proper assessment and the use of validated tools can help us recognise the injury.

    Things to look out for: pain over the spine on palpation or movement, obvious deformity of the spinal column, unexplained hypotension coupled with absence of a tachycardia, decreased motor and sensory function in upper or lower extremities; including pins-and-needles or loss of sensation (numbness), and weakness or loss of movement (paralysis).

    In penetrating trauma, SMR is not indicated unless the patient has the above signs and symptoms, and if the benefit of SMR outweighs the risk (mortality increases for the patient with penetrating trauma when we spend time with SMR rather than getting them to a theatre for definitive management).

    How do we clear C-spine?

    There are a handful of different guidelines that we can use to ‘clear’ C-spine, and they can help guide us in determining which patient should have SMR applied. It is out of the scope of practice of a Basic Ambulance Assistant (BAA) to ‘clear’ the c-spine. The Canadian C-Spine Rule is the one most used and widely advocated for. As per the 2018 Clinical Practice Guidelines, all prehospital providers can apply spinal motion restriction – “[Including] the use of all evidence-based spinal motion restriction devices”.

    Canadian C-Spine Rule

    (this has been validated for pre-hospital and in-hospital use)

    Long story short:

    • Spine/Trauma boards are out! (except to extricate)
    • Vacuum Mattress are in!
    • Standing takedowns are only fun for the provider and don’t provide any benefit
    • Hard collars are probably not ideal for most situations
    • Follow a rule to determine risk and therefore apply SMR or not
    • Assess your patient thoroughly and DOCUMENT your findings throughout the patient interaction

    Other reading:

    • For an online interaction on how to decide when to scan the spine or brain see this link.

    References:

    1 – Sundstrøm T, Asbjørnsen H, Habiba S, Sunde GA, Wester K. Prehospital use of cervical collars in trauma patients: a critical review. J Neurotrauma. 2014;31(6):531-540. doi:10.1089/neu.2013.3094

    2 – Stanton D et al. Cervical collars and immobilisation: A South African best practice recommendation. Afr J Emerg Med, (2017), doi.org/10.1016/j.afjem.2017.01.007. https://www.thennt.com/nnt/cervical-spine-motion-restriction-blunt-trauma/

    The study: Rapid Agitation control with Ketamine in the Emergency Department: A Blinded, Randomised Control Trial.

    Barbic, D., Andolfatto, G., Grunau, B. Scheuermeyer, F., Macewan, B., Qian, H., Wong, H., Barbic, S. and Honer, W. 2021. Annals of Emergency Medicine. Article in the press. Available online: https://trialsjournal.biomedcentral.com/articles/10.1186/s13063-018-2992-x [accessed 9 August 2021].

    The bottom line: Ketamine is a viable and possibly safe option for the management of the acute agitation (excited delirium) in the Emergency Department

     What did they do?

    • In this study, the use of two treatment regimes for the management of patients presenting with acute agitation (defined by a RASS score of 3+).
    • A RASS score of -1 or less was defined as sedation.

    The two regimes are noted below:

    The RASS score for reference:

    Source: https://rebelem.com/the-mends2-trial-dexmedetomidine-vs-propofol-for-sedation/rebel-review-101-richmond-agitation-sedation-scale-rass/

     

    How did they do this?

    • This study was set at a single center (a Canadian Unit in Vancouver), where two study arms were created, each with the medications as listed above. The patients who needed sedation for agitation were randomized to receive one of the medication regimes.
    • Staff treating the patients were blinded to the medication that the patient received, only the study nurse administering it knew what was being administered.
    • Adult patients between the ages of 19 and 60 were included in the study, everyone enrolled in the study was treated in a resus bay with CVS and Respiratory monitoring capability.
    • The study was conducted over a period of 21 months (June 2018 – March 2020) and was cut short by COVID-19. They enrolled 40 patients into each arm of the study, for a total of 80 patients.

    Strengths:

    • This was a randomized control study which blinded the treating practitioners to the treatment regime their patient was receiving.
    • The study took place in a large center which sees a large number of patients (90000 a year), with a large incidence of acute agitation presentations due to the population served (large homeless population with a concerning drug and alcohol use issue in the community).

    Weaknesses:

    • Single center trial, the results could have been more universal if more centers with different populations were studied.
    • COVID-19 cut the study enrollment time meaning the desired numbers for enrollment were not reached as planned (just less than half the required enrolments needed occurred)

    Findings:

    • Time to sedation in the Ketamine was superior when compared to the Haloperidol/Midazolam group in this study. The median time difference to adequate sedation was 7.7 minutes (this is significant with a possibly dangerous agitation patient).
    • Median time to sedation with Ketamine at 5mg/kg IMI was 5.8 minutes.
    • Safety in both arms were comparable with no patients in the study requiring intubation, equal numbers of patient requiring oxygen post sedation in both arms, and only one incidence out of 40 in the Ketamine arm experiencing laryngospasm (but not requiring intubation).
    • Apnea occurred in both groups with no escalation required to advanced airway management).

    It is noted that the procedure of sedation for control of agitation is possibly risky, it is recommended that all patients treated for acute agitation who require any form of sedation be managed in an area where there is access to appropriate monitoring devices, and sufficiently trained staff.

    Bottom Line:

    5mg/kg IVI Ketamine doses result in more rapid time to sedation in the management of acute agitation in the emergency department

    Although the study was not powered sufficiently to determine the safety of either arm, there is some evidence to suggest that Ketamine may be at least as safe as the alternative used in this study.

    1. Good Communicator

    A paramedic who is able to communicate effectively in high-stress environments is a “good paramedic”. This is the first thing that flies out of the window when people are faced with stressful, life and death situations. Being able to manage your own expectations and communicate effectively in these situations means that the patient you are treating is much more likely to so better than if you are unable to communicate.

    What makes communication good?

    • Listening
      • Allowing participation from the entire team involved and including all members of the complex teams found in pre-hospital care can be the difference between life and death for a patient. There is often something that one of the team members has spotted that the lead paramedic has not seen or noticed.  When a team is heard and appreciated there is a better chance that the patient receives better treatment, this also allows for more voices, meaning the best ideas are heard and implemented.
      • Communication is often less about talking and more about listening, being willing to listen to constructive feedback, and see every interaction as an attempt to do better rather than to insult the leader is very important.
    • Closing the loop
      • This means that although information usually flows down from a team leader to the team members, there is a need for almost as much information to flow back up to the team leader, this is why listening is important. When orders are given, the team leader needs feedback to know if they have been implemented as requested or if there are other problems stopping the instructions from being carried out. Closed-loop communication means everyone on the team is both listening and feeding back information as needed to solve the problem.
    • Courteous and pleasant
      • Teams do better for their patients when members are polite and courteous to each other, this results in a more friendly work environment (even amid an emergency) and makes the team leader more approachable, improving overall communication.

    A paramedic as a leader in the pre-hospital emergency care field also needs to possess the following to be “a good paramedic”.

    2. Empathy

    Although this is considered to be a basic human quality, sometimes we need to better at expressing it. In the harsh pre-hospital work environment, this is sometimes a quality that is lacking. Empathy towards patients and family members can often be more natural to express, while empathy towards the general public and work colleagues can be more difficult. A good paramedic is able to listen and identify with the struggles and problems of another person, without taking on the problems or struggles themselves. It is the quality of trying to see things from another person’s point of view and to assist them in the best way possible to meet all their needs. Empathy is also thought of the idea of “giving someone the benefit of the doubt”.

    3. Integrity

    Many situations in the pre-hospital environment will test the integrity of the paramedic, from having to treat suspected criminals, to having to work in harsh and challenging environments. Integrity to treat all human life as valuable in any situation can be really challenging. Being aware of the challenges and difficulties before being presented with them and having a plan for dealing with your own judgements and bias before being put into the circumstance will assist in the maintenance of integrity.

    4. Problem-solving ability and willingness to learn

    This is probably the quality that is most used by the paramedic in their day to day work. The environments and situations paramedics find patients and families in are often challenging and may be very different from what was taught in their training. Because the world is so dynamic and emergencies can present in very unique environments, its important for the paramedic to be adaptable and able to think outside the box in difficult situations, and most importantly, a paramedic needs to be able to take learning from other environments and apply it to new environments and problems all the time. This has to happen quickly.

    Adjunctive therapies for ACS patient

    We spend a lot of time talking about when to use fibrinolytic therapy for the ACS patient and when to refer the patient to cath-lab when we have this available, but we really don’t spend a lot of time covering the adjunctive therapy that should be considered for the AMI patient.

    The American Heart Association Algorithm for the management of the patient with suspected ACS should be reviewed for the purposes of the discussion that follows. 

    In this post we will not cover the indications for fibrinolysis, this will be covered in a separate post at a later date

    We are going to focus on the term “Adjunctive treatment” noted in the AHA ACS Algorithm (this content is copywrite protected and can be purchased here: https://www.worldpoint.com/20-3109).

     

    Fibrinolytic therapy or PCI?

    This all depends on what is available to you at the time, and the hospital in which you render service

    The information below covers the adjunctive treatment for both patients receiving PCI and Fibrinolytic therapy

    PCI vs Fibrinolytic

    ADJUNCTIVE TREATMENT: What does this mean in the EM space?

    Adjunctive therapies for ACS patient
    • There are some other options for adjunctive therapy that can be started either in the first 24 hours or immediately after PCI, however, these are usually at the treating cardiologist’s discretion. These are listed below:

    ACE inhibitors:

    • Generally started in the stable patient post AMI as they may assist with the remodelling of the muscle tissue post infarct and can reduce the amount of damage/scar tissue formed in the period immediately post AMI. Not routinely administered in the acute setting but might be considered if the patient is in the unit for a long period.

    GPIIB/IIIa Inhibitors

    • Abciximab, Eptifibatide
    • These are also not routinely administered and should be considered only on discussion with the receiving cardiologist
    • These are usually administered immediately before PCI if they are used

    P2Y12 Inhibitors
    These are medications that block platelet action through additional pathways (separate to aspirin) and include medications as well known as Clopidogrel, as well as a few others that may be less well known:

    1.Prasgrel

    2. Ticagrelor

    3. Ticlopidine

    In your ED/ward/service you should engage in conversation with the relevant treating cardiologists regarding the use of these medications as they are not routinely part of the emergency management of the patient.

    The simple summary!

    Adjunctive therapies for ACS patient

    References:

    The references below have been taken from: American Heart Association. 2015. Part 9: Acute Coronary Syndromes – Web-based Integrated 2010 & 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Available online: https://eccguidelines.heart.org/wp-content/themes/eccstaging/dompdf-master/pdffiles/part-9-acute-coronary-syndromes.pdf [accessed 09 June 2020].

    These references are the background evidence for the suggestions made above

    Evidence for the use of Aspirin

    Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany
    CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr., Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin
    JL, Hiratzka LF, Hunt SA, Jacobs AK. ACC/AHA guidelines for the management of patients with ST-elevation myocardial
    infarction–executive summary: a report of the Am College of Cardiology/Am Heart Association Task Force on Practice Guidelines
    (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation.
    2004;110:588–636.

    Barbash IM, Freimark D, Gottlieb S, Hod H, Hasin Y, Battler A, Crystal E, Matetzky S, Boyko V, Mandelzweig L, Behar S, Leor J.
    Outcome of myocardial infarction in patients treated with aspirin is enhanced by pre-hospital administration. Cardiology.
    2002;98:141–147.

    Stub D, Smith K, Bernard S, Nehme Z, Stephenson M, Bray JE, Cameron P, Barger B, Ellims AH, Taylor AJ, Meredith IT, Kaye DM;
    AVOID Investigators. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation. 2015;131:2143–2150. doi:
    10.1161/ CIRCULATIONAHA.114.014494.

    Gurfinkel EP, Manos EJ, Mejail RI, Cerda MA, Duronto EA, Garcia CN, Daroca AM, Mautner B. Low molecular weight heparin versus
    regular heparin or aspirin in the treatment of unstable angina and silent ischemia. J Am Coll Cardiol. 1995;26:313–318.

    Evidence for the use of GTN (SL)

    Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany
    CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr., Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin
    JL, Hiratzka LF, Hunt SA, Jacobs AK. ACC/AHA guidelines for the management of patients with ST-elevation myocardial
    infarction–executive summary: a report of the Am College of Cardiology/Am Heart Association Task Force on Practice Guidelines
    (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation.
    2004;110:588–636.

    Barbash IM, Freimark D, Gottlieb S, Hod H, Hasin Y, Battler A, Crystal E, Matetzky S, Boyko V, Mandelzweig L, Behar S, Leor J.
    Outcome of myocardial infarction in patients treated with aspirin is enhanced by pre-hospital administration. Cardiology.
    2002;98:141–147

    The Public Access Defibrillation Trial Investigators. Public-access defibrillation and survival after out-of-hospital cardiac arrest. N Engl J
    Med. 2004;351:637–646.

    Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R. Routine use of oxygen in the treatment of myocardial
    infarction: systematic review. Heart. 2009;95:198–202.

    Haynes BE, Pritting J. A rural emergency medical technician with selected advanced skills. Prehosp Emerg Care. 1999;3:343–346.

    Funk D, Groat C, Verdile VP. Education of paramedics regarding aspirin use. Prehosp Emerg Care. 2000;4:62–64.

    Verheugt FW, van der Laarse A, Funke-Kupper AJ, Sterkman LG, Galema TW, Roos JP. Effects of early intervention with low-dose
    aspirin (100 mg) on infarct size, reinfarction and mortality in anterior wall acute myocardial infarction. Am J Cardiol. 1990;66:267–270.

    Bussmann WD, Passek D, Seidel W, Kaltenbach M. Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin.
    Circulation. 1981;63:615–622.

    ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58 050
    patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. Lancet.
    1995;345():669–685.

    Diercks DB, Boghos E, Guzman H, Amsterdam EA, Kirk JD. Changes in the numeric descriptive scale for pain after sublingual
    nitroglycerin do not predict cardiac etiology of chest pain. Annals of emergency medicine. 2005;45:581–585.
    193. Henrikson CA, Howell EE, Bush DE, Miles JS, Meininger GR, Friedlander T, Bushnell AC, Chandra-S

     

    Evidence for Oxygen

    Montalescot G, Zeymer U, Silvain J, Boulanger B, Cohen M, Goldstein P, Ecollan P, Combes X, Huber K, Pollack C Jr, Bénezet JF,
    Stibbe O, Filippi E, Teiger E, Cayla G, Elhadad S, Adnet F, Chouihed T, Gallula S, Greffet A, Aout M, Collet JP, Vicaut E; ATOLL
    Investigators. Intravenous enoxaparin or unfractionated heparin in primary percutaneous coronary intervention for ST-elevation
    myocardial infarction: the international randomised open-label ATOLL trial. Lancet. 2011;378:693–703. doi: 10.1016/S0140-
    6736(11)60876-3. Part 9: Acute Coronary Syndromes.

    Rawles JM, Kenmure AC. Controlled trial of oxygen in uncomplicated myocardial infarction. Br Med J. 1976;1:1121–1123.

    Schünemann H, Broz?ek J, Guyatt G, Oxman A. GRADE Handbook. 2013. http://www.guidelinedevelopment.org/handbook/. Accessed
    May 6, 2015.

    Wilson AT, Channer KS. Hypoxaemia and supplemental oxygen therapy in the first 24 hours after myocardial infarction: the role of
    pulse oximetry. J R Coll Physicians Lond. 1997;31:657–661.

    Kilgannon JH, Jones AE, Shapiro NI, Angelos MG, Milcarek B, Hunter K, Parrillo JE, Trzeciak S; Emergency Medicine Shock Research
    Network (EMShockNet) Investigators. Association between arterial hyperoxia fol- lowing resuscitation from cardiac arrest and inhospital mortality. JAMA. 2010;303:2165–2171. doi: 10.1001/jama.2010.707.

    Janz DR, Hollenbeck RD, Pollock JS, McPherson JA, Rice TW. Hyperoxia is associated with increased mortality in patients treated with
    mild therapeutic hypothermia after sudden cardiac arrest. Crit Care Med. 2012;40:3135–3139. doi: 10.1097/CCM.0b013e3182656976.

    Wang CH, Chang WT, Huang CH, Tsai MS,Yu PH, Wang AY, Chen NC, Chen WJ. The effect of hyperoxia on survival following adult
    cardiac arrest: a sys- tematic review and meta-analysis of observational studies. Resuscitation. 2014;85:1142–1148. doi:
    10.1016/j.resuscitation.2014.05.021.

    Ukholkina GB, Kostianov IIu, Kuchkina NV, Grendo EP, Gofman IaB. [Effect of oxygenotherapy used in combination with reperfusion in
    patients with acute myocardial infarction]. Kardiologiia. 2005;45:59.

    Ranchord AM, Argyle R, Beynon R, Perrin K, Sharma V, Weatherall M, Simmonds M, Heatlie G, Brooks N, Beasley R. Highconcentration versus titrated oxygen therapy in ST-elevation myocardial infarction: a pilot ran- domized controlled trial. Am Heart J.
    2012;163:168–175. doi: 10.1016/j. ahj.2011.10.013.

    Evidence for Clopidogel and Tigarelor

    Montalescot G, Wiviott SD, Braunwald E, Murphy SA, Gibson CM, McCabe CH, Antman EM; TRITON-TIMI 38 investigators. Prasugrel
    compared with clopidogrel in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (TRITONTIMI 38): double-blind, randomised controlled trial. Lancet. 2009;373:723–731. doi: 10.1016/S0140-6736(09)60441-4.

    Wallentin et Al. Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes. N Engl J Med 2009; 361:1045-1057.

    Xavier Scheuermeyer F, Wong H, Yu E, Boychuk B, Innes G, Grafstein E, Gin K, Christenson J. Development and validation of a
    prediction rule for early discharge of low-risk emergency department patients with potential ischemic chest pain. CJEM.
    2014;16:106–119.

    Evidence for Opioids

    Giannopoulos G et al. P2Y12 Receptor Antagonists and Morphine: A Dangerous Liaison? Circ Cardiovasc Interv 2016. PMID: 27586412

    Hobl EL et al. Morphine Decreases Clopidogrel concentrations and Effects: A Randomized, Double-Blind, Placebo-Controlled Trial. J Am Coll Cardiol 2014. PMID: 24315907

    Hobl EL et al. Morphine Decreases Ticagrelor Concentrations but not its Antiplatelet Effects: A Randomized Trial in Healthy Volunteers. Eur J Clin Invest 2016. PMID: 26449338

    Hobl EL et al. Morphine Interaction with Prasugrel: A Double-Blind Cross-Over Trial in Healthy Volunteers. Clin Res Cardiol. 2016. PMCID: PMC4805697

    Parodi G et al. Morphine is Associated with a Delayed Activity of Oral Antiplatelet Agents in Patients with ST-Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circ Cardiovasc Interv. 2014. PMID: 25552565

    Meine TJ et al. Association of Intravenous Morphine Use and Outcomes in Acute Coronary Syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J 2005. PMID: 15976786

    Puymirat E et al. Correlates of Pre-Hospital Morphine Use in ST-Elevation Myocardial Infartion Patients and its Association with In-Hospital Outcomes and Long-Term Mortality: The FAST-MI (French Registry of Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction) Programme. Eur Heart J 2016. PMID: 26578201

    Iakobishvili Z et al. Effect of Narcotic Treatment on Outcomes of Acute Coronary Syndromes. Am J Cardiol 2010. PMID: 20346305

    Weldon ER et al. Comparison of Fentanyl and Morphine in the Prehospital Treatment of Ischemic Type Chest Pain. Prehosp Emerg Care 2016. PMID: 26727338

    Amsterdam EA et al. 2014 AHA/ACC Guideline for the Mangement of Patients with Non-ST-Elevation Acute coronary Syndromes: A Report of the American college of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am coll Cardiol 2014. PMID: 25260718

    This post builds on the post linked here.

    Where the linked post discusses the ventilation of a patient who presents in the emergency setting, in need of lung protective ventilation, and safe parameters to avoid injury to the lung and possible ARDS, this post will cover the slightly more challenging approach to ventilation of the patient who is trapping air due to an obstructive disease process (usually the patient with status asthmaticus or an exacerbation of COPD).

    There are two major references for the data contained in this post which have been linked here:

    1: Mechanical Ventilation of the Severe Asthmatic Patient

    2: Managing Initial Mechanical Ventilation in the ED  

    A summary of the ventilation of the patient with obstructive lung disease patient is below:

    ventilating obstructed lungs

    The problem with obstructive lungs that need ventilation

    We often think of asthma (and COPD) as a problem of getting air out, however by the time the patient presents with a need for invasive airway management and ventilation, the problem also becomes one of getting air in.

    One of the big challenges with ventilating the patient with obstructive pathology, is that simply placing an ETT and placing the patient on mechanical ventilation does nothing to help the patient, in fact, forcing more air, under more pressure is more likely to increase the danger to the patient and possibly worsen the condition.

    OK, so what do I do then?

    Let’s say we do get to the point where the patient with an obstructive lung pathology needs to be ventilated… first of all, what does this look like?

    • Patient who is starting to tire with the massively increased work of breathing to move adequate tidal volumes
    • Patient who is starting to not move adequate tidal volumes
    • Increasing CO2 levels on ABG (or even on ETCO2 if you have been monitoring this throughout)
    • Severe cyanosis and signs of hypoxia (PaO2 < 60mmHg or trending down despite maximal therapy)
    • Level of consciousness starts to decrease
    • Silent chest (despite maximal therapy) and respiratory arrest would be good indicators that you are not winning, but also may be a bit late 

    If the above symptoms progress despite maximal therapy, then the patient may need to be escalated to airway management and invasive ventilation.

    There are some things you should already have considered and have already tried to prevent this downward spiral of trapping of air and increasing pressure:

    1. Oxygen administered preferably humidified (increasing flow to meet oxygen demand) but be careful of administering oxygen and causing hyperoxia (see notes below)
    2. Nebulised Beta 2 stimulants and Ipratropium Bromide (ongoing and continuous if needed)
    3. IV/Oral or IM Steroids (corticosteroids)
    4. Magnesium Sulphate IV infusion
    5. Adrenalin subcutaneously in the case that the patient is getting worse despite therapy (or first line in the case of a silent chest)
    6. Consider IV Beta2 Stimulants (being careful not to delay other more effective treatments

     

    The fix here is NOT to push more air into the chest, rather to ventilate in a way that limits the pressure buildup within the chest, and thus decreases the risk of hypotension, hypoxia and death. The whole aim of intubating this patient for ventilation is to maximize the expiatory time and decrease the pressure buildup within the thorax, to buy time for the medications you are still administering to work. The aims of mechanical ventilation are:

    • to decrease the work of breathing
    • maintain oxygenation
    • assist alveolar ventilation without causing more harm

    Let’s have a look at the physiology and pathophysiology associated with the acute exacerbation of asthma/COPD leading to air trapping (this is a fairly complicated explanation that is summarised below).

    How does a normal lung work to inflate and deflate?

    Normally, the brain senses an increase in the concentration of CO2 in the system through chemoreceptors located in the arch of the aorta, the carotid bodies, and measuring CSF at the medulla oblongata. This increase leads to stimulation of the respiratory centre, increasing rate and volume of ventilation (to increase the minute volume).

    Messages are sent down the phrenic nerve (that innervates the diaphragm) and other nerves that innervate the intercostal muscles to contract these muscles, making the volume inside the thorax larger, and the pressure inside the thorax lower.

    This causes a rush of air into the lungs from the outside, in an attempt to equalize the pressure, and the lungs fill with air. As can be seen this is an active process as the pressure within the thorax needs to be decreased by increasing the volume of space within to allow for air movement.

    ventilating obstructed lungs

    In the patient who is trapping air, this is really difficult as the resting pressure within the thorax is already a lot higher when compared to the normal patient above, this results in a resting positive pressure within the thorax. In order to get air to move, this patient still needs to create a negative pressure but because their starting point is much higher, the patient needs to work much harder to move the same amount of air.

    Often the patient with bronchospasm or air trapping will have a prolonged expiratory phase, but as they struggle more and more with increasing pressure, the expiration may not always come to an end before the hypoxia and air hunger drives the next breath. The patient is not yet finished breathing out, when they are triggered by their brains to take a new breath in, and more air is inevitably trapped.

    ventilating obstructed lungs

    The trick comes in here, that even if we were able to (and we are to an extent), decrease how hard the patient has to work to move air (by increasing the external pressure of the air that moves into the lungs by blowing it in under pressure), this doesn’t really solve the problem. It only buys a little time, after which; the pressure inside the thorax will still be larger (due to air being blown in and still trapped by the bronchoconstriction) than the external pressure.

    The pressure being used to assist the patient will need to be increased again to allow for some air movement. This can be only be done to a certain limit, as the chest wall can only expand to a point. Once the pressure driving the air in reaches equilibrium with the pressure trapped, there is no way that air can move in the lungs. This is when the patient often arrests or ends up with a “Silent Chest” when there is not enough pressure generated to move air into the lungs

    These patients arrest for a few reasons:

    1. The lungs are not able to allow for any movement of oxygen-rich air into the space as the pressure inside may be greater than the pressure outside the lungs, therefore hypoxia is a major contributor. The only way to overcome this is to increase the FiO2.
    2. The increased pressure in the chest, leads to decreased venous return (dynamic hyperinflation), as the pressure in the inferior vena cava is very low. It doesn’t take much extra intrathoracic pressure to drop the venous return, leaving the heart empty, and unable to push any blood to the lungs or body. The patient presents with a form of obstructive shock.
    3. Smaller airways collapse during expiration, trapping even more gas as the tiny airways just before the alveoli do not contain any cartilage and are made only of muscle, which under the extreme exertion of attempting to expire, can easily collapse just because the patient tries to force air out of their lungs. This means the above two problems are worsened.
    4. Hypercapnia (as well as the hypoxia described above) sets in and the patient starts to lose consciousness, resulting in a decrease in the ability to breathe both in and out. The extreme activity of trying to force air out as well as create a negative pressure to suck air in causes the movement of air to cease.

     

    The image below shows the effect of massive expiratory pressure on the smaller airways, resulting in collapse, leading to an increase in trapping.

    ventilating obstructed lungs

    As if all the other stuff we have already covered is not enough… We also need to be careful about ending up in a situation where hyperoxia occurs (where we administer too much oxygen). This is a problem as the hypoxic vasoconstriction in the pulmonary circuit actually helps to maximise perfusion to the areas that are better ventilated and will begin to decrease if there is too much oxygen administered, and resulting in a worsening V/Q mismatch.

    ventilating obstructed lungs

    If all we are going to do is intubate the patient so we can force air under greater pressure into the lungs, we are not helping the patient at all. If your vent settings are such that we can minimise the pressure, and maximize the expiration, whilst allowing the medication we are still administering time to work, then we will be able to actually assist this patient.

    Right…so we are at the point where we need to intubate and ventilate this patient… HELP!

    Some things we have to get right from the start:

    1. The largest size ETT we can place in the airway is the one that should be placed. Increasing the size of the ETT decreases the pressure against which the patient has to breathe to get the air out.
    2. Delayed Sequence Intubation might be needed especially for the patient who is combative (using Ketamine in high doses will allow control of the patient while you try to better oxygenate the patient before intubation)

     

    Ventilator Settings:

    • Volume control modes of ventilation may be safer for this patient, as a controlled tidal volume can be administered, and even if there are dynamic changes in the compliance of the lungs then a safe tidal volume will be administered). See the post on ventilation for more information on this point.
    • Select a safe tidal volume (lung protective), this usually means anywhere from 5-7ml/kg
      • the higher the tidal volume, the higher the pressure will go as more air will need to flow through the same space leading to increases in pressure
    • Set PEEP that is reasonable (this DOESN’T MEAN ZERO)
      • set a PEEP that will be low enough not to add to the pressure in the thorax, but high enough that it might help to splint the smaller airways open against the forced expiration
      • Anywhere from 2-6cmH20 should be safe, start lowish and stay low and see how the patient does
      • There is some evidence that in the paralysed patient, PEEP may not add any positive effect (as there is no work of breathing and no forced expiration), but in the patient who is spontaneously breathing, adding low levels of PEEP may be beneficial to decrease work of breathing and fight against the collapse of the smaller airways on forced expiration (Laher and Buchanan, 2018).
    • Decrease the respiratory rate to around 10-12 for an adult patient (for paeds it gets a bit tricky, but perhaps lower than normal)
      • This one seems counter intuitive, but at this point we want as long a time as possible for expiration, and this will assist with minimising pressure build up in the chest
      • Decreasing the respiratory rate is MUCH more powerful in terms of increasing expiratory time than using the I:E ratio.
    • Think about setting a higher than normal I:E ratio once the respiratory rate is set, this will be 1:3 or 1:4
      • This will maximise the expiratory time a little further, but wait and see if the reduced rate works to fix the problem
    • Try to maintain the following pressures in safe parameters:
      • Plateau pressure should not exceed 25cmH20 – 30cmH20. Rremember this is the pressure applied to the elastic airways or alveoli, and shouldn’t be too high as the air can’t really get there easily.
      • Peak pressures are going to alarm (this is the pressure applied to the conducting airways), and although we usually don’t want this to go above 35cmH20, it likely will. Set the high pressure alarm higher than usual and monitor it as you may need to go as high as 50-70cmH20 or even higher to achieve a tidal volume that meets the patients minimum requirement.
      • Call for help early in the ventilation of these patients
    • Think about paralysing the patient in the early stages to gain control of the pressure in the thorax and to get the patient not to breathe too fast
      • This patient will be air hungry, hypoxic and hypercapneic, and will likely want to breathe at a much faster rate than the 10-12b/min you set, this will be counter-productive as the faster the patient breathes the more pressure is trapped in the lungs.
      • Paralyse the patient with a longer acting paralytic to better control their ventilation

    Anticipate that there will be a MUCH higher PaCO2 level than you might be comfortable with as a result of the slower respiratory rate and lower tidal volume. This will have to be accepted for the period whilst the patient is still trapping pressure. Permissive hypercapnia is the term used to describe this where you may have to accept PaCO2 levels that are very high. Provided the pH doesn’t drop below 7.2, this is considered to be safe.

    If the patient’s condition is complicated by RICP (or some other disease process where CO2 level maintenance should be within strict norms) then this is not the best approach to take.

    The screenshots below are from a ventilator simulator that can help understand these concepts.

    Affecting Expiratory Time

    The screenshots below are from a ventilator simulator that can help understand these concepts.

    ventilating obstructed lungs
    ventilating obstructed lungs
    ventilating obstructed lungs

    Follow this link to play with a ventilator simulator that will help you understand the relationships between the I:E ratio, ventilator rate, pressure and time for expiration.

    References:

    Kenny, J. 2019. ICU Physiology in 1000 Words: Asthmatic Mechanics. Pulm CCM. Available online: https://pulmccm.org/review-articles/icu-physiology-in-1000-words-asthmatic-mechanics/ [accessed 19 May 2020].

    Laher AE, Buchanan SK: Mechanically ventilating the severe asthmatic. Journal of intensive care medicine 2018, 33(9):491-501.

    Rezaie, S. 2015.  REBEL Cast Episode 11: The Crashing Asthmatic. REBEL EM blog, June 1, 2015. Available at: https://rebelem.com/rebelcast-crashing-asthmatic/ [accessed 18 May 2020]

    Yartsev, A. 2019. Ventilation strategies for Status Asthmaticus. Deranged Physiology. Available online: https://derangedphysiology.com/main/required-reading/respiratory-medicine-and-ventilation/Chapter%20611/ventilation-strategies-status-asthmaticus-0 [accessed: 26 May 2020].

    Figuring out a mechanical ventilator, and understanding the basic modes of ventilation can be a difficult task. At the end of this brief summary, you should have a better understanding of what is meant by the some of the different terms used when ventilating a patient mechanically, and you should leave with a basic understanding of how pressure and volume controlled ventilation work.

    For the purposes of this post, we will not be going into the different modes of ventilation, these will be covered in more depth in a different post, however, these definitions will set you up with a better understanding for all the ventilation chapters to follow.

    First some definitions

    Volume control

    • In this mode of ventilation, the parameter that is controlled is the volume administered to the patient (tidal volume)
    • Safe tidal volumes of around 4-8ml/kg are recommended for most patients, with somewhere near the 6ml/kg mark being a safe starting point

    Pressure control

    • In this mode of ventilation, the controlled parameter is the pressure
    • The peak airway pressure is constant, and is used to achieve a tidal volume which may vary depending on many factors

    Peak Inspiratory Pressure

    • This is the highest level of pressure applied to the lungs during inspiration
    • This is a factor of airway resistance, PEEP and compliance of the lungs
    • Pressure that is generally applied to the larger airways (those that are not involved in gaseous exchange) and the airways not capable of distending (conducting airways)
    • Ideally this pressure should not exceed 35cmH20 in lungs that are not obstructed. The ventilation of the patient with obstructive lung disease is discussed in a different post)

    Mean Airway Pressure

    • This is the average pressure applied to the lungs throughout the respiratory cycle (on inspiration and expiration) – see the graph below
    • The mean airway pressure can be increased by allowing more time to be spent under higher pressures; increasing PEEP; increasing inspiratory time and increasing inspiratory pressure
    ventilation

    Mean Airway Pressure (Image from Kevin Kuo, MD – Link can be found HERE)

    PEEP

    • Positive END-Expiratory pressure
    • This is the baseline pressure left over in the lungs once expiration is complete. It can be set by the ventilator, or may be a reading of the intrinsic pressure that is left over due to air trapping in the asthma/COPD patient for instance
    • This is the pressure that allows the alveoli to stay partially open throughout the respiratory cycle (too much PEEP = too little tidal volume, too little PEEP – increased effort to open the alveoli and oxygenateP

    Plateau Pressure

    • This is the pressure applied to the alveoli and is measured at the end of inspiration (or during an inspiratory hold). It is the pressure that is exerted on the actual tissues which can distend in the lungs
    • Ideally this pressure should not exceed 30cmH20

    Driving Pressure

    This is a measurement of the difference between the plateau pressure and the PEEP in the system. The higher the driving pressure, the more the lung is placed under stress. A driving pressure of around 14cmH20 – 18cmH20 is recommended when following the “open lung” or lung protective ventilation strategy. The lower, the better (provided that the appropriate tidal volume is produced for the patient).

    I:E Ratio

    • This is the time in the respiratory cycle that is allocated to the inspiration of air, and expiration of air, normally a person breathes at a ratio of 1:2 (inspiration is usually 1/2 as long as expiration). This is usually as a result of the active nature of inspiration (it is driven by actively moving muscle), whilst expiration is about relaxing muscle and so usually takes a bit longer.
    • In advanced ventilation, the inspiratory time can be made equal to or more than the expiratory time to maximize mean airway pressure and increase oxygenation, this is called inverse ratio ventilation and is NOT recommended in normal ventilation in the EM setting.

    Tidal Volume

    This is the volume of air required to distend the lungs in one single breath (normal breath without any active work to get more air in) and is normally around 7ml/kg when a person is at rest

    Pressure Support

    This is a preset pressure value that is delivered when the patient triggers a breath. It is a pressure mode of ventilation, that assists an existing drive to breathe. It makes the work of breathing easier by decreasing the effort the patient has to put in to achieve an appropriate tidal volume

    Respiratory Cycle

    The respiratory cycle includes two phases: inspiration of environmental air and the expiration of gases from inside the lung including carbon dioxide

    Trigger

    This refers to the method used by the ventilator to decide when to give the next breath

    • Time trigger: uses time alone to determine when the next breath should be given. It does not really take the patient into account at all, and uses the respiratory rate to determine the time between breaths (example: rate set at 12b/min, a breath will be given every 5 seconds regardless of the patient’s desire to breath at a different time)
    • Pressure trigger: this trigger is patient driven and uses the fact that spontaneous breaths create negative pressure. When a certain amount of negative pressure is generated in the ventilator circuit by the patient, then the ventilator will deliver the breath. Because the patient needs to generate a change in pressure, it requires that the patient work relatively hard to get a breath.
    • Flow trigger: When the patient makes an inspiratory effort, some of the gas that was previously flowing continuously through the circuit is diverted to the patient. The ventilator senses the decrease in flow returning through the circuit, and a breath is triggered, this requires much less work than the pressure trigger but also requires a flow sensor to be calibrated and in place on the ventilator with constant monitoring
    ventilation

    Pressure Modes

    In a pressure controlled mode of ventilation, the inspiratory pressure is the control variable (this is the one you can set), and is maintained during the inspiratory phase. The volume will be variable depending on a number of different things and can vary on a breath to breath basis.

    On all ventilators there are three specific parameters/graphs that indicate how a breath has been delivered, based on the pressure, flow and volumes.

    The graphs below are representative of a pressure-controlled mode of ventilation for the following reasons:

    1. The pressure graph is the same for each breath. There is a pressure that has been set and this is achieved for each breath
    2. The pressure waveform is square
    3. The flow graph shows what is called a “decelerating waveform” with the highest flow present at the start of inspiration, which then tapers off at the end of the inspiratory time. This mode most closely resembles the flow pattern of “normal” breathing.
    4. The tidal volume varies with each breath as this is dependent on the pressure reached and the pressure set
    5. You cannot see the plateau pressure, this is really only visible in the volume control mode of ventilation
    ventilation

    Why is pressure controlled ventilation good?

    Pressure controlled ventilation means that:

    • There is increased mean airway pressure which helps to assist in the improvement of oxygenation. The more time the airway (and specifically the alveoli) are exposed to pressure, the longer the time for oxygen movement across the membrane. BUT because it is not “normal” for the time of inspiration to be longer than the expiratory time, this benefit is mostly achieved through the use of PEEP (we tend not to ventilate a patient with I:E ratios that favor prolonged inspiratory time unless we run out of options)
    • Increased alveolar recruitment occurs with pressure ventilation as the pressure is applied to the alveoli from the start, meaning they open up earlier and remain open longer, exposing them to oxygen for a longer period. The pressure is exerted evenly across the alveoli and not directed down the path of least resistance (as sometimes happens with volume-controlled ventilation), so de-recruited alveoli are more likely to distend with this mode of ventilation.
    • Pressure is limited to the set level, and the risk of barotrauma is limited, however changes in compliance can result in changes in tidal volume, so volume trauma, or hypo-ventilation are still possible.
    • Patient comfort may be improved because the flow curve simulates “normal” negative pressure ventilation the closest, with a decelerating waveform, offering the highest flow at the start of the inspiration and tapering off towards the end of inspiration
    • Leaks in the circuit can be accounted for as the pressure that is required will be achieved by adding more pressure (this will accommodate for a leak)

    Why is pressure controlled ventilation not so good?

    • Tidal volume is completely variable depending on a lot of different things. If the patient has any dysynchrony then the ventilator will not be able to deliver the breath (the patient will breath against the ventilator and the pressure limit will be reached without any tidal volume being delivered). If the patient is ventilated for a longer time, there needs to be a close watch on the tidal volume and minute volume achieved to ensure adequate control of the carbon dioxide levels. As compliance decreases, so the pressure increases and the tidal volume decreases.
    • Because of the fact that tidal volume is totally variable, there are risks for the sudden increase in tidal volumes if compliance improves, this may risk damage to the elastic recoil of the lungs
    • Flow rates set too high may cause the pressure limitation to be reached (the high pressure alarm) especially if there is an increase in airway resistance, this would mean a breath would not be delivered and the patient would not receive any tidal volume on that breath.

    Examples of pressure controlled modes:

    • CPAP
    • BiPAP
    • Pressure assist control
    • Pressure Support
    • Pressure controlled SIMV
    • APRV

    These and more will be discussed in detail  in a different post.

    Volume Modes

    In volume-controlled modes of ventilation, the tidal volume is the control variable (this is the one you can set), depending on a whole lot of different parameters, the pressure will be variable from breath to breath.

    On all ventilators there are three specific parameters/graphs that indicate how a breath has been delivered, based on the pressure, flow and volumes.

    The graphs below are representative of a volume-controlled mode of ventilation for the following reasons:

    1. The volume graph is exactly the same for each breath, as the set tidal volume is achieved (the only time it will look different is if the pressure alarm limit is reached before the volume is fully delivered)
    2. The flow waveform is square as the flow is delivered in the same way with each breath, exactly the same flow throughout inspiration
    3. The pressure waveform is variable, as different breaths will result in different pressures depending on the patient at the time of the breath
    4. The pressure waveform slopes up early in the breath and then plateaus at the end of the breath
    5. Plateau pressure can be measured here if an inspiratory hold is completed (pushing the hold button at the end of inspiration)
    ventilation

    If lung compliance increases, the pressure applied to the lungs will decrease, and if lung compliance increases, the pressure required to achieve an appropriate tidal volume (distend the elastic tissues) will decrease. In theory, or at least long ago when ventilators only had the ability to control one or the other parameter, this was dangerous as high levels of pressure could be achieved.

    Most ventilators now will allow you to set a volume or pressure as their static parameter, but also set limits on the other parameter to allow for safer ventilation, this will be discussed in more depth in further posts (Ventilation modes and what they mean).

    Why is volume controlled ventilation good?

    • Tidal volume is set and won’t change and is helpful in cases where the carbon dioxide levels need to be carefully maintained (patient with increased ICP (intra-cranial pressure) for instance)
    • Minute volume also does not change unless respiratory rate changes even if there are large changes in lung compliance, the ventilation and tidal volumes and well as minute volumes remain fairly static
    • Flow rate is lower at the start of inspiration and can reduce the risk of reaching a pressure limitation (meaning early termination of the breath is less likely and the patient is more likely to receive their full tidal volume as required than if pressure control was used (especially in cases with higher airway pressures)

    Why is volume controlled ventilation not so good?

    • Mean Airway pressure is not as high as with pressure-controlled ventilation due to the variable pressure waves and time under the curve. For the hypoxic patient this might be a concern as the increased mean pressure results in increased oxygenation
    • Volume-controlled ventilation tends to ventilate the “easier” to ventilate alveoli, those that are already open and able to distend easily. This might result in a ventilation perfusion mismatch as the “good” alveoli are over ventilated whilst the others are under ventilated. Recruitment of alveoli is better achieved with pressure than volume.
    • If there is a leak, the volume-controlled mode is not as good at accommodating for it as the pressure-controlled mode. The volume will leak into the open space and be counted as delivered even though it didn’t go to the patient
    • If there is not enough flow at the start of inspiration, the patient may become agitated and air-hungry. Flow is not always a setting than can be adjusted on all ventilators and so might be difficult to get the patient settled if they are requiring more flow at the start of inspiration.

    Examples of volume controlled modes:

    • Volume Mandatory controlled ventilation
    • Volume assist control
    • Volume controlled SIMV

    These and more will be discussed in detail  in a different post.

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    References:

    Deden, K. (2015) ‘Ventilation Modes in Intensive Care’, Dräger, p. 72. Available at: http://www.draeger.com/sites/assets/PublishingImages/Generic/UK/Booklets/rsp_new_nomenclature_ventilation_modes_ICU_booklet_9066477_en.pdf.

    Modes of Mechanical Ventilation (no date). Available at: https://www.openanesthesia.org/modes_of_mechanical_ventilation/ (Accessed: 12 May 2020).

    Simplifying Mechanical Ventilation – Part I: Types of Breaths – REBEL EM – Emergency Medicine Blog (no date). Available at: https://rebelem.com/simplifying-mechanical-ventilation-part/ (Accessed: 12 May 2020).

    Yartsev, A. 2015. Practical differences between pressure and volume controlled ventilation. Deranged Physiology. Blog available online: https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%20542/practical-differences-between [accessed 15 May 2020].

    PPE

    Personal Protective Equipment and their proper use will assist in protection against the COVID-19 and exposure to the virus for healthcare workers, ancillary staff and other people within the healthcare system.

    Putting on PPE and getting it off again can present some serious challenges!

    First of all, what should I wear?

    Different hospitals and systems have different recommendations, however the NICD COVID-19 Disease: Infection Prevention and Control Guidelines (published at this link)  provide the following guidance:

    Covid deceased management

    The PPE for clinical staff is different for those providing care with possible aerosol creation, and then those who are not at risk of aerosol creation. This changes the PPE requirement somewhat.

    We will discuss the following:

    • How to properly DON PPE for protection against aerosol creation
    • How to DOFF PPE for these procedures
    • What mask should I wear and when? (cloth vs surgical vs N95)
    • What is the deal with gloves?
    • Can I use PPE more than once?

    Donning and Doffing PPE

    The University of Cape Town has published some really useful videos on the application and removal of PPE before and after contact with patients where contact with possible aerosol of the virus may be a risk, watch the video linked below.

    This process must be a slow and thoughtful process, being very careful not to expose yourself or others to any risk

    1. Donning the PPE

    • Clean hands using alcohol cleaner or washing your hands with soap and water
    • Put apron (or gown) on (over your head and tie it at the back)
    • Place the mask on your face (N95 if aerosol generating procedures will be performed)
      • One strap above the ears and one strap below
      • Mold the mask to the face and check a positive and negative pressure seal to make sure it fits the face really well
    • Place goggles or face visor over the eyes, making sure they interface with the mask well and comfortably
      • Make sure no hair gets trapped in the seal
    • Apply gloves to your hands

    Go and treat the patient as needed

    2. Doffing procedure (this is the dangerous part)

    You will need a bin (red bin to place all soiled items into)

    • Step 1 is to remove the gloves first. These will be the most heavily soiled pieces of equipment
      • Peel the first one off and then place the clean finger under the cuff against your skin and peel off the second glove
      • Place the gloves into the bin immediately
    • Clean your hands after the gloves are removed (this will allow for any exposure with the gloves to be mitigated against)
    • Remove the apron
      • Using your hands to tear the apron from the back (where you tied it) or undo the knot you made to loosen the apron/gown
      • Pull the apron/gown using the “clean” surface that was against your body, away from your body and allow the neck part to tear away from you (if you are wearing a gown this should be pulled forward to remove)
      • Place the apron/gown in a bin immediately
    • Remove the goggles
      • Avoid touching the front of the goggles and rather use your hands to pull the elastic of the mask off the head
      • The goggles will need to be cleaned and disinfected according to your hospital’s policy
    • Remove the mask again, by avoiding contact with the front surface, using the elastic straps to pull the mask off your head and immediately place in a bin
    • Clean your hands and forearms immediately after the doffing procedure

     If you are working in a COVID-19 ward and are moving from patient to patient, you won’t need to remove the goggles and mask with each interaction, only the gloves and gown. Remember to perform good hand hygiene between as noted above at each of the intervals noted above to avoid contamination of yourself or other patients.  The re-use of PPE will be discussed later in this post, this will also depend on the system where you work.

    3. What mask should I wear and when? (cloth vs surgical vs N95)

    Cloth masks

    These masks are not for use in the healthcare setting and are only recommended for use when people are out in public spaces. The mask does not provide the greatest protection. Social distancing and hand washing remain the best recommendation for prevention of spread.

     

    Public areas of the hospital and areas where there is not likely to be exposure to a COVID-19 positive patient is where these masks might be used:

    • Canteens
    • Outdoor areas
    • Public waiting spaces
    PPE Recommendations

    Why not cloth masks for healthcare workers?

    Cotton masks are not indicated for healthcare work because there is no filtration or protection against droplets or splashes. There is also the “wicking effect” which increases the risk of mucous membrane contamination. Cotton draws moisture towards the skin so if the cotton mask does get soiled, there is no protection for the healthcare worker. As this risk is low in a public space, the mask is recommended for use. HOWEVER, if the mask does get soiled in a public space, it should rather be removed and replaced.

    PPE Recommendations

    Cloth masks also need to conform to the following criteria to be helpful:

    • The mouth and nose are fully covered
    • The covering fits snugly against the sides of the face so there are no gaps
    • There should be no difficulty breathing while wearing the cloth face covering
    • The cloth face covering can be tied or otherwise secured to prevent slipping
    • The cloth mask should be made of multiple layers of cloth
    • The cloth mask must be washable and should be able to be ironable (these cloths should be washed after they are used each day)

    Surgical Face Masks

    These masks are for use in the healthcare setting for providers who are working in general wards and around patients who may present with possible COVID-19 infection. Any staff in contact with patients should ideally wear this kind of mask (reception staff, cleaning staff, clinical staff). They are waterproof and provide protection against splashes and droplets. They are multiplayer masks and provide a higher level of protection. Because these masks are specialised, they should be reserved for use by healthcare workers only.

     

    The following recommendations apply to these masks:

    These masks are for use in the healthcare setting for providers who are working in general wards and around patients who may present with possible COVID-19 infection. Any staff in contact with any patient should ideally wear this kind of mask (reception staff, cleaning staff, clinical staff). They are waterproof and provide protection against splashes and droplets. They are multilayer masks and provide a higher level of protection. Because these masks are specialized, they should be reserved for use by healthcare workers only.

    PPE Recommendations

    N95/FFP2-3 Masks

    PPE Recommendations

    These masks are for use by healthcare providers only, and only when they are expecting to be exposed to a possible aerosol creating procedure.

    These procedures can be found below:

    Swabbing of the patient for COVID-19 testing is also considered high risk, and the appropriate PPE should be in place. 

    PPE Recommendations

    4. What is the deal with gloves?

    Gloves are for use in single interaction situations where the hands need to be protected from possible exposure to the virus. The general rule with gloves is to treat them as heavily soiled pieces of equipment, this means they should NEVER touch your face, your personal belongings, the inside of your pockets, your mask, or anything except the patient that is being treated at the time.

    These are single use protective devices and should be used along with exceptional hand hygiene to manage the spread of infection.

    Below are a few images of how gloves SHOULD NOT BE USED, these should make you very uncomfortable.

    PPE Recommendations
    PPE Recommendations

    5. Can I use PPE more than once

    The table below has been taken from the NICD SA guidelines  which specify when and what PPE may be reused

    PPE Recommendations

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    References:

    Department of Health. 2020. COVID-19 Disease: Infection Prevention and Control Guidelines Version 1 April 2020 . Published by the Department of Health. available online: https://www.idealhealthfacility.org.za/docs/Manuals-and-Handbooks/COVID%2019%20Disease%20Infection%20Prevention%20and%20Control%20Guidelines%20Version%201%20-%20%20April%202020.pdf [accessed: 08 May 2020)

    This post will deal with the role of the Emergency Medical provider in the management of the deceased patient who is either positive for COVID-19, or is suspected of having the infection (in the case where the patient was not able to be tested prior to their demise).

    There are government regulations and recommendations for the management of the deceased with possible COVID-19 infection available. These NICD Guidelines have been linked HERE for more information.

    Handling the body immediately after death

    The good news is that there appears to be very little risk of spreading the disease through the management and handling of the deceased post-mortem. However, there does exist the potential risk for the transmission of the virus through direct contact (without appropriate PPE), as well as contact with body fluids which may contain the virus.

    There is also the potential risk that through handling of the body there may be a chance that aerosol is created in movement. Although this risk is incredibly low, the standard precautions for the virus should be maintained with the deceased, as they are with care of the COVID-19 patient. There is a higher risk of exposure to the staff performing post-mortem examinations than to the emergency care provider.

     

    The following guidance has been summarized:

    1. A body bag should be used when transporting the deceased from the place of death to any other place (mortuary/hospital mortuary) as movement of the body can cause small amounts of air to be expelled from the lungs which poses a minor risk.
    2. All personnel handling the deceased are required to don full PPE (as noted below in the table for Clinical Staff)
    3. The hospital trolley/Ambulance stretcher transporting the deceased as well as the outer surface of the body bag should be decontaminated, preferably by 2 individuals in PPE, prior to leaving the ward/unit/scene.
    4. Prior to placing the deceased in the body bag, it may be acceptable for family to view the body, however they should be in full PPE, and there should be little or no contact with the deceased at all, this will limit infection spread. One or two family representatives may be elected to view the body if the family wish, but ideally limit the number of people allowed into contact with the body if possible.
    5. “The CDC recommends not touching, kissing or hugging the deceased, though acknowledges that touching a hand or clothing after the body has been prepared for viewing is lower risk if hand-washing can then immediately occur” (Wilson, 2020).
    6. After use, body bags should be treated and disposed as a health care risk waste along with all PPE from the room/area/scene.

    Appropriate PPE

    As with all the recommendations with PPE, the wearer must be able to don and doff the PPE appropriately for their own protection

    Recommendations as per the standard guidance for care of a potential COVID-19 patient are to be adhered to:

    • Gown/apron to be worn (preferably a long-sleeved, waterproof gown if contact with the body is expected)
    • FFP2/FFP3 mask is to be worn if there is the risk of aerosol generation (surgical mask may be acceptable if this risk is considered to be low)
    • Eye protection to be worn
    • Gloves to be worn

    The table below should be used as a guide for PPE requirements (the reference for the table can be found HERE).

    Each company/hospital will have different protocols, ensure that you are aware of and able to follow the protocols laid out by the system in which you work.

    Covid deceased management

    Cleaning the area after death

    Once the deceased has been packaged and removed to the appropriate space either within the hospital, or to the mortuary (depending on the circumstances), the treatment area will need to be cleaned and decontaminated.

    • The person cleaning the space should don appropriate PPE (see above)
    • All equipment used in the care of the patient should be disinfected as per service/hospital protocol, all disposables should be disposed of into medical waste bins and removed
    • Surfaces are to be sprayed and wiped down physically with an appropriate cleaning solution (bleach solution mixed according to the table below, or hospital cleaning products which are recommended for the prevention of virus spread).
    • Solutions containing >70% alcohol may also be used to wipe down these surfaces
    • If the hospital/service has access to the use of ultraviolet light cleaners, these may be used in the room/environment to clean the surfaces and the general spaces after the surfaces have been cleaned with soap and water/other recommended cleaner as noted above (there are a number of regulations for the use of these devices and the manufacturer recommendations should be followed)
    Covid deceased management

    Post-Mortem: who should be referred?

    It is important to note that if the death of a patient is considered is confirmed to be Covid-19, an autopsy is unlikely to be necessary and a medical certificate with the cause of death should be given.

    If the death is due to a forensic case, then a full autopsy needs to be conducted (Hanley et al., 2020). Follow the usual referral pathways for Autopsy in your setting/centre and ensure that the laws of the country are followed for these situations.

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    References:

    European Centre For Disease Prevention and Control (2020) ‘Considerations related to the safe handling of bodies of deceased persons with suspected or confirmed COVID-19 Scope of this document’, pp. 1–4.

    Guidelines for the Preparation of Mass Burials and Cremation of COVID-19 Victims – South African Cemeteries Association (no date). Available at: http://sa-cca.org.za/guidelines-for-the-preparation-of-mass-burials-and-cremation-of-covid-19-victims/ (Accessed: 4 May 2020).

    Hanley, B. et al. (2020) ‘Autopsy in suspected COVID-19 cases’, Journal of clinical pathology, pp. 239–242. doi: 10.1136/jclinpath-2020-206522.

    National Department of Health, S. A. (2020) ‘COVID-19 Disease: Infection Prevention and Control Guidelines’, (April). Available at: https://j9z5g3w2.stackpathcdn.com/wp-content/uploads/2020/04/Covid-19-Infection-and-Prevention-Control-Guidelines-1-April-2020.pdf.

    Republic of South Africa. (2020) ‘Government Gazette – updated guidelines on burial’.

    WHO Interm Guidance (2020) ‘Infection Prevention and Control for the safe management of a dead body in the context of COVID-19’, Journal of Hospital Infection, 104(3), pp. 246–251. doi: 10.1016/j.jhin.2020.01.022.

    Wilson, L. 2020. How to avoid infection after a COVID-19 death – an Ebola response veteran explains. The Conversation. Published online 20 April 2020: https://theconversation.com/how-to-avoid-infection-after-a-covid-19-death-an-ebola-response-veteran-explains-135904 [accessed 04 May 2020].