PHEMCAST

PHEMCAST

By Tim Nutbeam and Clare BosankoMedicine
Download on the App Store

PHEMCAST episodes

  • Episode 28: LOST

    https://phemcast.co.uk/wp-content/uploads/2018/04/lost-final.mp3

     

    Cardiac arrest is the end point, it is the symptom, not the diagnosis. The pathophysiological process varies, and this is particularly relevant in trauma vs medical. In medical cardiac arrest, the pathological processes tend to affect the heart’s ability to pump: eg primary cardiac event, chemical/electrolyte abnormality, but full circulation. In trauma the process is generally not primarily due to pump failure, but due to hypovolaemia or obstruction. It might be better to consider traumatic cardiac arrest as a completely different disease eg LOST: Low Output State due to Trauma

    The 2015 European Resuscitation Council and UK Resuscitation Council Algorithms for Traumatic Cardiac Arrest:

     

    To read the whole ERC guideline on special circumstances cardiac arrest including trauma, click here.

    Ultrasound during TCA: Cureton et al. The heart of the matter: utility of ultrasound of cardiac activity during traumatic arrest. J Trauma. 2012; 73: 102-10.

    The outcomes from different resuscitative interventions in a haemorrhagic shock model in porcine model:

    From: Watts et al. Closed chest compressions reduce survival in a model of haemorrhagic-induced traumatic cardiac arrest . EMJ 2017; 34: 860-900. (A866)

    Impact brain apnoea: Wilson et al. Impact brain apnoea – A forgotten cause of cardiovascular collapse in trauma. Resuscitation. 2016; 105: 52-58.

    References
    1. Barnard et al. Epidemiology and aetiology of TCA in England… Resuscitation; 110 (2017): 90-94.
    2. Russell RJ et al. The role of trauma scoring in developing trauma clinical governance in the Defence Medical Services. Phil Trans R Soc. 2011; 366. Doi: 1098/rstb.2010.0232
    3. Wise et al. Emergency thoracotomy ‘how to do it’. EMJ; 2005: 22-24.
    4. Morrison et al. Resuscitative thoracotomy following wartime injury.
    5. Jeffcoach DR et al. Use of CPR in hemorrhagic shock, a dog model.
    6. Lockey et al. Traumatic cardiac arrest: who are the survivors? Annals of Emergency Medicine; 2006.
    7. Grasner et al. Cardiopulmonary resuscitation in traumatic cardiac arrest – there are survivors. Critical Care; 2011.
    8. Zwingmann et al. Survival and neurological outcome after OOH TCA in pediatric & adult populations: a systematic review. Critical Care; 2012.
    9. Slessor et al. To Be Blunt: are we wasting our time? Emergency Deaprtment Thoracotomy following blunt trauma: a systematic review & meta-analysis. Anneals of EM; 2015: 297-307.
    10. Leis CC et sl. TCA: should advanced life support be initiated? J Trauma. 2013; 74: 634-8.
    11. Jacobs et al. Effect of adrenaline on survival in out of hospital cardiac arrest: randomised double-blind placebo controlled trial. Resuscitation. 2011; 82: 1138-43.
    12. Smith et al. Traumatic Cardiac Arrest. Journal of Royal Society of Medicine. 2015; 108: 11-16.
    13. Sperry et al. Early use of vasopressors after injury: caution before constriction. J Trauma. 2008; 64: 9-14/
      14. 29 min
    14. Episode 27: Checklists

      https://phemcast.co.uk/wp-content/uploads/2018/01/checklists_final.mp3

      We recommend reading Atul Gawande’s book ‘The Checklist Manifesto’. It’s a well written, fascinating story about the introduction of the WHO Safer Surgery checklist and the impact it had. This link will take you straight to Amazon if you want to buy a copy (other internet retailers exist!!)

      To understand the how human factors failed in the death of Martin’s wife, Elaine, please watch this video:

      The fabulous Life in the Fast Lane have also produced a blog on the case.

      There are lots of resources available on the Clinical Human Factors Group website.

      52 min
    15. Episode 26: Tranexamic Acid

      https://phemcast.co.uk/wp-content/uploads/2018/01/txa-final.mp3

       

      The paper which we discuss in the interview is available open access here

      How does tranexamic acid work?

      Taken from: https://pbrainmd.wordpress.com/2015/10/15/1335/

      Critical appraisal aids

      To understand more about hierachy of evidence and how a systematic review fits into this please have a look at these resources available from the Cochrane group.

      http://consumers.cochrane.org/levels-evidence

      http://training.cochrane.org/path/grade-approach-evaluating-quality-evidence-pathway

      The CASP checklist can be used for assessing the quality of a meta-analysis.

      More TXA research trials

      Want to know more about the ongoing Crash 3 trial?

      Want to know more about the Halt it trial?

       

      References
      • CRASH-2 (available open access here)
      • The WOMAN Trial (available Open access here)
      • The meta-analysis of topical tranexamic acid which Ian mentions is a Cochrane review, available here.
        • 38 min
      • Episode 25: Tension pneumothorax 2

        https://phemcast.co.uk/wp-content/uploads/2017/12/tp2-final-11_11_2017-00-30.mp3

        Where can you undertake decompression of a pneumothorax?

        Be particularly careful when using the 2nd intercostal space mid-clavicular line that you are sufficiently lateral. For example, here are the locations identified as ‘2nd ICS mid clavicular line’ amongst 25 EM physicians in a 2005 EMJ paper.

        From http://emj.bmj.com/content/22/11/788

        The Three Kings: George Clooney’s recommended approach to decompression of a tension pneumothorax. Note – again please do not use this location!

        Devices used for decompression:

         

        Dressings available for covering an open pneumothorax +/- thoracostomy in a spontaneously breathing patient:

         

        References

        • Ball, C. G., Wyrzykowski, A. D., Kirkpatrick, A. W., Dente, C. J., Nicholas, J. M., Salomone, J. P., et al. (2010). Thoracic needle decompression for tension pneumothorax: clinical correlation with catheter length. Canadian Journal of Surgery Journal Canadien De Chirurgie, 53(3), 184–188.
        • Barton, E. D., Epperson, M., Hoyt, D. B., Fortlage, D., & Rosen, P. (1995). Prehospital needle aspiration and tube thoracostomy in trauma victims: a six-year experience with aeromedical crews. The Journal of Emergency Medicine, 13(2), 155–163.
        • Beckett, A., Savage, E., Pannell, D., Acharya, S., Kirkpatrick, A., & Tien, H. C. (2011). Needle Decompression for Tension Pneumothorax in Tactical Combat Casualty Care: Do Catheters Placed in the Midaxillary Line Kink More Often Than Those in the Midclavicular Line? The Journal of Trauma, 71, S408–S412. http://doi.org/10.1097/TA.0b013e318232e558
        • Cullinane, D., Morris, J., Bass, J., & Rutherford, E. (2001). Needle thoracostomy may not be indicated in the trauma patient. Injury, 32, 749–752.
        • Ferrie, E. P., Collum, N., & McGovern, S. (2005). The right place in the right space? Awareness of site for needle thoracocentesis. Emergency Medicine Journal, 22(11), 788–789. http://doi.org/10.1136/emj.2004.015107
        • Fitzgerald, M., Mackenzie, C. F., Marasco, S., Hoyle, R., & Kossmann, T. (2008). Pleural decompression and drainage during trauma reception and resuscitation. Injury, 39(1), 9–20. http://doi.org/10.1016/j.injury.2007.07.021
        • Givens, M. L., Ayotte, K., & Manifold, C. (2004). Needle thoracostomy: implications of computed tomography chest wall thickness. Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine, 11(2), 211–213. http://doi.org/10.1197/j.aem.2003.09.015
        • Harcke, H. T., Mabry, R. L., & Mazuchowski, E. L. (2013). Needle thoracentesis decompression: observations from postmortem computed tomography and autopsy. Journal of Special Operations Medicine : a Peer Reviewed Journal for SOF Medical Professionals, 13(4), 53–58.
        • Inaba, K., Branco, B. C., Eckstein, M., Shatz, D. V., Martin, M. J., Green, D. J., et al. (2011). Optimal positioning for emergent needle thoracostomy: a cadaver-based study. The Journal of Trauma, 71(5), 1099–103– discussion 1103. http://doi.org/10.1097/TA.0b013e31822d9618
        • Inaba, K., Ives, C., McClure, K., Branco, B. C., Eckstein, M., Shatz, D., et al. (2012). Radiologic evaluation of alternative sites for needle decompression of tension pneumothorax. Archives of Surgery (Chicago, Ill : 1960), 147(9), 813–818. http://doi.org/10.1001/archsurg.2012.751
        • Jadder, U., & McAuley, D. (2005). Transthoracic ultrasonography to diagnose pneumothorax in trauma. BestBETS.org, 1–3.
        • Jones, R., & Hollingsworth, J. (2002). Tension pneumothoraces not responding to needle thoracocentesis. Emergency Medicine Journal, 19, 176–177.
        • MD, A. R. M., MD, M. E. R., MD, C. S. C., & MD, J. L. M. (2015). Ultrasound determination of chest wall thickness: implications for needle thoracostomy. The American Journal of Emergency Medicine, 1–5. http://doi.org/10.1016/j.ajem.2010.06.030
        • MD, B. B., & MD, J.-M. T. (2012). Initial Management and Resuscitation of Severe Chest Trauma. Emergency Medicine Clinics of NA, 30(2), 377–400. http://doi.org/10.1016/j.emc.2011.10.010
        • MD, E. J. C., MD, C. H. C., BS, R. M., PHD, C. L. A., RDMS, C. A. K. M. M., RDMS, S. S. M., & RDMS, J. C. F. M. (2013). Ultrasound in Emergency Medicine. The Journal of Emergency Medicine, 44(1), 142–149. http://doi.org/10.1016/j.jemermed.2012.02.032
        • Netto, F. A. C. S., Shulman, H., Rizoli, S. B., Tremblay, L. N., Brenneman, F., & Tien, H. (2008). Are needle decompressions for tension pneumothoraces being performed appropriately for appropriate indications? The American Journal of Emergency Medicine, 26(5), 597–602. http://doi.org/10.1016/j.ajem.2007.08.016
        • Rathinam, S., Grobler, S., Bleetman, A., Kink, T., & Steyn, R. (2014). Evolved design makes ThoraQuik safe and user friendly in the management of pneumothorax and pleural effusion. Emergency Medicine Journal, 31(1), 59–64. http://doi.org/10.1136/emermed-2012-201821
        • Rathinam, S., Quinn, D. W., Bleetman, A., Wall, P., & Steyn, R. S. (2011). Evaluation of ThoraQuik: a new device for the treatment of pneumothorax and pleural effusion. Emergency Medicine Journal, 28(9), 750–753. http://doi.org/10.1136/emj.2009.082297
        • Sanchez, L. D., Straszewski, S., Saghir, A., Khan, A., Horn, E., Fischer, C., et al. (2011). Anterior versus lateral needle decompression of tension pneumothorax: comparison by computed tomography chest wall measurement. Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine, 18(10), 1022–1026. http://doi.org/10.1111/j.1553-2712.2011.01159.x
        • Wax, D. B., & Leibowitz, A. B. (2007). Radiologic assessment of potential sites for needle decompression of a tension pneumothorax. Anesthesia and Analgesia, 105(5), 1385–8– table of contents. http://doi.org/10.1213/01.ane.0000282827.86345.ff
        • Yamagiwa, T., Morita, S., Yamamoto, R., Seki, T., Sugimoto, K., & Inokuchi, S. (2012). Determination of the appropriate catheter length for needle thoracostomy by using computed tomography scans of trauma patients in Japan. Injury, 43(1), 42–45. http://doi.org/10.1016/j.injury.2010.11.022
        • Zengerink, I., Brink, P. R., Laupland, K. B., Raber, E. L., Zygun, D., & Kortbeek, J. B. (2008). Needle thoracostomy in the treatment of a tension pneumothorax in trauma patients: what size needle? The Journal of Trauma, 64(1), 111–114.  http://doi.org/10.1097/01.ta.0000239241.59283.03
          • 29 min
        • Episode 24: Tension pneumothorax 1

          https://phemcast.co.uk/wp-content/uploads/2017/12/tp-1-fin-11_11_2017-00-08.mp3

          Firstly, go and read Simon and Tim Harris’ great 2005 paper on the subject which we reference repeatedly in the podcast. It is available free open access here.

          A pneumothorax exists when air accumulates in the potential space between the visceral and parietal pleura:

          From: www.wisdomjobs.com

          A tension pneumothorax exists when the air in the pleural cavity is under high pressure resulting in compression of the surrounding structures.

          Simon mentions Rutherford’s diagram in the podcast. This is taken from a 1968 paper examining the progressive pathophysiology of a tension pneumothorax. The graph shows the changes in intrapleural pressure (on the ipsilateral and contralateral sides) in spontaneously breathing goats who had air injected into one side of their chest. We can’t find the full article free/open access anywhere I’m afraid. But this is the reference: THE PATHOPHYSIOLOGY OF PROGRESSIVE, TENSION PNEUMOTHORAX. Rutherford RB, Hurt HH, Brickman RD, Tubb JM. Journal of Trauma and Acute Care Surgery, March 1968,8(2):212-227

          The imaging findings of tension pneumothorax might look like this:

          From: http://www.unboundedmedicine.com

          More plain film images are available in this article on the Radiopaedia website.

          And you can see what a CT scan of a patient with tension pneumothorax looks like in this vimeo shared on the Life in the Fast Lane website.

          If you want to know about ultrasound findings of pneumothorax, check out this great R.E.B.E.L.EM post.

          References:

          Leigh-Smith S, Harris T. Tension pneumothorax—time for a re-think? EMJ. 2005; 22:8-16.  doi.org/10.1136/emj.2003.010421

          Roberts DJ, Leigh-Smith S et al. Clinical Presentation of patients with a Tension Pneumothorax – a systematic review. Annals of Surgery. 2015; 261: 1068-78. doi: 10.1097/SLA.0000000000001073

          43 min
        • Episode 23: Intraosseus access

          https://phemcast.co.uk/wp-content/uploads/2017/11/io-fin-10-11-2017-22-41.mp3

          The various devices which Tony discusses are:

          This video shows the rapidity of infusion entering the circulation from a humeral IO.

          This is the paper mentioned by Tony, which shows the stepwise improvement in mortality amongst combat casualties from military conflict 2003-2012, including the ‘unicorn’ graph:

          Anatomy of bones and the humerus related to intraosseus access

          Long bone anatomy

          Humeral anatomy

           

          The surface anatomy of the shoulder

          The bony anatomy of the shoulder

          Muscular attachments of the shoulder

          Blood vessels and nerves around the proximal humerus

          A demonstration of the landmarking process for humeral intraosseus insertion is available here.

          Want to know more about EZ-IO access?

          The education resources which Tom mentions are available here.

           

          50 min
        • Episode 20: End Tidal Carbon Dioxide

          Guest contributor: Lauren Weekes

          https://phemcast.co.uk/wp-content/uploads/2017/09/et-06092017-16-24.mp3

          What is ETCO2?

          • % or partial pressure of carbon dioxide measured somewhere near the mouth at the end of a normal exhalation (hence end tidal, end of tidal volume breath)
          • To get a measurement the following systems need to be functioning:
            • Metabolically active tissue to produce CO2
            • Circulation & cardiac output to carry that CO2 to the lungs in blood
            • Transfer of CO2 between the blood and the air in the lung
            • Gas in and out of the lung to excrete the CO2
            • Brilliant monitor in anaesthesia in that in elective cases, we start off with healthy patients are looking for deviations from the norm- and a normal ETCO2 trace tells you that all those components are functioning.
            • It is still extremely useful in prehospital care, but we just have to remember that an abnormal trace or value may be caused by problems with one or more of those systems i.e circulation, gas exchange, ventilation (rarely tissue metabolism)
            • Much better than pulse oximetry, because of the difference in lag time between clinical change occurring and being able to see it on the monitor- less than 3 seconds for sidestream capnography, compared to up to 90s for pulse oximetry

              •  

              How does ETCO2 relate to arterial CO2?

              • What we’re REALLY interested in is arterial CO2 as this is the clinically significant value in a number of clinical scenarios; for example in the brain-injured patient, we want to keep arterial CO2 values normal as we know that this determines the state of cerebral vasoconstriction or dilation, and thus affects ICP. In non-brain injured patients, high arterial CO2 can lead to a respiratory acidosis, and low pH values are harmful to most body tissues, in particular the clotting cascade (because of its reliance on enzymes, which function best in a narrow range of pH), and cardiac contractility.
              • In healthy people, ETCO2 is usually 0.5-1kPA LOWER than the arterial value. Why is this? CO2 is only found in parts of the lung which participate in gas exchange, i.e are perfused with blood. So the trachea and first few generations of bronchi do not participate in gas exchange and are known as the dead space. They ARE however filling with gas during breaths, and as such gas from this dead space DILUTES the gas containing CO2 that has come predominantly from the alveoli.
              • What we are assuming when we ask ETCO2 to substitute for arterial CO2 is that there is normal matching of ventilation to perfusion occurring in the lungs, so that all the mixed venous CO2 returning to the lungs from respiring tissue can equilibrate with alveolar gas and be eliminated via ventilation

                •  

                What causes a discrepancy between arterial and ETCO2?

                1. Artefact

                  2. Loose connections, not having nasal prongs up nose, dilution with high oxygen flows (partic when using nasal prongs)

                  1. Failure of venous CO2 to cross to ventilated alveoli

                    2. Alveolar dead space- alveoli are ventilated but not perfused

                    Classically low cardiac output states, PE, etc

                    1. Failure of alveolar gas to be transported out of the lungs because alveoli are perfused but not ventilated (shunt):
                      • pneumonia and pulmonary edema, pulm haemorrhage (alveoli filled with fluid)
                      • tissue trauma: alveolar wall swelling
                      • atelectasis: collapse of alveoli from failure to expand, or absorption of the air out of the alveoli without replacing it
                      • mucous/vomit plugging
                      • Global ventilation failure e.g airway obstruction, hypoventilation esp where tidal volume is very low- dead space is fixed, so as a proportion of each breath it gets higher as tidal volume reduces until there is minimal ALVEOLAR ventilation

                        •  

                         

                        How do we measure it? 

                        • Usually by infra-red absorption- CO2 absorbs infra-red light in a manner proportional to its concentration in the sampled gas.
                        • Can be measured from a breathing circuit attached to an invasive airway device e.g supraglottic airway or endotracheal tube, or from a number of methods in the spontaneously breathing patient, such as a specific nasal cannula, or a sampling tube attached to an oxygen mask. Important to note that the waveform, and values for ETCO2 are very different in the spontaneously breathing patient, and we’ll come back to that later.
                        • Might be measured directly from the breathing circuit (mainstream) or sucked out of the circuit in a sampling tube (sidestream).
                        • Might display results as a waveform with a value given for ETCO2, or simply a number (capnometry) although the latter much less useful.
                        • Colorimetric devices are available which change colour, based loosely on percentage of gas present. pH related. Occasionally used as an adjunct to waveform

                          •  

                          What does the waveform mean?

                          • The classic waveform that you will see in textbooks come from CO2 measured in the ventilated patient.
                          • The graph has time in seconds along the x axis and partial pressure in kPa along the y axis
                          • Phase I (inspiratory baseline) reflects inspired gas, which is normally devoid of carbon dioxide.
                          • Phase II (expiratory upstroke) is the transition between dead space and alveolar gas from the respiratory bronchioles and alveoli.
                          • Phase III is the alveolar plateau, when largely homogenous gas from the alveoli empties. This is the most accurate reflection of arterial co2
                          • Phase 0  is the inspiratory downstroke, the beginning of the next inspiration
                          • In the spontaneously breathing patient, there is not usually a plateau phase, which makes interpretation of ETCO2 values more difficult

                            •  

                            EVIDENCE

                            ETT placement

                            • All major anaesthetic organisations mandate the use of ETCO2 to confirm ETT placement
                            • Good evidence that the trace is not completely flat even in cardiac arrest- Silvestri Ann Emerg Med 2005
                            • Should seen >7 waveforms to exclude oesophageal (Orinato 1993)

                              •  

                              Cardiac arrest- general

                              • 2010 & 2015 ERC guidelines recommend use of waveform capnography
                              • Not new- 1978 paper Kalenda in Resuscitation described the use of capnogram as a guide to CPR efficacy

                                •  

                                Predicting ROSC

                                • Grmec 2003 & 2011 in Critical Care
                                • ETCO2 of >2.4kpa after 20min predictive of rosc , <1.3 = no ROSC
                                • Alwens 2001 used cut off 10mmHg
                                • Systematic review in 2013 Resuscitation used cut off of 1.3kPa but this wasn’t 100% sensitive across all studies
                                • Concerns also raised by Norwegian paper in Resuscitation again 2011 showing a number of confounding factors made interpretation of etco2 problematic inc rhythm, bystander CPR, cause of arrest

                                  •  

                                  CPR quality

                                  • As noted in 1978, ETCO2 drops off when chest compressions become ineffective.
                                  • Qvigstad et al showed in again in Resuscitation in 2013, confirming inter-individual variation in effectiveness of CPR using ETCO2 as a surrogate for CO

                                    •  

                                    Trauma

                                    • Deakin et al. (J. trauma 2004) showed that end-tidal CO2 may be of value in predicting outcome from major trauma (19). In a study of 191 blunt trauma patients, only 5% of patients with an end-tidal CO2 determination of 3.25 kPa survived to discharge

                                      •  

                                       

                                      PRACTICAL USE

                                      When should we use ETCO2 monitoring in the prehospital setting?

                                      • Mandatory if intubating (RSI, cardiac arrest)
                                      • Mandatory if performing procedural sedation where consciousness impaired
                                      • Highly recommended in cardiac arrest
                                      • Highly recommended in all critically ill patients

                                        •  

                                        In cardiac arrest:

                                        Attach to circuit/ BVM at soonest available opportunity

                                        Use it to confirm intubation (if using)

                                        Use it as a guide:

                                        • If ETCO2 has been steady during CPR but then begins to fall, consider changing rescuer
                                        • As corroborating evidence around decision making- if there has been no ROSC after 20min of full ALS protocol and ETCO2 remains below 1.3kPA, you are highly unlikely to resuscitate that patient
                                        • If there is a sudden increase in ETCO2- well done, you’ve achieved ROSC (even if you can’t yet feel a pulse- in fact, maybe you needn’t do a pulse check if you’ve got ETCO2)
                                        • Optimise ventilation post ROSC as you are now dealing with a head-injured patient.

                                          •  

                                          In the critically ill patient:

                                          • If I can only have one monitor on an entrapped patient, I’d pick capnography
                                          • You will learn more quickly than any other method when your patient is deteriorating- e.g in blood loss, ETC02 will gradually fall. In the head injured patient who’s coning, you’ll see apnoeas and gradually rising ETCO2. In the heart failure patient who’s about to arrest, you’ll see their ETCO2 fall precipitously almost before anything else. In the comatose patient, you’ll be able to see that their airway is obstructed on the capnography a full 30 to 60s before their sats drop (by which point you’re already a long way down the oxygen dissociation curve).
                                          • You can also see when your treatment is working- if you give a patient in septic shock some fluid and improve their CO, you’ll see a rise in ETC02
                                          • You can confirm adequacy of respiratory function in the fitting or post-ictal patient when all other methods fail

                                            •  

                                            PITFALLS

                                            Device failure- lines blocking, batteries running out, pump failure.

                                            Test by blowing

                                            Over-interpreting the accuracy of non-invasive capnography

                                            • Those lovely graphs showing curare clefts, rebreathing, bronchospasm etc you see on lots of different websites and in textbooks? They are almost all referring to capnography in the intubated and ventilated patient, who has a constant tidal volume.
                                            • Numbers are often wildly inaccurate in the critically unwell population, and there may be an ET-arterial gradient of 10kPA.
                                            • What CAN you tell from it? 1. Ventilation is occurring (accurate RR) 2. There is a cardiac output 3. You can interpret trends ie a gradual rise or fall in CO2, in the given clinical context 4. Very low is bad whichever way you look at it

                                              •  

                                              Sometimes a low ETCO2 value is due to hyperventilation (because as we all remember, arterial CO2 concentration is almost linearly related to alveolar minute ventilation) BUT it may be hypoventilation with increased proportion of dead space ventilation compared to alveolar ventilation

                                               

                                              Not using capnography

                                              • The more you use it, the more familiar with various patterns you will become
                                              • Stick it on everyone –it causes no harm. See what happens when you give a decent dose of morphine:
                                                • slows respiratory rate but breaths are normal volume
                                                • You get reduced alveolar MINUTE ventilation but normal alveolar TIDAL ventilation
                                                • Therefore what you see at ETCO2 is reasonably representative of arterial concentration because the same number of alveoli are ventilated and have opportunity to equilibrate with the blood CO2
                                                • This is unlike when a patient is making low tidal volume breaths, because then you’re largely ventilating dead space, and a much smaller number of alveoli are ventilated and thus equilibrium cannot occur between blood and gas

                                                  • Demonstration traces: 

                                                  From: Capnography Outside the Operating Rooms, Anesthes. 2013;118(1):192-201. doi:10.1097/ALN.0b013e318278c8b6

                                                  A Prolonged phase II, increased α angle, and steeper phase III suggest bronchospasm or airway obstruction.

                                                  B Expiratory valve malfunction resulting in elevation of the baseline, and the angle between the alveolar plateau and the downstroke of inspiration is increased from 90°. This is due to rebreathing of expiratory gases from the expiratory limb during inspiration.

                                                  C Inspiratory valve malfunction resulting in rebreathing of expired gases from inspiratory limb during inspiration (reference 5 for details).

                                                  D Capnogram with normal phase II but with increased slope of phase III. This capnogram is observed in pregnant subjects under general anesthesia (normal physiologic variant and details in reference 9).

                                                  E Curare cleft: Patient is attempting to breathe during partial muscle paralysis. Surgical movements on the chest and abdomen can also result in the curare cleft.

                                                  F Baseline is elevated as a result of carbon dioxide rebreathing.

                                                  G Esophageal intubation resulting in the gastric washout of residual carbon dioxide and subsequent carbon dioxide will be zero.

                                                  H  Spontaneously breathing carbon dioxide waveforms where phase III is not well delineated.

                                                  I  Dual capnogram in one lung transplantation patient. The first peak in phase III is from the transplanted normal lung, whereas the second peak is from the native disease lung. A variation of dual capnogram (steeple sign capnogram – dotted line) is seen if there is a leak around the sidestream sensor port at the monitor. This is because of the dilution of expired PCO2with atmospheric air.

                                                  J Malignant hyperpyrexia where carbon dioxide is raising gradually with zero baseline suggesting increased carbon dioxide production with carbon dioxide absorption by the soda lime.

                                                  K Classic ripple effect during the expiratory pause showing cardiogenic oscillations. These occur as a result of to-and-for movement of expired gases at the sensor due to motion of the heartbeat during expiratory pause when respiratory frequency of mechanical ventilation is low. Ripple effect like wave forms also occur when forward flow of fresh gases from a source during expiratory pause intermingles with expiratory gases at the sensor.

                                                  L  Sudden raise of baseline and the end-tidal PCO2(PETCO2) due to contamination of the sensor with secretions or water vapor. Gradual rise of baseline and PETCO2occurs when soda lime is exhausted.

                                                  M Intermittent mechanical ventilation (IMV) breaths in the midst of spontaneously breathing patient. A comparison of the height of spontaneous breaths compared to the mechanical breaths is useful to assess spontaneous ventilation during weaning process.

                                                  N  Cardiopulmonary resuscitation: capnogram showing positive waveforms during each compression suggesting effective cardiac compression generating pulmonary blood.

                                                  O  Capnogram showing rebreathing during inspiration. This is normal in rebreathing circuits such as Mapleson D or Bain circuit.

                                                  Useful links: 

                                                  https://lifeinthefastlane.com/ccc/capnography-waveform-interpretation/

                                                  http://www.capnography.com/new/index.php?option=com_content&view=article&id=131&Itemid=993

                                                  40 min
                                                • Episode 19: Surgical Airway

                                                  https://phemcast.co.uk/wp-content/uploads/2017/07/surg.mp3

                                                   

                                                  The West Midlands surgical skills course offers cadaveric training for PHEM and EM practitioners on rare life saving procedures. Click here to go straight to their page.

                                                  Anatomy

                                                  The Guidelines

                                                  Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. C. Frerk et al. Difficult Airway Society: Intubation guidelines working group. British Journal of Anaesthesia, 115 (6): 827–848 (2015) doi:10.1093/bja/aev371

                                                  For more information, have a look at the Difficult Airway Society website.

                                                  AAGBI Safer Prehospital Anaesthesia

                                                  Click here for the 2017 guidelines

                                                  The Kit

                                                  Know what your service carries, practice with that equipment, then you will be familiar with the kit you are using in the heat of the moment.

                                                  Minimal kit: scalpel, bougie, tube

                                                  Tracheal dilators and tracheal hook

                                                  The Technique

                                                  For a demonstration of the DAS recommended technique for surgical front of neck access, have a look at this video, recorded by colleagues over at openairway.org:

                                                  Just a Routine operation

                                                  The video we mention in the podcast produced by Martin Bromiley after the death of his wife, Elaine, in a can’t intubate can’t oxygenate scenario is available here:

                                                  https://www.youtube.com/watch?v=JzlvgtPIof4

                                                  And have a look at the website for more of Martin’s work with the Clinical Human Factors group.

                                                  Other fantastic #FOAM resources regarding airway management are available:

                                                  From Nicholas Chrimes  at http://vortexapproach.org

                                                  From the fabulous people over at Life in the Fast Lane including a video demo from Scott Weingart from EMCrit: https://lifeinthefastlane.com/ccc/surgical-cricothyroidotomy/

                                                  References

                                                  This is Tim’s recent publication we mention in the ‘cast!: Nutbeam, T., Clarke, R., Luff, T., Enki, D. and Gay, D. (2017), The height of the cricothyroid membrane on computed tomography scans in trauma patients. Anaesthesia. doi:10.1111/anae.13905

                                                  Aslani, A., Ng, S.-C., Hurley, M., McCarthy, K. F., McNicholas, M., & McCaul, C. L. (2012). Accuracy of identification of the cricothyroid membrane in female subjects using palpation: an observational study. Anesthesia and Analgesia, 114(5), 987–992. http://doi.org/10.1213/ANE.0b013e31824970ba
                                                  Bair, A. E., & Chima, R. (2015). The Inaccuracy of Using Landmark Techniques for Cricothyroid Membrane Identification: A Comparison of Three Techniques. Academic Emergency Medicine : Official Journal of the Society for Academic Emergency Medicine, 22(8), 908–914. http://doi.org/10.1111/acem.12732
                                                  Bennett, J. D., Guha, S. C., & Sankar, A. B. (1996). Cricothyrotomy: the anatomical basis. Journal of the Royal College of Surgeons of Edinburgh, 41(1), 57–60.
                                                  Boon, J. M., Abrahams, P. H., Meiring, J. H., & Welch, T. (2004). Cricothyroidotomy: a clinical anatomy review. Clinical Anatomy (New York, NY), 17(6), 478–486. http://doi.org/10.1002/ca.10231
                                                  Buonopane, C. E., Pasta, V., Sottile, D., Del Vecchio, L., Maturo, A., Merola, R., et al. (2014). Cricothyrotomy performed with the Melker set or the QuickTrach kit: procedure times, learning curves and operators’ preference. Il Giornale Di Chirurgia, 35(7-8), 165–170.
                                                  Cook, T., Woodall, N., & Frerk, C. (2015). Appendix 4 NAP4 Summary: major complications of airway management in the United Kingdom. British Journal of Anaesthesia (2011) 106 (5): 617-631. https://doi.org/10.1093/bja/aer058
                                                  Dover, K., Howdieshell, T. R., & Colborn, G. L. (1996a). The dimensions and vascular anatomy of the cricothyroid membrane: relevance to emergent surgical airway access. Clinical Anatomy (New York, NY), 9(5), 291–295. http://doi.org/10.1002/(SICI)1098-2353(1996)9:5<291::AID-CA1>3.0.CO;2-G
                                                  Frerk, C., Mitchell, V. S., & McNarry, A. F. (2015). Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. British Journal of Anaesthesia (2015) 115 (6): 827-848. https://doi.org/10.1093/bja/aev371
                                                  Hubert, V., Duwat, A., Deransy, R., Mahjoub, Y., & Dupont, H. (2014). Effect of simulation training on compliance with difficult airway management algorithms, technical ability, and skills retention for emergency cricothyrotomy. Anesthesiology, 120(4), 999–1008. http://doi.org/10.1097/ALN.0000000000000138
                                                  Langvad, S., Hyldmo, P. K., Nakstad, A. R., Vist, G. E., & Sandberg, M. (2013a). Emergency cricothyrotomy–a systematic review. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 21, 43. http://doi.org/10.1186/1757-7241-21-43
                                                  Nakstad, A. R., Bredmose, P. P., & Sandberg, M. (2013). Comparison of a percutaneous device and the bougie-assisted surgical technique for emergency cricothyrotomy: an experimental study on a porcine model performed by air ambulance anaesthesiologists. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 21, 59. http://doi.org/10.1186/1757-7241-21-59
                                                   Navsa, N., Tossel, G., & Boon, J. M. (2005). Dimensions of the neonatal cricothyroid membrane – how feasible is a surgical cricothyroidotomy? Paediatric Anaesthesia, 15(5), 402–406. http://doi.org/10.1111/j.1460-9592.2005.01470.x
                                                   Prithishkumar, I. J., & David, S. S. (2010). Morphometric analysis and clinical application of the working dimensions of cricothyroid membrane in south Indian adults: With special relevance to surgical cricothyroidotomy. Emergency Medicine Australasia, 22(1), 13–20. http://doi.org/10.1111/j.1742-6723.2009.01245.x
                                                   The clinical anatomy of several invasive procedures. American Association of Clinical Anatomists, Educational Affairs Committee. (1999). The clinical anatomy of several invasive procedures. American Association of Clinical Anatomists, Educational Affairs Committee. Clinical Anatomy (New York, NY), 12(1), 43–54. http://doi.org/10.1002/(SICI)1098-2353(1999)12:1<43::AID-CA7>3.0.CO;2-W

                                                   

                                                   

                                                  26 min

                                                About PHEMCAST

                                                From the publisher's feed

                                                A UK Prehospital Emergency Medicine Podcast.