Refusal Heuristic Traps:    How to avoid heuristic traps:      Competency Vs Capacity: Competency is a global assessment and legal determination made by a judge in court. Capacity is a functional assessment and a clinical determination about a specific decision that can be made by any clinician familiar with a patient’s case. How does a patient demonstrate capacity? •Understanding – The ability to understand, i.e., knows the information being presented. Consider a patient who is having a COPD exacerbation, they know they have it, the treatment for it, and the benefits and risks of the treatment for COPD. •Expressing a choice – Can clearly communicate their choice when you present multiple options. A patient that frequently changes their choice (if they have some neurologic condition) could indicate they lack capacity. •Appreciation – They can apply the facts that you present to their own life and understands it’s relevance. If they do not acknowledge their illness or facts about their illness due to some delusions may lack capacity. •Reasoning – The ability to compare options and to infer consequences of a choice. Ask “How is not being transported to the hospital better than being transported”. This should illicit the patients values, which will require the patient to compare the consequences of what they want to do compared to what they do not want to do.         References Dastidar, J., 2011. How Do I Determine If My Patient Has Decision-Making Capacity?. [online] The-hospitalist.org. Available at:  [Accessed 23 January 2021]. Karlawish, J., 2021. Uptodate. [online] Uptodate.com. Available at:  [Accessed 23 January 2021]. McCammon, I., 2002. [online] Arc.lib.montana.edu. Available at:  [Accessed 23 January 2021]. Selde, W., 2015. Know When And How Your Patient Can Legally Refuse Care - JEMS. [online] JEMS. Available at:  [Accessed 23 January 2021].

Refusal Heuristic Traps: How to avoid heuristic traps: Competency Vs Capacity: Competency is a global assessment and legal determination made by a judge in court. Capacity is a functional assessment and a clinical determination about a specific decision that can be made by any clinician familiar with a patient’s case. How does a patient demonstrate capacity? •Understanding – The ability to understand, i.e., knows the information being presented. Consider a patient who is having a COPD exacerbation, they know they have it, the treatment for it, and the benefits and risks of the treatment for COPD. •Expressing a choice – Can clearly communicate their choice when you present multiple options. A patient that frequently changes their choice (if they have some neurologic condition) could indicate they lack capacity. •Appreciation – They can apply the facts that you present to their own life and understands it’s relevance. If they do not acknowledge their illness or facts about their illness due to some delusions may lack capacity. •Reasoning – The ability to compare options and to infer consequences of a choice. Ask “How is not being transported to the hospital better than being transported”. This should illicit the patients values, which will require the patient to compare the consequences of what they want to do compared to what they do not want to do.       References Dastidar, J., 2011. How Do I Determine If My Patient Has Decision-Making Capacity?. [online] <a href="http://The-hospitalist.org" rel="nofollow" target="_blank">The-hospitalist.org</a>. Available at: [Accessed 23 January 2021]. Karlawish, J., 2021. Uptodate. [online] <a href="http://Uptodate.com" rel="nofollow" target="_blank">Uptodate.com</a>. Available at: [Accessed 23 January 2021]. McCammon, I., 2002. [online] <a href="http://Arc.lib.montana.edu" rel="nofollow" target="_blank">Arc.lib.montana.edu</a>. Available at: [Accessed 23 January 2021]. Selde, W., 2015. Know When And How Your Patient Can Legally Refuse Care - JEMS. [online] JEMS. Available at: [Accessed 23 January 2021].

Refusal Heuristics

Joined by Peter D. Akpunonu, MD, Haedan Eager and Ben Doty, we discuss their recent paper on "Managing the Effects of Riot Control Agents" and throw in a little trivia - and discuss relevant and practical management principles for patients exposed to incapacitating agents.

Joined by Peter D. Akpunonu, MD, Haedan Eager and Ben Doty, we discuss their recent paper on "Managing the Effects of Riot Control Agents" and throw in a little trivia - and discuss relevant and practical management principles for patients exposed to incapacitating agents.

Chemical Casualties: Incapacitating Agents

Ryan Mynatt

Don't you wish someone explained what viral load, viral shedding, and all those other words we use loosely when talking about COVID-19? Well.... our guest on this podcast did, and we think you'll really enjoy getting back to the basics, and then some.   Dr. Ryan Mynatt is a practicing PharmD specializing in infectious disease, and like most academics who know anything about anything, he's responses were a little guarded - which is most appropriate right now.   You can view any of his many publications here.   Oh, he's also on Twitter.   Let us know what you think of the podcast...

Don't you wish someone explained what viral load, viral shedding, and all those other words we use loosely when talking about COVID-19? Well.... our guest on this podcast did, and we think you'll really enjoy getting back to the basics, and then some. Dr. Ryan Mynatt is a practicing PharmD specializing in infectious disease, and like most academics who know anything about anything, he's responses were a little guarded - which is most appropriate right now. You can view any of his many publications <a href="https://www.researchgate.net/profile/Ryan_Mynatt" rel="nofollow" target="_blank">here</a>. Oh, he's also on <a href="https://twitter.com/rp_mynatt" rel="nofollow" target="_blank">Twitter</a>. Let us know what you think of the podcast...

Ryan Mynatt, PharmD on Virology

In this podcast we discuss a gift box of items regarding treatment considerations for reducing aerosol generating procedures. As with the previous podcast, this is a dynamic situation, and the information is not guaranteed to be accurate. Please share your thoughts and what you are doing at your own department. 

In this podcast we discuss a gift box of items regarding treatment considerations for reducing aerosol generating procedures. As with the previous podcast, this is a dynamic situation, and the information is not guaranteed to be accurate. Please share your thoughts and what you are doing at your own department.

COVID-19 Update: Avoiding the Aerosols

Let's start by saying that I am not an expert. But, specific guidance from the CDC for managing these patients is available, but I feel like the dispersal of this information is critical to front line EMS providers. For links to important sites and to see images of the BVM and ventilator setup, go to curbtobed.com

Let's start by saying that I am not an expert. But, specific guidance from the CDC for managing these patients is available, but I feel like the dispersal of this information is critical to front line EMS providers. For links to important sites and to see images of the BVM and ventilator setup, go to <a href="http://curbtobed.com" rel="nofollow" target="_blank">curbtobed.com</a>

COVID-19 - EMS Considerations

In this episode we take a new look at the pathophysiology behind tension pneumothorax and how it presents in the real world population, and discuss why we should pause before inserting the needle in the 2nd intercostal space. 

In this episode we take a new look at the pathophysiology behind tension pneumothorax and how it presents in the real world population, and discuss why we should pause before inserting the needle in the 2nd intercostal space.

C2B Podcast 24 - Needle Thoracostomy

Hyperkalemia Intro    Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction. Serum measured potassium is typically between 3.5 and 5.0 mEq/L. Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia. Potassium is mostly excreted via the kidneys, and the "classic" hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness.    Causes of HyperK    Most commonly, renal failure.  Transcelluar shift   DKA Acidosis  Other acid-base disturbances   Medications   RAAS or ACE inhibitors      Effects of HyperK     Most drastically affect cardiac myocytes   Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased.   Leads to ominous “sine wave” pattern on ECG.    Arrythmogenic  May produce classic tall, “peaked” T waves on ECG.   Stepwise ECG changes in hyperkalemia:  5.5-6.5 mEq/L - Peaked T Waves 6.5-7.5 mEq/L - P waves amplitude becomes smaller and PR intervals prolong 7.5-8.0 mEq/L - QRS becomes wide   ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG.  Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result.  Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present - but are also not reliable findings.     Management     Prioritized by a strategy of:  Stabilization of cardiac cell membranes  Shifting potassium back into the cells  Eliminating potassium   Calcium (Chloride or gluconate) administered to stabilize cell membranes   Stabilizing effect is transient and relatively short lived  Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs.  Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes  Calcium Chloride - generally, 1 gram is administered over 3 minutes. Calcium Gluconate - 1 gram over 2-3 minutes  Repeat either q5min   Albuterol / Beta 2 agonists  These act on beta 2 receptors to assist in moving potassium back into the intracellular space  Albuterol - 10-20mg (inhalation), with most effect noted in 30 minutes    IV Insulin   Drives K back into the cells (shift) Generally administered with dextrose unless the patient’s BGL is below 250mg/dL 10 units IVP followed by 25G dextrose Incidence of hypoglycemia is high, and this therapy should be administered cautiously   Dialysis  Treating reversible cause  d/c RASS or ACE inhibiting medicaitions  Volume administration   

Hyperkalemia Intro <ol> <li>Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction.</li> <li>Serum measured potassium is typically between 3.5 and 5.0 mEq/L.</li> <li>Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia.</li> <li>Potassium is mostly excreted via the kidneys, and the "classic" hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness.</li> </ol> Causes of HyperK <ol> <li>Most commonly, renal failure. </li> <li>Transcelluar shift  <ol> <li>DKA</li> <li>Acidosis </li> <li>Other acid-base disturbances</li> </ol> </li> <li>Medications  <ol> <li>RAAS or ACE inhibitors</li> </ol> </li> </ol> Effects of HyperK  <ol> <li>Most drastically affect cardiac myocytes  <ol> <li>Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased.  <ol> <li>Leads to ominous “sine wave” pattern on ECG. </li> </ol> </li> <li>Arrythmogenic </li> <li>May produce classic tall, “peaked” T waves on ECG.</li> </ol> </li> <li>Stepwise ECG changes in hyperkalemia: <ol> <li>5.5-6.5 mEq/L - Peaked T Waves</li> <li>6.5-7.5 mEq/L - P waves amplitude becomes smaller and PR intervals prolong</li> <li>7.5-8.0 mEq/L - QRS becomes wide</li> </ol> </li> <li>ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG. </li> <li>Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result. </li> <li>Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present - but are also not reliable findings. </li> </ol> Management  <ol> <li>Prioritized by a strategy of: <ol> <li>Stabilization of cardiac cell membranes </li> <li>Shifting potassium back into the cells </li> <li>Eliminating potassium</li> </ol> </li> <li>Calcium (Chloride or gluconate) administered to stabilize cell membranes  <ol> <li>Stabilizing effect is transient and relatively short lived </li> <li>Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs. </li> <li>Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes </li> <li>Calcium Chloride - generally, 1 gram is administered over 3 minutes.</li> <li>Calcium Gluconate - 1 gram over 2-3 minutes </li> <li>Repeat either q5min</li> </ol> </li> <li>Albuterol / Beta 2 agonists <ol> <li>These act on beta 2 receptors to assist in moving potassium back into the intracellular space </li> <li>Albuterol - 10-20mg (inhalation), with most effect noted in 30 minutes </li> </ol> </li> <li>IV Insulin  <ol> <li>Drives K back into the cells (shift)</li> <li>Generally administered with dextrose unless the patient’s BGL is below 250mg/dL</li> <li>10 units IVP followed by 25G dextrose</li> <li>Incidence of hypoglycemia is high, and this therapy should be administered cautiously</li> </ol> </li> <li>Dialysis </li> <li>Treating reversible cause <ol> <li>d/c RASS or ACE inhibiting medicaitions </li> <li>Volume administration</li> </ol> </li> </ol>

C2B Podcast 23 - Hyperkalemia

Transporting a sick DKA patient is challenging. Surprisingly, there's a bit more to it than "just" administering fluid and monitoring an insulin infusion. Read more and find references at curbtobed.com

Transporting a sick DKA patient is challenging. Surprisingly, there's a bit more to it than "just" administering fluid and monitoring an insulin infusion. Read more and find references at <a href="http://curbtobed.com" rel="nofollow" target="_blank">curbtobed.com</a>

Diabetic Ketoacidosis

In our first official “vodcast”, we discuss pearls and pitfalls of transcutaneous pacing, and how it’s much more difficult than “you either have capture or you don’t”. “Phantom” complexes are rarely reported on or discussed in Paramedic school, but one monitor manufacturer appreciates how they can make verifying true electrical capture very difficult. The folks over at ems12lead.com have put a lot of work into providing education and spreading the word around the problem of false capture. 

In our first official “vodcast”, we discuss pearls and pitfalls of transcutaneous pacing, and how it’s much more difficult than “you either have capture or you don’t”. “Phantom” complexes are rarely reported on or discussed in Paramedic school, <a href="https://www.physio-control.com/uploadedFiles/learning/clinical-topics/Pacing_Artifact_3207454-000.pdf" rel="nofollow" target="_blank">but one monitor manufacturer</a> appreciates how they can make verifying true electrical capture very difficult. The folks over at <a href="http://ems12lead.com" rel="nofollow" target="_blank">ems12lead.com</a> have put a lot of work into providing education and spreading the word around the <a href="http://ems12lead.com/2008/11/15/transcutaneous-pacing-tcp-the-problem-of-false-capture/" rel="nofollow" target="_blank">problem of false capture</a>.

Rethinking Transcutaneous Pacing

First, there are two proposed mechanisms of CPR, brilliantly summarized in this paper: Cardiac Pump Mechanism:  “blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.”  Thoracic Pump Mechanism:  “With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.”  It is likely that both mechanisms are at play:  …In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory.   Is there any evidence that M-CPR Devices improve outcomes – since they’re marketed as “life saving devices”? A Meta Analysis from Gates et. al. concluded: Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest. However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse. Gonzales et. al. compared “pit crew” resuscitation with “scripted” mCPR implementation and found: In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge.   Why might this be the case? We know based off work by Hwang et. al. who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients! In another study, anderson et. al. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root.  All of these studies and more are explained in a wonderful video created by Felipe Teran: The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR:  TEE to save lives, guide compressions, and guide interventions Pt 1. #FOAMED.  p.s. – checkout cabofest2018.com     But, how do we do we know that we’re compressing the LV without TEE? Well, we don’t exactly. However, Qvigstad E et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.” They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2. They found that there’s not “one superior hand position”, and that optimal positioning varies:   How does this explain when we should place mCPR? It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle.   Are we applying mCPR too early? Poole et. al discuss this in a paper titled: Mechanical CPR: Who? When? How? In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5) The authors continue and note that… subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p

First, there are two proposed mechanisms of CPR, brilliantly summarized in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6028802/" rel="nofollow" target="_blank">this paper:</a> Cardiac Pump Mechanism: “blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.” Thoracic Pump Mechanism: “With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.” It is likely that both mechanisms are at play: …In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory. Is there any evidence that M-CPR Devices improve outcomes – since they’re marketed as “life saving devices”? A <a href="https://www.ncbi.nlm.nih.gov/pubmed/26190673" rel="nofollow" target="_blank">Meta Analysis</a> from Gates et. al. concluded: Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest. However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse. <a href="https://www.ncbi.nlm.nih.gov/pubmed/30119989/" rel="nofollow" target="_blank">Gonzales et. al.</a> compared “pit crew” resuscitation with “scripted” mCPR implementation and found: In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge. Why might this be the case? We know based off work by <a href="https://www.ncbi.nlm.nih.gov/pubmed/19732038" rel="nofollow" target="_blank">Hwang et. al.</a> who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients! In another study, <a href="https://www.ncbi.nlm.nih.gov/pubmed/27918847" rel="nofollow" target="_blank">anderson et. al</a>. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root.  All of these studies and more are explained in a wonderful video created by Felipe Teran: The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR: <a href="http://www.ultrasoundpodcast.com/2017/02/tee-save-lives-guide-compressions-guide-interventions-pt-1-foamed-p-s-checkout-cabofest2018-com/" rel="nofollow" target="_blank"> TEE to save lives, guide compressions, and guide interventions Pt 1. #FOAMED.  p.s. – checkout cabofest2018.com </a> But, how do we do we know that we’re compressing the LV without TEE? Well, we don’t exactly. However, <a href="https://www.ncbi.nlm.nih.gov/pubmed/?term=Qvigstad%20E%5BAuthor%5D&amp;cauthor=true&amp;cauthor_uid=23499897" rel="nofollow" target="_blank">Qvigstad E</a> et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.” They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2. They found that there’s not “one superior hand position”, and that optimal positioning varies: How does this explain when we should place mCPR? It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle.  Are we applying mCPR too early? Poole et. al discuss this in a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5975402/" rel="nofollow" target="_blank">paper</a> titled: Mechanical CPR: Who? When? How? In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5) The authors continue and note that… subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p

Are we Placing mCPR Devices too Early?

Free open access Prehospital Medical education for the front line EMS Provider. This podcast does not replace your institutions policies, procedures, protocols, or guidelines. Please go to our website for a full disclaimer:www.curbtobed.com

Andrew Fisher

Join us as we interview Andrew Fisher on the multiplicity of managing civilian trauma patients. Although the complexity of trauma management is often understated, the basics are often not managed appropriately, and can have an appreciable affect on trauma outcomes.   We discuss TEG, blood product administration, acute traumatic coagulopathy, the MARCH algorithm, and when it comes to permissive hypotension, just how low can you go?

Join us as we interview Andrew Fisher on the multiplicity of managing civilian trauma patients. Although the complexity of trauma management is often understated, the basics are often not managed appropriately, and can have an appreciable affect on trauma outcomes. We discuss TEG, blood product administration, acute traumatic coagulopathy, the MARCH algorithm, and when it comes to permissive hypotension, just how low can you go?

An Assault on Preventable Trauma Deaths With Andrew Fisher

Wantabe et al. (2018) "Is Use of Warning Lights and Sirens Associated With Increased Risk of Ambulance Crashes?" was the first to definitively link L&amp;S use with ambulance crashes.     Data extrapolated from Wantabe et al. (2018)  Response Crash Rate:  4.6 / 100,000 without L&amp;S  5.4 / 100,000 with L/S   Transport Crash Rate:   7 / 100,000 without L&amp;S   17.1 / 100,000 with L&amp;S   The authors theorize a driving reason behind their observations as such: “During response two providers are in the front and share the cognitive load required to operate an ambulance”.   NHTSA - Proposed L&amp;S Response Benchmark:    Reduce L/S use to less than 50% during response. Less than 5% during transport.    Common arguments for the use of L/S:    Saves time Time is brain/muscle Public expectation     History   The general attitude may stem from the genesis of EMS, where First Aid attendants were not trusted to discern if a patient was stable or not. Ergo, the strategy of the time was to rapidly transport all patients with the underlying presumption that all patients “would” deteriorate unless proven otherwise AFTER arrival at a hospital.   With current advances in prehospital care, the vast majority of injury/illnesses can be effectively managed during the out-of-hospital phase of patient care.    Increased vehicle safety should be championed along with the need to decrease the use of L&amp;S.    Lime Green colors decreases rate of overall crashes Lime Green: 28.2 crashes per 1 million miles travelled Red/White: 62.1 crashes per 1 million miles travelled    The average rate of car crashers per 1 million miles is 2.6 / 1 million miles of travel. (Solomon, 1995)    Does it save lives?   (Anderson, 2014) Study in Denmark looked for morbidity by studying 94,488 patients transported without L&amp;S and found only 152 patients (0.16%) that died the same day as their ambulance transport. A panel of prehospital anesthesiologists reviewed the patient care reports and found 13 (0.02%) with potentially preventable deaths. If every one of these deaths could have been prevented with L&amp;S transport, the “number needed to treat” would have been 5000 extra L&amp;S transports. (Anderson 2014)  (Kupas 1994) Protocol is used to identify patients that may benefit by the time saved with L&amp;S transport. When using this protocol on 1625 patients, only 130 (8%) were transported using L&amp;S. A review of the 92% of cases where L&amp;S was not used, the receiving physicians did not identify any cases of possible morbidity due to a slower transport.  (Merlin 2012) Merlin developed an even simpler medical protocol for L&amp;S transport, which reduced L&amp;S transport in this urban New Jersey community from 49.6% to 29.0% for patients transported by ALS providers.  (Marques-Batista 2010) 112 patients transported with L&amp;S found that only five of those patients received a time-critical intervention upon arrival to the emergency department, and none of these procedures was done within the 2.62 minutes saved by L&amp;S transport  (Newgard 2010) The Resuscitation Outcomes Consortium studied the outcomes for injured patients treated by 146 EMS agencies, transporting to 51 Level I and II trauma centers, in ten North American communities. This large study found no association between survival and EMS time intervals – including response time and transport time.   Does it save time?   L&amp;S use generally only shortens response and transport time intervals by 1.7-3.6 minutes, and transport time only by 0.7-3,8 minutes. Greenville, NC; Saved average of 43.5 seconds    Fatalities:   9.6 fatalities per 100,000 people per capita related to transportation. Rear Occupants are 2.7 times more likely to die in a crash (Kahn, 2001)    Exceeds rate for LEOs and FFs Rear occupants 2.7 times more likely to be killed in ambulance crash    But our Fracile Response Time needs to be 8 minutes!    Stems from 1979 study in Seattle of cardiac arrests What matters more is when the first arriving aid is present. Now we have widespread T-CPR, rapid dispatch, bystander CPR, and LEO responses w/ AEDs.    EMSA Response Time Standards:    Priority one calls - 10.59 Priority two calls - 24.59 Respond to only 33% of calls w/ L/S Have NOT observed any changes in cardiac arrest survival rates.    Time Critical Conditions:    Rendering a coronary intervention sooner by 10 minutes would decrease death by only 0.4%  Rather, work on earlier notification, reduced scene times, and in-hospital workflow.   Best chance of survival from OOHCA is to obtain ROSC on scene.    Public Perception:  Anecdotally, it is possible some patients hesitate to call EMS for medical emergencies, because they are uncomfortable with L&amp;S responses and increased attention. See the ubiquitous "caller requests no lights or sirens" dispatch.  A 1988 phone survey of the public in Connecticut cited sirens and noise (67/604 respondents) as the primary reason for being uncomfortable in calling EMS during an emergency, and this response was followed by “getting lots of attention” (49/604 respondents). (Smackery 1988) Critz reported that the families of terminally ill patients who died at home sometimes felt anger with EMS, and L&amp;S response was listed as one of the reasons for this.   One-third of drivers responding to a survey in the United Kingdom reported feeling stress when navigating away from approaching emergency vehicles with L&amp;S, and the authors believed that drivers found the interactions with emergency vehicles inconvenient and potentially dangerous. (Saunders 2003)   Legal:   Wolfberg 1996 found that ambulance crashes are the most common cause of insurance claims greater than 10,000 dollars in EMS agencies

Wantabe et al. (2018) "Is Use of Warning Lights and Sirens Associated With Increased Risk of Ambulance Crashes?" was the first to definitively link L&amp;S use with ambulance crashes. Data extrapolated from Wantabe et al. (2018) Response Crash Rate: 4.6 / 100,000 without L&amp;S 5.4 / 100,000 with L/S Transport Crash Rate: 7 / 100,000 without L&amp;S 17.1 / 100,000 with L&amp;S The authors theorize a driving reason behind their observations as such: “During response two providers are in the front and share the cognitive load required to operate an ambulance”. NHTSA - Proposed L&amp;S Response Benchmark: <ul> <li>Reduce L/S use to less than 50% during response.</li> <li>Less than 5% during transport.</li> </ul> Common arguments for the use of L/S: <ul> <li>Saves time</li> <li>Time is brain/muscle</li> <li>Public expectation </li> </ul> History The general attitude may stem from the genesis of EMS, where First Aid attendants were not trusted to discern if a patient was stable or not. Ergo, the strategy of the time was to rapidly transport all patients with the underlying presumption that all patients “would” deteriorate unless proven otherwise AFTER arrival at a hospital. With current advances in prehospital care, the vast majority of injury/illnesses can be effectively managed during the out-of-hospital phase of patient care. Increased vehicle safety should be championed along with the need to decrease the use of L&amp;S. <ul> <li>Lime Green colors decreases rate of overall crashes</li> <li>Lime Green: 28.2 crashes per 1 million miles travelled</li> <li>Red/White: 62.1 crashes per 1 million miles travelled</li> </ul> The average rate of car crashers per 1 million miles is 2.6 / 1 million miles of travel. (Solomon, 1995) Does it save lives? (Anderson, 2014) Study in Denmark looked for morbidity by studying 94,488 patients transported without L&amp;S and found only 152 patients (0.16%) that died the same day as their ambulance transport. A panel of prehospital anesthesiologists reviewed the patient care reports and found 13 (0.02%) with potentially preventable deaths. If every one of these deaths could have been prevented with L&amp;S transport, the “number needed to treat” would have been 5000 extra L&amp;S transports. (Anderson 2014) (Kupas 1994) Protocol is used to identify patients that may benefit by the time saved with L&amp;S transport. When using this protocol on 1625 patients, only 130 (8%) were transported using L&amp;S. A review of the 92% of cases where L&amp;S was not used, the receiving physicians did not identify any cases of possible morbidity due to a slower transport. (Merlin 2012) Merlin developed an even simpler medical protocol for L&amp;S transport, which reduced L&amp;S transport in this urban New Jersey community from 49.6% to 29.0% for patients transported by ALS providers. (Marques-Batista 2010) 112 patients transported with L&amp;S found that only five of those patients received a time-critical intervention upon arrival to the emergency department, and none of these procedures was done within the 2.62 minutes saved by L&amp;S transport (Newgard 2010) The Resuscitation Outcomes Consortium studied the outcomes for injured patients treated by 146 EMS agencies, transporting to 51 Level I and II trauma centers, in ten North American communities. This large study found no association between survival and EMS time intervals – including response time and transport time. Does it save time? L&amp;S use generally only shortens response and transport time intervals by 1.7-3.6 minutes, and transport time only by 0.7-3,8 minutes. Greenville, NC; Saved average of 43.5 seconds Fatalities: 9.6 fatalities per 100,000 people per capita related to transportation. Rear Occupants are 2.7 times more likely to die in a crash (Kahn, 2001) <ul> <li>Exceeds rate for LEOs and FFs</li> <li>Rear occupants 2.7 times more likely to be killed in ambulance crash</li> </ul> But our Fracile Response Time needs to be 8 minutes! <ul> <li>Stems from 1979 study in Seattle of cardiac arrests</li> <li>What matters more is when the first arriving aid is present.</li> <li>Now we have widespread T-CPR, rapid dispatch, bystander CPR, and LEO responses w/ AEDs.</li> </ul> EMSA Response Time Standards: <ul> <li>Priority one calls - 10.59</li> <li>Priority two calls - 24.59</li> <li>Respond to only 33% of calls w/ L/S</li> <li>Have NOT observed any changes in cardiac arrest survival rates.</li> </ul> Time Critical Conditions: <ul> <li>Rendering a coronary intervention sooner by 10 minutes would decrease death by only 0.4% <ul> <li>Rather, work on earlier notification, reduced scene times, and in-hospital workflow.</li> </ul> </li> <li>Best chance of survival from OOHCA is to obtain ROSC on scene.</li> </ul> Public Perception: Anecdotally, it is possible some patients hesitate to call EMS for medical emergencies, because they are uncomfortable with L&amp;S responses and increased attention. See the ubiquitous "caller requests no lights or sirens" dispatch. A 1988 phone survey of the public in Connecticut cited sirens and noise (67/604 respondents) as the primary reason for being uncomfortable in calling EMS during an emergency, and this response was followed by “getting lots of attention” (49/604 respondents). (Smackery 1988) Critz reported that the families of terminally ill patients who died at home sometimes felt anger with EMS, and L&amp;S response was listed as one of the reasons for this. One-third of drivers responding to a survey in the United Kingdom reported feeling stress when navigating away from approaching emergency vehicles with L&amp;S, and the authors believed that drivers found the interactions with emergency vehicles inconvenient and potentially dangerous. (Saunders 2003) Legal: Wolfberg 1996 found that ambulance crashes are the most common cause of insurance claims greater than 10,000 dollars in EMS agencies

Wailing for Risk Reduction

Regan Baum

Goals on Initiation Reverse shock and increase tissue perfusion:  Improve blood flow  BP (MAP &gt;65) perfuse coronaries and brain Mental status End tidal CO2 Maybe:  urine output (if Foley present) &amp; capillary refill time   Increase venous return Avoid ischemia &amp; other adverse events   Which vasopressor do I choose? It depends.  For the prehospital provider, most of these are not an option. However, having one pressor that you're familiar with that can be implemented safely and rapidly is probably more beneficial to the patient than not using a pressor at all, or worse, using it incorrectly. Currently, norepinephrine is recommended as first line in the vast majority of shock states. However,  this is only commercially available in a vial as a concentrated solution, requiring drip preparation. Most EMS Providers in our area are either more familiar with dopamine or have it as their only option per Protocol.  This is likely due to it being a commercially available pre-mixed drip.  In short term, may be fine, but is more arrhythmogenic than norepinephrine. Alternatively, "Dirty" Epi is an option:  1 mg into a 1,000 mL NS (conc 1 mcg/mL). Maximum rate of infusion will vary with catheter size, IV bag height, and squeeze on the bag; however, with a wide-open 18-gauge IV, the patient will receive about 20-30 mL/min (or 20-30 mcg/min) of epinephrine, which is similar to the recommended push-dose epi (0.1 mg or 100 mcg over 5 minutes = 20 mcg per min Run wide open in your peripheral IV or IO until the patient’s hemodynamics stabilize. Can set up the pump, follow  protocols, and perform double-checks. Adequate labeling is important to mitigate errors.  Or, compel your service administrators to buy the right equipment (IV Pumps) and the right vasopressor (Norepi).   Vasopressors Turn Unstressed Volume Into Stressed Volume  Unstressed Volume - Vol­ume of fluid to fill the vascular bed to the point where its presence exerts force on the vessel walls Stresssed Volume - Anything greater ⇒ which will exert an increasing degree of pressure on the venous vascular bed ⇒ determines flow   Vasopressor Classification - A Simpler Approach  Pure vasopresors (isolated vessel squeeze)  Phenylephrine Vasopressin   Vasopressor with ionotrophy (both vessel &amp; heart squeeze)  Norepinephrine Epinephrine Dopamine   Ionotropes with vasodilators (heart squeeze &amp; vasodilation)  Dobutamine Milrinone      Maximum doses vary greatly between institutions.  It is likely that your hospital or agency has set a maximum dose for each vasopressor.  Maximum doses can be exceeded if needed to maintain hemodynamics.  When to Titrate (frequency)   Peripheral Administration Tips for peripheral administration:  Use well functioning 18-20G IV proximal to the wrist Place BP cuff on opposite arm Regularly inspect IV site for signs of extravasation Ask patient to report discomfort around IV site Be prepared to manage extravasation Prolonged administration = Central access   Extravasation Management   Compatibility   Sterility When properly mixing Push Dose Epinephrine, repeated entries into any one container should be limited to maintain integrity/sterility of the original container. Ways to limit puncturing the carpuject, as described by Dr. Baum in the podcast:  Instead of puncturing the carpuject, it may be more more sterile to remove needleless cap from the Epi and insert it into the tip of the 10 cc syringe. Or...  Purchase a Luer Lock-to-Luer Lock  connector so you don't have to expose a needle. Care Transitions Be cautious when stopping drips when delivering patient to the hospital.  This is especially important with agents like vasopressors as they have short half-lives.  Patients needing these for support may decline.  Best practice is to transition to hospital product before discontinuing. Reporting of infusion rates during hand off:   Medication infusions need to be reported in a concentration per time  Examples: mg/hr or mcg/kg/min or units/hr ml/hr is NEVER appropriate due to differing concentrations of medication infusions   Vasopressors may be dosed in mcg/min or mcg/kg/min beware of units IV fluids like normal saline and lactate ringers ml/hr is appropriate.  Special thanks to Dr. Regan Baum for providing us with these notes and images. A few additions were made by Curbside to Bedside.

Goals on Initiation Reverse shock and increase tissue perfusion: <ul> <li>Improve blood flow <ul> <li>BP (MAP &gt;65) perfuse coronaries and brain</li> <li>Mental status</li> <li>End tidal CO2</li> <li>Maybe:  urine output (if Foley present) &amp; capillary refill time</li> </ul> </li> <li>Increase venous return</li> <li>Avoid ischemia &amp; other adverse events</li> </ul> Which vasopressor do I choose? It depends. For the prehospital provider, most of these are not an option. However, having one pressor that you're familiar with that can be implemented safely and rapidly is probably more beneficial to the patient than not using a pressor at all, or worse, using it incorrectly. Currently, norepinephrine is recommended as first line in the vast majority of shock states. However,  this is only commercially available in a vial as a concentrated solution, requiring drip preparation. Most EMS Providers in our area are either more familiar with dopamine or have it as their only option per Protocol.  This is likely due to it being a commercially available pre-mixed drip.  In short term, may be fine, but is more arrhythmogenic than norepinephrine. Alternatively, "Dirty" Epi is an option: <ul> <li>1 mg into a 1,000 mL NS (conc 1 mcg/mL).</li> <li>Maximum rate of infusion will vary with catheter size, IV bag height, and squeeze on the bag; however, with a wide-open 18-gauge IV, the patient will receive about 20-30 mL/min (or 20-30 mcg/min) of epinephrine, which is similar to the recommended push-dose epi (0.1 mg or 100 mcg over 5 minutes = 20 mcg per min</li> <li>Run wide open in your peripheral IV or IO until the patient’s hemodynamics stabilize.</li> <li>Can set up the pump, follow  protocols, and perform double-checks.</li> <li>Adequate labeling is important to mitigate errors.</li> </ul> Or, compel your service administrators to buy the right equipment (IV Pumps) and the right vasopressor (Norepi). Vasopressors Turn Unstressed Volume Into Stressed Volume <ul> <li>Unstressed Volume - Vol­ume of fluid to fill the vascular bed to the point where its presence exerts force on the vessel walls</li> <li>Stresssed Volume - Anything greater ⇒ which will exert an increasing degree of pressure on the venous vascular bed ⇒ determines flow</li> </ul> Vasopressor Classification - A Simpler Approach <ol> <li>Pure vasopresors (isolated vessel squeeze) <ol> <li>Phenylephrine</li> <li>Vasopressin</li> </ol> </li> <li>Vasopressor with ionotrophy (both vessel &amp; heart squeeze) <ol> <li>Norepinephrine</li> <li>Epinephrine</li> <li>Dopamine</li> </ol> </li> <li>Ionotropes with vasodilators (heart squeeze &amp; vasodilation) <ol> <li>Dobutamine</li> <li>Milrinone</li> </ol> </li> </ol> Maximum doses vary greatly between institutions.  It is likely that your hospital or agency has set a maximum dose for each vasopressor.  Maximum doses can be exceeded if needed to maintain hemodynamics. When to Titrate (frequency) Peripheral Administration Tips for peripheral administration: <ol> <li>Use well functioning 18-20G IV proximal to the wrist</li> <li>Place BP cuff on opposite arm</li> <li>Regularly inspect IV site for signs of extravasation</li> <li>Ask patient to report discomfort around IV site</li> <li>Be prepared to manage extravasation</li> <li>Prolonged administration = Central access</li> </ol> Extravasation Management Compatibility Sterility When properly mixing Push Dose Epinephrine, repeated entries into any one container should be limited to maintain integrity/sterility of the original container. Ways to limit puncturing the carpuject, as described by Dr. Baum in the podcast: Instead of puncturing the carpuject, it may be more more sterile to remove needleless cap from the Epi and insert it into the tip of the 10 cc syringe. Or... Purchase a Luer Lock-to-Luer Lock  connector so you don't have to expose a needle. Care Transitions Be cautious when stopping drips when delivering patient to the hospital.  This is especially important with agents like vasopressors as they have short half-lives.  Patients needing these for support may decline.  Best practice is to transition to hospital product before discontinuing. Reporting of infusion rates during hand off:  <ul> <li>Medication infusions need to be reported in a concentration per time <ul> <li>Examples: mg/hr or mcg/kg/min or units/hr</li> <li>ml/hr is NEVER appropriate due to differing concentrations of medication infusions</li> </ul> </li> <li>Vasopressors may be dosed in mcg/min or mcg/kg/min beware of units</li> <li>IV fluids like normal saline and lactate ringers ml/hr is appropriate.</li> </ul> Special thanks to Dr. Regan Baum for providing us with these notes and images. A few additions were made by Curbside to Bedside.

Under Pressure - Vasopressor PEARLS with Dr. Regan Baum

Topics Discussed in the Podcast:  Provider bias and the pulse oximeter. CO oximetry. Pulse oximeter lag.  Approach to the well-appearing patient with a low SpO2 reading.  Relation of vascular tone to pleth wave amplitude and variability.  Using the pulse ox waveform to confirm mechanical capture during transcutaneous pacing. Odds and ends...  Pulse oximetry is more than just a measurement of oxygenation: The pulse oximetry plethysmograph is a pulsatile waveform that can be thought of as an arterial waveform. However, this waveform is influenced by cardiac output and systemic vascular resistance.  Thinking of the SpO2 pleth as a pulsatile waveform,  variations in the patients cardiac output should be transmitted to the fingertip arteries, which results in variations in the pulse ox waveform amplitude. The implications of this are far reaching. In patients who are mechanically ventilated, cyclical changes in intrathoracic pressures can produce measurable variations in the pulse oximetry waveform of a preload dependent patient, which suggesst a potentially fluid-responsive patient. Do we really need to remove fingernail polish? You can save your department some money because it's unlikely to affect the SpO2 measurement to any clinically relevant degree. However, if you are concerned,  just turn it sideways. Is this the silver bullet of measuring fluid responsiveness, non-invasively? No. At least not yet. The majority of studies evaluating pulse oximetry utilization in this application were conducted under controlled conditions, such as mechanically ventilated patients with consistent respiratory changes in a proper sedation. Additionally, pulse oximetry waveform variations can be difficult to measure during increased systemic vascular resistance (How many patients on mechanical ventilation also require vasopressor support?). Then there's the issue with variations in vascular tone. The fingertip is much more susceptible to these changes as opposed to the vessels in the forehead, nose, or ear. To visualize what pulse wave variability looks like, here's a helpful picture: [caption id="" align="alignnone" width="600"] Extreme respiratory variation in a mechanically ventilated patient[/caption]            Bendjelid, K. (2008). The pulse oximetry plethysmographic curve revisited. Current Opinion in Critical Care. http://doi.org/10.1097/MCC.0b013e3282fb2dc9 Cannesson, M., Besnard, C., Durand, P. G., Bohé, J., &amp; Jacques, D. (2005). Relation between respiratory variations in pulse oximetry plethysmographic waveform amplitude and arterial pulse pressure in ventilated patients. Crit Care. http://doi.org/10.1186/cc3799 Cannesson, M., &amp; Talke, P. (2009). Recent advances in pulse oximetry. F1000 Medicine Reports. http://doi.org/10.3410/M1-66 Chan, E. D., Chan, M. M., &amp; Chan, M. M. (2013). Pulse oximetry: Understanding its basic principles facilitates appreciation of its limitations. Respiratory Medicine. http://doi.org/10.1016/j.rmed.2013.02.004 DeMeulenaere, S. (2007). Pulse Oximetry: Uses and Limitations. Journal for Nurse Practitioners. http://doi.org/10.1016/j.nurpra.2007.02.021 Gesche, H., Grosskurth, D., Küchler, G., &amp; Patzak, A. (2012). Continuous blood pressure measurement by using the pulse transit time: Comparison to a cuff-based method. European Journal of Applied Physiology. http://doi.org/10.1007/s00421-011-1983-3 Goldman, J. M., Petterson, M. T., Kopotic, R. J., &amp; Barker, S. J. (2000). Masimo signal extraction pulse oximetry. Journal of Clinical Monitoring and Computing. http://doi.org/10.1023/A:1011493521730 Hinkelbein, J., &amp; Genzwuerker, H. V. (2008). Fingernail polish does not influence pulse oximetry to a clinically relevant dimension. Intensive and Critical Care Nursing. http://doi.org/10.1016/j.iccn.2007.04.007 Jubran, A. (2012). Pulse oximetry. In Applied Physiology in Intensive Care Medicine 1: Physiological Notes - Technical Notes - Seminal Studies in Intensive Care, Third Edition. http://doi.org/10.1007/978-3-642-28270-6_12 Mendelson, Y. (1992). Pulse oximetry: Theory and applications for noninvasive monitoring. In Clinical Chemistry. Nitzan, M., Romem, A., &amp; Koppel, R. (2014). Pulse oximetry: Fundamentals and technology update. Medical Devices: Evidence and Research. http://doi.org/10.2147/MDER.S47319 Petterson, M. T., Begnoche, V. L., &amp; Graybeal, J. M. (2007). The effect of motion on pulse oximetry and its clinical significance. Anesthesia and Analgesia. http://doi.org/10.1213/01.ane.0000278134.47777.a5 Pizov, R., Eden, A., Bystritski, D., Kalina, E., Tamir, A., &amp; Gelman, S. (2010). Arterial and plethysmographic waveform analysis in anesthetized patients with hypovolemia. Anesthesiology. http://doi.org/10.1097/ALN.0b013e3181da839f Pretto, J. J., Roebuck, T., Beckert, L., &amp; Hamilton, G. (2014). Clinical use of pulse oximetry: Official guidelines from the Thoracic Society of Australia and New Zealand. Respirology. http://doi.org/10.1111/resp.12204 Sinex, J. E. (1999). Pulse oximetry: Principles and limitations. American Journal of Emergency Medicine. http://doi.org/10.1016/S0735-6757(99)90019-0

Topics Discussed in the Podcast: <ul> <li>Provider bias and the pulse oximeter.</li> <li>CO oximetry.</li> <li>Pulse oximeter lag. </li> <li>Approach to the well-appearing patient with a low SpO2 reading. </li> <li>Relation of vascular tone to pleth wave amplitude and variability. </li> <li>Using the pulse ox waveform to confirm mechanical capture during transcutaneous pacing.</li> <li>Odds and ends...</li> </ul> Pulse oximetry is more than just a measurement of oxygenation: The pulse oximetry plethysmograph is a pulsatile waveform that can be thought of as an arterial waveform. However, this waveform is influenced by cardiac output and systemic vascular resistance.  Thinking of the SpO2 pleth as a pulsatile waveform,  variations in the patients cardiac output should be transmitted to the fingertip arteries, which results in variations in the pulse ox waveform amplitude. The implications of this are far reaching. In patients who are mechanically ventilated, cyclical changes in intrathoracic pressures can produce measurable variations in the pulse oximetry waveform of a preload dependent patient, which suggesst a potentially fluid-responsive patient. Do we really need to remove fingernail polish? You can save your department some money because it's unlikely to affect the SpO2 measurement to any clinically relevant degree. However, if you are concerned, <a href="https://journal.chestnet.org/article/S0012-3692(16)34864-4/fulltext" rel="nofollow" target="_blank"> just turn it sideways</a>. Is this the silver bullet of measuring fluid responsiveness, non-invasively? No. At least not yet. The majority of studies evaluating pulse oximetry utilization in this application were conducted under controlled conditions, such as mechanically ventilated patients with consistent respiratory changes in a proper sedation. Additionally, pulse oximetry waveform variations can be difficult to measure during increased systemic vascular resistance (How many patients on mechanical ventilation also require vasopressor support?). Then there's the issue with variations in vascular tone. The fingertip is much more susceptible to these changes as opposed to the vessels in the forehead, nose, or ear. To visualize what pulse wave variability looks like, here's a helpful picture: [caption id="" align="alignnone" width="600"] <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297625/" rel="nofollow" target="_blank">Extreme respiratory variation in a mechanically ventilated patient</a>[/caption]   Bendjelid, K. (2008). The pulse oximetry plethysmographic curve revisited. Current Opinion in Critical Care. <a href="http://doi.org/10.1097/MCC.0b013e3282fb2dc9" rel="nofollow" target="_blank">http://doi.org/10.1097/MCC.0b013e3282fb2dc9</a> Cannesson, M., Besnard, C., Durand, P. G., Bohé, J., &amp; Jacques, D. (2005). Relation between respiratory variations in pulse oximetry plethysmographic waveform amplitude and arterial pulse pressure in ventilated patients. Crit Care. <a href="http://doi.org/10.1186/cc3799" rel="nofollow" target="_blank">http://doi.org/10.1186/cc3799</a> Cannesson, M., &amp; Talke, P. (2009). Recent advances in pulse oximetry. F1000 Medicine Reports. <a href="http://doi.org/10.3410/M1-66" rel="nofollow" target="_blank">http://doi.org/10.3410/M1-66</a> Chan, E. D., Chan, M. M., &amp; Chan, M. M. (2013). Pulse oximetry: Understanding its basic principles facilitates appreciation of its limitations. Respiratory Medicine. <a href="http://doi.org/10.1016/j.rmed.2013.02.004" rel="nofollow" target="_blank">http://doi.org/10.1016/j.rmed.2013.02.004</a> DeMeulenaere, S. (2007). Pulse Oximetry: Uses and Limitations. Journal for Nurse Practitioners. <a href="http://doi.org/10.1016/j.nurpra.2007.02.021" rel="nofollow" target="_blank">http://doi.org/10.1016/j.nurpra.2007.02.021</a> Gesche, H., Grosskurth, D., Küchler, G., &amp; Patzak, A. (2012). Continuous blood pressure measurement by using the pulse transit time: Comparison to a cuff-based method. European Journal of Applied Physiology. <a href="http://doi.org/10.1007/s00421-011-1983-3" rel="nofollow" target="_blank">http://doi.org/10.1007/s00421-011-1983-3</a> Goldman, J. M., Petterson, M. T., Kopotic, R. J., &amp; Barker, S. J. (2000). Masimo signal extraction pulse oximetry. Journal of Clinical Monitoring and Computing. <a href="http://doi.org/10.1023/A:1011493521730" rel="nofollow" target="_blank">http://doi.org/10.1023/A:1011493521730</a> Hinkelbein, J., &amp; Genzwuerker, H. V. (2008). Fingernail polish does not influence pulse oximetry to a clinically relevant dimension. Intensive and Critical Care Nursing. <a href="http://doi.org/10.1016/j.iccn.2007.04.007" rel="nofollow" target="_blank">http://doi.org/10.1016/j.iccn.2007.04.007</a> Jubran, A. (2012). Pulse oximetry. In Applied Physiology in Intensive Care Medicine 1: Physiological Notes - Technical Notes - Seminal Studies in Intensive Care, Third Edition. <a href="http://doi.org/10.1007/978-3-642-28270-6_12" rel="nofollow" target="_blank">http://doi.org/10.1007/978-3-642-28270-6_12</a> Mendelson, Y. (1992). Pulse oximetry: Theory and applications for noninvasive monitoring. In Clinical Chemistry. Nitzan, M., Romem, A., &amp; Koppel, R. (2014). Pulse oximetry: Fundamentals and technology update. Medical Devices: Evidence and Research. <a href="http://doi.org/10.2147/MDER.S47319" rel="nofollow" target="_blank">http://doi.org/10.2147/MDER.S47319</a> Petterson, M. T., Begnoche, V. L., &amp; Graybeal, J. M. (2007). The effect of motion on pulse oximetry and its clinical significance. Anesthesia and Analgesia. <a href="http://doi.org/10.1213/01.ane.0000278134.47777.a5" rel="nofollow" target="_blank">http://doi.org/10.1213/01.ane.0000278134.47777.a5</a> Pizov, R., Eden, A., Bystritski, D., Kalina, E., Tamir, A., &amp; Gelman, S. (2010). Arterial and plethysmographic waveform analysis in anesthetized patients with hypovolemia. Anesthesiology. <a href="http://doi.org/10.1097/ALN.0b013e3181da839f" rel="nofollow" target="_blank">http://doi.org/10.1097/ALN.0b013e3181da839f</a> Pretto, J. J., Roebuck, T., Beckert, L., &amp; Hamilton, G. (2014). Clinical use of pulse oximetry: Official guidelines from the Thoracic Society of Australia and New Zealand. Respirology. <a href="http://doi.org/10.1111/resp.12204" rel="nofollow" target="_blank">http://doi.org/10.1111/resp.12204</a> Sinex, J. E. (1999). Pulse oximetry: Principles and limitations. American Journal of Emergency Medicine. <a href="http://doi.org/10.1016/S0735-6757(99)90019-0" rel="nofollow" target="_blank">http://doi.org/10.1016/S0735-6757(99)90019-0</a>

Pulse Oximetry Basics and Biases 

The following is a short list of salient points related to the podcast and the corresponding source literature. As always, read the source literature and critically appraise it for yourself. Take none of the following as a substitution for local protocol or procedure. 2018 NAEMSP Spinal Immobilization paper   https://naemsp.org/resources/position-statements/spinal-immobilization/  Securing a patient to the stretcher mattress significantly reduces lateral motion:  Am J Emerg Med. 2016 Apr;34(4):717-21. doi: 10.1016/j.ajem.2015.12.078. Epub 2015 Dec 30.  C-Collar limits visible external motion in the intact spine, but not internal motion in the unstable injured spine:  Horodyski M, DiPaola CP, Conrad BP, Rechtine GR 2nd. Cervical collars are insufficient for immobilizing an unstable cervical spine injury. J Emerg Med. 2011 Nov;41(5):513-9. doi: 10.1016/j.jemermed.2011.02.001. Epub 2011 Mar 12. PubMed PMID: 21397431.  C-Collar increases ICP:  Davies G, Deakin C, Wilson A. The effect of a rigid collar on intracranial pressure. Injury. 1996 Nov;27(9):647-9. PubMed PMID: 9039362.  C-Collar causes distraction of unstable C-spine:  Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010 Aug;69(2):447-50. doi:10.1097/TA.0b013e3181be785a. PubMed PMID: 20093981. Lador R, Ben-Galim P, Hipp JA. Motion within the unstable cervical spine during patient maneuvering: the neck pivot-shift phenomenon. J Trauma. 2011 Jan;70(1):247-50; discussion 250-1. doi: 10.1097/TA.0b013e3181fd0ebf. PubMed PMID: 21217496.  Spinal immobilization negatively impacts the physical exam:  March J et al. Changes In Physical Examination Caused by Use of Spinal Immobilization. Prehosp Emerg Care 2002; 6(4): 421 – 4. PMID: 12385610 Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994 Jan;23(1):48-51. PubMed PMID: 8273958. Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med. 1996 May-Jun;14(3):293-8. PubMed PMID: 8782022.  Even Manual In Line Stabilization alone increased difficulty during intubation and increases forces applied to the neck:  Thiboutot F, Nicole PC, Trépanier CA, Turgeon AF, Lessard MR. Effect of manual in-line stabilization of the cervical spine in adults on the rate of difficult orotracheal intubation by direct laryngoscopy: a randomized controlled trial. Can J Anaesth. 2009 Jun;56(6):412-8. doi: 10.1007/s12630-009-9089-7. Epub 2009 Apr 24. PubMed PMID: 19396507. Santoni BG, Hindman BJ, Puttlitz CM, Weeks JB, Johnson N, Maktabi MA, Todd MM. Manual in-line stabilization increases pressures applied by the laryngoscope blade during direct laryngoscopy and orotracheal intubation. Anesthesiology. 2009 Jan;110(1):24-31. doi: 10.1097/ALN.0b013e318190b556. PubMed PMID: 19104166.  Spinal immobilization makes it harder to breath and decreases forced expiratory volume: “...produce a significantly restrictive effect on pulmonary function in the healthy, nonsmoking man.”  Chan, D., Goldberg, R., Tascone, A., Harmon, S., &amp; Chan, L. (1994). The effect of spinal immobilization on healthy volunteers. Annals of Emergency Medicine, 23(1), 48–51. https://doi.org/10.1016/S0196-0644(94)70007-9 Schafermeyer RW, Ribbeck BM, Gaskins J, Thomason S, Harlan M, Attkisson A. Respiratory effects of spinal immobilization in children. Ann Emerg Med. 1991 Sep;20(9):1017-9. PubMed PMID: 1877767. Totten VY, Sugarman DB. Respiratory effects of spinal immobilization. Prehosp Emerg Care. 1999 Oct-Dec;3(4):347-52. PubMed PMID: 10534038.  Prehospital providers can effectively apply selective immobilization criteria without causing harm:  Domeier, R. M., Frederiksen, S. M., &amp; Welch, K. (2005). Prospective performance assessment of an out-of-hospital protocol for selective spine immobilization using clinical spine clearance criteria. Annals of Emergency Medicine, 46(2), 123–131. https://doi.org/10.1016/j.annemergmed.2005.02.004  Out of 32,000 trauma encounters, a prehospital clearance protocol resulted in ONE patient with an unstable injury that was not immobilized. This patient injured her back one week prior, required fixation, but had no neurological injury:  Burton, J.H., Dunn, M.G., Harmon, N.R., Hermanson, T.A., and Bradshaw, J.R. A statewide, prehospital emergency medical service selective patient spine immobilization protocol. J Trauma. 2006; 61: 161–167  Ambulatory patients self extricating with a cervical collar results in less cervical spine motion than with the use of a backboard:  Shafer, J. S., &amp; Naunheim, R. S. (2009). Cervical Spine Motion During Extrication: A Pilot Study. Western Journal of Emergency Medicine, 10(2), 74–78. https://doi.org/10.1016/j.jemermed.2012.02.082 Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS. Cervical spine motion during extrication. J Emerg Med. 2013 Jan;44(1):122-7. doi:10.1016/j.jemermed.2012.02.082. Epub 2012 Oct 15. PubMed PMID: 23079144  Lift and slide technique is superior to log roll:  Boissy, P., Shrier, I., Brière, S. et al. Effectiveness of cervical spine stabilization techniques. Clin J Sport Med. 2011; 21: 80–88  Despite there not being any randomized control trials evaluating spinal immobilization, patients transferred to hospitals immobilized have more disability than those transported without immobilization:  Hauswald, M., Ong, G., Tandberg, D., and Omar, Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998; 5: 214–219  “Mechanism of injury does not affect the ability of clinical criteria to predict spinal injury”  Domeier, R.M., Evans, R.W., Swor, R.A. et al. The reliability of prehospital clinical evaluation for potential spinal injury is not affected by the mechanism of injury.Prehosp Emerg Care. 1999; 3: 332–337  Spinal immobilization in penetrating trauma is associated with an increased risk of death:  Vanderlan, W.B., Tew, B.E., and McSwain, N.E. Jr. Increased risk of death with cervical spine immobilisation in penetrating cervical trauma. Injury. 2009; 40: 880–88 Stuke, L.E., Pons, P.T., Guy, J.S., Chapleau, W.P., Butler, F.K., and McSwain, N.E.Prehospital spine immobilization for penetrating trauma-review and recommendations from the Prehospital Trauma Life Support Executive Committee. J Trauma. 2011; 71: 763–769  “The number needed to treat with spine immobilization to potentially benefit one patient was 1,032. The number needed to harm with spine immobilization to potentially contribute to one death was 66.”  Haut, E.R., Kalish, B.T., Efron, D.T. et al. Spine immobilization in penetrating trauma: more harm than good?. J Trauma. 2010; 68: 115–121 Vanderlan WB, Tew BE, Seguin CY, Mata MM, Yang JJ, Horst HM, Obeid FN, McSwain NE. Neurologic sequelae of penetrating cervical trauma. Spine (Phila Pa 1976). 2009 Nov 15;34(24):2646-53. doi: 10.1097/BRS.0b013e3181bd9df1. PubMed PMID: 19881402. Velopulos CG, Shihab HM, Lottenberg L, Feinman M, Raja A, Salomone J, Haut ER. Prehospital spine immobilization/spinal motion restriction in penetrating trauma: A practice management guideline from the Eastern Association for the Surgery of Trauma (EAST). J Trauma Acute Care Surg. 2018 May;84(5):736-744. doi:10.1097/TA.0000000000001764. PubMed PMID: 29283970.  Use of LSB can cause sufficient pressure to create pressure ulcers in a short period of time:  Cordell W:H, Hollingsworth JC, Olinger ML, Stroman SJ, Nelson DR. Pain and tissue-interface pressures during spine-board immobilization. Ann Emerg Med. 1995 Jul;26(1):31-6. PubMed PMID: 7793717.  The natural progression of some C-spine injuries is to get worse, sometimes because we force them into immobilization devices, sometimes because of hypotension, vascular injury, or hypoxia, but surprisingly not because of EMS providers…  Harrop JS, Sharan AD, Vaccaro AR, Przybylski GJ. The cause of neurologic deterioration after acute cervical spinal cord injury. Spine (Phila Pa 1976). 2001 Feb 15;26(4):340-6. PubMed PMID: 11224879.  Reports of asymptomatic but clinically important spine injuries are, at best, dubious:  McKee TR, Tinkoff G, Rhodes M. Asymptomatic occult cervical spine fracture: case report and review of the literature. J Trauma. 1990 May;30(5):623-6. Review. PubMed PMID: 2188001. Bresler MJ, Rich GH. Occult cervical spine fracture in an ambulatory patients. Ann Emerg Med. 1982 Aug;11(8):440-2. PubMed PMID: 7103163. 

The following is a short list of salient points related to the podcast and the corresponding source literature. As always, read the source literature and critically appraise it for yourself. Take none of the following as a substitution for local protocol or procedure. 2018 NAEMSP Spinal Immobilization paper <ul> <li> <a href="https://naemsp.org/resources/position-statements/spinal-immobilization/" rel="nofollow" target="_blank">https://naemsp.org/resources/position-statements/spinal-immobilization/</a></li> </ul> Securing a patient to the stretcher mattress significantly reduces lateral motion: <ul> <li>Am J Emerg Med. 2016 Apr;34(4):717-21. doi: 10.1016/j.ajem.2015.12.078. Epub 2015 Dec 30.</li> </ul> C-Collar limits visible external motion in the intact spine, but not internal motion in the unstable injured spine: <ul> <li>Horodyski M, DiPaola CP, Conrad BP, Rechtine GR 2nd. Cervical collars are insufficient for immobilizing an unstable cervical spine injury. J Emerg Med. 2011 Nov;41(5):513-9. doi: 10.1016/j.jemermed.2011.02.001. Epub 2011 Mar 12. PubMed PMID: 21397431.</li> </ul> C-Collar increases ICP: <ul> <li>Davies G, Deakin C, Wilson A. The effect of a rigid collar on intracranial pressure. Injury. 1996 Nov;27(9):647-9. PubMed PMID: 9039362.</li> </ul> C-Collar causes distraction of unstable C-spine: <ul> <li>Ben-Galim P, Dreiangel N, Mattox KL, Reitman CA, Kalantar SB, Hipp JA. Extrication collars can result in abnormal separation between vertebrae in the presence of a dissociative injury. J Trauma. 2010 Aug;69(2):447-50. doi:10.1097/TA.0b013e3181be785a. PubMed PMID: 20093981.</li> <li>Lador R, Ben-Galim P, Hipp JA. Motion within the unstable cervical spine during patient maneuvering: the neck pivot-shift phenomenon. J Trauma. 2011 Jan;70(1):247-50; discussion 250-1. doi: 10.1097/TA.0b013e3181fd0ebf. PubMed PMID: 21217496.</li> </ul> Spinal immobilization negatively impacts the physical exam: <ul> <li>March J et al. Changes In Physical Examination Caused by Use of Spinal Immobilization. Prehosp Emerg Care 2002; 6(4): 421 – 4. PMID: 12385610</li> <li>Chan D, Goldberg R, Tascone A, Harmon S, Chan L. The effect of spinal immobilization on healthy volunteers. Ann Emerg Med. 1994 Jan;23(1):48-51. PubMed PMID: 8273958.</li> <li>Chan D, Goldberg RM, Mason J, Chan L. Backboard versus mattress splint immobilization: a comparison of symptoms generated. J Emerg Med. 1996 May-Jun;14(3):293-8. PubMed PMID: 8782022.</li> </ul> Even Manual In Line Stabilization alone increased difficulty during intubation and increases forces applied to the neck: <ul> <li>Thiboutot F, Nicole PC, Trépanier CA, Turgeon AF, Lessard MR. Effect of manual in-line stabilization of the cervical spine in adults on the rate of difficult orotracheal intubation by direct laryngoscopy: a randomized controlled trial. Can J Anaesth. 2009 Jun;56(6):412-8. doi: 10.1007/s12630-009-9089-7. Epub 2009 Apr 24. PubMed PMID: 19396507.</li> <li>Santoni BG, Hindman BJ, Puttlitz CM, Weeks JB, Johnson N, Maktabi MA, Todd MM. Manual in-line stabilization increases pressures applied by the laryngoscope blade during direct laryngoscopy and orotracheal intubation. Anesthesiology. 2009 Jan;110(1):24-31. doi: 10.1097/ALN.0b013e318190b556. PubMed PMID: 19104166.</li> </ul> Spinal immobilization makes it harder to breath and decreases forced expiratory volume: “...produce a significantly restrictive effect on pulmonary function in the healthy, nonsmoking man.” <ul> <li>Chan, D., Goldberg, R., Tascone, A., Harmon, S., &amp; Chan, L. (1994). The effect of spinal immobilization on healthy volunteers. Annals of Emergency Medicine, 23(1), 48–51. <a href="https://doi.org/10.1016/S0196-0644(94)70007-9" rel="nofollow" target="_blank">https://doi.org/10.1016/S0196-0644(94)70007-9</a></li> <li>Schafermeyer RW, Ribbeck BM, Gaskins J, Thomason S, Harlan M, Attkisson A. Respiratory effects of spinal immobilization in children. Ann Emerg Med. 1991 Sep;20(9):1017-9. PubMed PMID: 1877767.</li> <li>Totten VY, Sugarman DB. Respiratory effects of spinal immobilization. Prehosp Emerg Care. 1999 Oct-Dec;3(4):347-52. PubMed PMID: 10534038.</li> </ul> Prehospital providers can effectively apply selective immobilization criteria without causing harm: <ul> <li>Domeier, R. M., Frederiksen, S. M., &amp; Welch, K. (2005). Prospective performance assessment of an out-of-hospital protocol for selective spine immobilization using clinical spine clearance criteria. Annals of Emergency Medicine, 46(2), 123–131. <a href="https://doi.org/10.1016/j.annemergmed.2005.02.004" rel="nofollow" target="_blank">https://doi.org/10.1016/j.annemergmed.2005.02.004</a></li> </ul> Out of 32,000 trauma encounters, a prehospital clearance protocol resulted in ONE patient with an unstable injury that was not immobilized. This patient injured her back one week prior, required fixation, but had no neurological injury: <ul> <li>Burton, J.H., Dunn, M.G., Harmon, N.R., Hermanson, T.A., and Bradshaw, J.R. A statewide, prehospital emergency medical service selective patient spine immobilization protocol. J Trauma. 2006; 61: 161–167</li> </ul> Ambulatory patients self extricating with a cervical collar results in less cervical spine motion than with the use of a backboard: <ul> <li>Shafer, J. S., &amp; Naunheim, R. S. (2009). Cervical Spine Motion During Extrication: A Pilot Study. Western Journal of Emergency Medicine, 10(2), 74–78. <a href="https://doi.org/10.1016/j.jemermed.2012.02.082" rel="nofollow" target="_blank">https://doi.org/10.1016/j.jemermed.2012.02.082</a></li> <li>Engsberg JR, Standeven JW, Shurtleff TL, Eggars JL, Shafer JS, Naunheim RS. Cervical spine motion during extrication. J Emerg Med. 2013 Jan;44(1):122-7. doi:10.1016/j.jemermed.2012.02.082. Epub 2012 Oct 15. PubMed PMID: 23079144</li> </ul> Lift and slide technique is superior to log roll: <ul> <li>Boissy, P., Shrier, I., Brière, S. et al. Effectiveness of cervical spine stabilization techniques. Clin J Sport Med. 2011; 21: 80–88</li> </ul> Despite there not being any randomized control trials evaluating spinal immobilization, patients transferred to hospitals immobilized have more disability than those transported without immobilization: <ul> <li>Hauswald, M., Ong, G., Tandberg, D., and Omar, Z. Out-of-hospital spinal immobilization: its effect on neurologic injury. Acad Emerg Med. 1998; 5: 214–219</li> </ul> “Mechanism of injury does not affect the ability of clinical criteria to predict spinal injury” <ul> <li>Domeier, R.M., Evans, R.W., Swor, R.A. et al. The reliability of prehospital clinical evaluation for potential spinal injury is not affected by the mechanism of injury.Prehosp Emerg Care. 1999; 3: 332–337</li> </ul> Spinal immobilization in penetrating trauma is associated with an increased risk of death: <ul> <li>Vanderlan, W.B., Tew, B.E., and McSwain, N.E. Jr. Increased risk of death with cervical spine immobilisation in penetrating cervical trauma. Injury. 2009; 40: 880–88</li> <li>Stuke, L.E., Pons, P.T., Guy, J.S., Chapleau, W.P., Butler, F.K., and McSwain, N.E.Prehospital spine immobilization for penetrating trauma-review and recommendations from the Prehospital Trauma Life Support Executive Committee. J Trauma. 2011; 71: 763–769</li> </ul> “The number needed to treat with spine immobilization to potentially benefit one patient was 1,032. The number needed to harm with spine immobilization to potentially contribute to one death was 66.” <ul> <li>Haut, E.R., Kalish, B.T., Efron, D.T. et al. Spine immobilization in penetrating trauma: more harm than good?. J Trauma. 2010; 68: 115–121</li> <li>Vanderlan WB, Tew BE, Seguin CY, Mata MM, Yang JJ, Horst HM, Obeid FN, McSwain NE. Neurologic sequelae of penetrating cervical trauma. Spine (Phila Pa 1976). 2009 Nov 15;34(24):2646-53. doi: 10.1097/BRS.0b013e3181bd9df1. PubMed PMID: 19881402.</li> <li>Velopulos CG, Shihab HM, Lottenberg L, Feinman M, Raja A, Salomone J, Haut ER. Prehospital spine immobilization/spinal motion restriction in penetrating trauma: A practice management guideline from the Eastern Association for the Surgery of Trauma (EAST). J Trauma Acute Care Surg. 2018 May;84(5):736-744. doi:10.1097/TA.0000000000001764. PubMed PMID: 29283970.</li> </ul> Use of LSB can cause sufficient pressure to create pressure ulcers in a short period of time: <ul> <li>Cordell W:H, Hollingsworth JC, Olinger ML, Stroman SJ, Nelson DR. Pain and tissue-interface pressures during spine-board immobilization. Ann Emerg Med. 1995 Jul;26(1):31-6. PubMed PMID: 7793717.</li> </ul> The natural progression of some C-spine injuries is to get worse, sometimes because we force them into immobilization devices, sometimes because of hypotension, vascular injury, or hypoxia, but surprisingly not because of EMS providers… <ul> <li>Harrop JS, Sharan AD, Vaccaro AR, Przybylski GJ. The cause of neurologic deterioration after acute cervical spinal cord injury. Spine (Phila Pa 1976). 2001 Feb 15;26(4):340-6. PubMed PMID: 11224879.</li> </ul> Reports of asymptomatic but clinically important spine injuries are, at best, dubious: <ul> <li>McKee TR, Tinkoff G, Rhodes M. Asymptomatic occult cervical spine fracture: case report and review of the literature. J Trauma. 1990 May;30(5):623-6. Review. PubMed PMID: 2188001.</li> <li>Bresler MJ, Rich GH. Occult cervical spine fracture in an ambulatory patients. Ann Emerg Med. 1982 Aug;11(8):440-2. PubMed PMID: 7103163.</li> </ul>

Modern Spinal Care 

Ben Newman

“The value of experience is not in seeing much, but in seeing wisely.”  ― Sir William Osler   Deciphering signal from noise as it relates to modern stroke care can be challenging and conflicting, especially as it pertains to the out of hospital environment. In this podcast, we brought the knowledge and experience of Dr. Ben Newman: a neurosurgeon and endovascular therapy expert to discuss advances, challenges, and strategies in caring for our stroke patients. When to Bypass Perhaps the most challenging decision to make when presented with a patient experiencing an acute stroke is the transport decision. Should we transport them to a Comprehensive Stroke Center (CSC), or to a "thrombolytic capable center"?  The 2018 AHA/ASA Stroke Guidelines state that: When several IV alteplase–capable hospital options exist within a defined geographic region, the benefit of bypassing the closest to bring the patient to one that offers a higher level of stroke care, including mechanical thrombectomy, is uncertain. Further research is needed. They also state that the   Mission: Lifeline Severity–based Stroke Triage Algorithm for EMS may be reasonable in some circumstances. This algorithm recommends, in some circumstances, transporting the patient to a comprehensive center only if the transport time is "

“The value of experience is not in seeing much, but in seeing wisely.” ― Sir William Osler Deciphering signal from noise as it relates to modern stroke care can be challenging and conflicting, especially as it pertains to the out of hospital environment. In this podcast, we brought the knowledge and experience of Dr. Ben Newman: a neurosurgeon and endovascular therapy expert to discuss advances, challenges, and strategies in caring for our stroke patients. When to Bypass Perhaps the most challenging decision to make when presented with a patient experiencing an acute stroke is the transport decision. Should we transport them to a Comprehensive Stroke Center (CSC), or to a "thrombolytic capable center"?  The <a href="https://www.strokeassociation.org/idc/groups/stroke-public/@wcm/@hcm/@sta/documents/downloadable/ucm_499252.pdf" rel="nofollow" target="_blank">2018 AHA/ASA Stroke Guidelines</a> state that: When several IV alteplase–capable hospital options exist within a defined geographic region, the benefit of bypassing the closest to bring the patient to one that offers a higher level of stroke care, including mechanical thrombectomy, is uncertain. Further research is needed. They also state that the  <a href="https://www.heart.org/-/media/files/professional/quality-improvement/mission-lifeline/severitybased-stroke-triage-algorithm-for-ems-ucm_498615.pdf?la=en&amp;hash=B7B28286E1DEE20045BC00CCEB1442D09A20E768" rel="nofollow" target="_blank"> Mission: Lifeline Severity–based Stroke Triage Algorithm for EMS</a> may be reasonable in some circumstances. This algorithm recommends, in some circumstances, transporting the patient to a comprehensive center only if the transport time is "

Seeing Wisely: Decoding Stroke Care with Dr. Ben Newman

Jeff Jarvis

In this episode, we're graced by the presence of Airway Jedi Dr. Jeff Jarvis. We discuss a novel approach to the standardization of airway management in order to prevent peri-intubation hypoxia and valuable insight into the organizational culture required to make it successful. Link to Dr. Jarvis' paper "Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia": (Note, at the time of publishing, this article was open-access). https://www.annemergmed.com/article/S0196-0644(18)30071-4/abstract Link to the FOAMfrat Q&amp;A with Dr. Jarvis: https://www.foamfrat.com/single-post/2018/09/29/Why-Do-You-QA-w-Jeff-Jarvis Link to "EMS Intubation Improves with King Vision Video Laryngoscopy" (Non-open access) https://www.tandfonline.com/doi/abs/10.3109/10903127.2015.1005259 Williamson County EMS YouTube Channel: https://www.youtube.com/channel/UCkMY9plbu_4aTUuSXXm46gg

In this episode, we're graced by the presence of Airway Jedi Dr. Jeff Jarvis. We discuss a novel approach to the standardization of airway management in order to prevent peri-intubation hypoxia and valuable insight into the organizational culture required to make it successful. Link to Dr. Jarvis' paper "Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia": (Note, at the time of publishing, this article was open-access). <a href="https://www.annemergmed.com/article/S0196-0644(18)30071-4/abstract" rel="nofollow" target="_blank">https://www.annemergmed.com/article/S0196-0644(18)30071-4/abstract</a> Link to the FOAMfrat Q&amp;A with Dr. Jarvis: <a href="https://www.foamfrat.com/single-post/2018/09/29/Why-Do-You-QA-w-Jeff-Jarvis" rel="nofollow" target="_blank">https://www.foamfrat.com/single-post/2018/09/29/Why-Do-You-QA-w-Jeff-Jarvis</a> Link to "EMS Intubation Improves with King Vision Video Laryngoscopy" (Non-open access) <a href="https://www.tandfonline.com/doi/abs/10.3109/10903127.2015.1005259" rel="nofollow" target="_blank">https://www.tandfonline.com/doi/abs/10.3109/10903127.2015.1005259</a> Williamson County EMS YouTube Channel: <a href="https://www.youtube.com/channel/UCkMY9plbu_4aTUuSXXm46gg" rel="nofollow" target="_blank">https://www.youtube.com/channel/UCkMY9plbu_4aTUuSXXm46gg</a>

Avoiding Airway Disasters with Dr. Jeff Jarvis

What is SCAPE?   For this podcast, we're discussing the acute pulmonary edema presentation.  This patient is hypertensive (SBP &gt;140mmHg), severely dyspneic, with diffuse rales and clearly anxious. The "no-shitter, drowning-before-your-very-eyes" type of pulmonary edema.   This is the SCAPE patient. SCAPE = Sympathetic Crashing Acute Pulmonary Edema.  Patho Quick Hits   The core causative factor in the SCAPE patient is an acute increase in left ventricular filling pressure.  There are a myriad of causes for a sudden increase in LV pressure, but the end result is a redistribution of fluid into the lungs.  1) Acute increase in LV filling pressure. 2) Fluid redistribution into the lungs and alveolar space. 3) Hypoxia ensues. 4) Catecholamine production and increase in SVR. 5) Activation of the RAAS.  It's important to remember that the majority of these patients are not volume overloaded. This is a fluid distribution problem due to increased LV pressure. As the RV continues to pump fluid into the pulmonary circulation, the LV cannot move that fluid forward because of the increased afterload. This creates a pressure gradient that transmits that pressure back into the pulmonary capillaries.  5 Major Causes of SCAPE - Exacerbation of chronic LV failure - Acute myocardial ischemia or infarction involving 25% or more of the myocardial mass - Severe systemic hypertension - Left sided valvular disorders - Acute tachydysrhythmias and bradysrhythmias  Treatment   In the out of hospital realm, the core treatments are Non Invasive Positive Pressure Ventilation (NIPPV) via CPAP or BiPAP, coupled with nitroglycerine as a first-line medication.  For the "regular guy" toolbox, the treatment pathway looks a little like this:  1) Treating the underlying cause if evident. 2) NIPPV 3) NTG 4) More NTG 5) More NTG 6) More NTG   Do not delay NIPPV to see if other therapies (like a NRB) will work first. In the awake patient maintaining their own airway presenting with SCAPE, have a low threshold to apply your NIPPV mode of choice.  These patients need PEEP: they generally have an oxygenation problem, and not a ventilation problem.  To that point, most prehospital disposable CPAP systems do not deliver 100% FiO2.  The O_two and Pulmodyne O2-MAX systems we generally use are either fixed FiO2 or provide a titration of FiO2 based on oxygen flow.  The O_two system will provide between 59% and 77% FiO2 at oxygen flow rates between 8L/min and 25 L/min respectively.  The Pulmodyne O2-MAX system provides 30% FiO2 regardless of PEEP, or with an additional adapter may provide 30%, 60%, or 90% FiO2 independent of the set PEEP.  Nitrogylcerin  If sublingual NTG is all you have, give it. Often, too. Lifting up the CPAP mask for 20 seconds is highly unlikely to cause clinically relevant harm.  If you have the option of IV NTG, that should be your go-to.  Standard dosing strategies for IV NTG of 5-40mcg/min are likely ineffective, and there is literature to support higher dosing strategies.  Consider that we bolus 400mcg of SL NTG, and that the bioequivalence of SL NTG is comparable to around an IV NTG dose of 60-80mcg/min, so rapid titration of IV NTG even up to 100mcg/min is not entirely unreasonable and largely supported by current literature.  Bibliography   Dec, G. W. (2007). Management of Acute Decompensated Heart Failure. Current Problems in Cardiology, 32(6), 321–366. https://doi.org/10.1016/j.cpcardiol.2007.02.002 Mosesso, V. N. J., Dunford, J., Blackwell, T., &amp; Griswell, J. K. (2003). Prehospital therapy for acute congestive heart failure: state of the art. Prehospital Emergency Care : Official Journal of the National Association of EMS Physicians and the National Association of State EMS Directors, 7(1), 13–23. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=reference&amp;D=med4&amp;NEWS=N&amp;AN=12540139 Aguilar, S., Lee, J., Castillo, E., Lam, B., Choy, J., Patel, E., … Serra, J. (2013). Assessment of the addition of prehospital continuous positive airway pressure (CPAP) to an urban emergency medical services (EMS) system in persons with severe respiratory distress. The Journal of Emergency Medicine, 45(2), 210–9. https://doi.org/10.1016/j.jemermed.2013.01.044 Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., … Zalenski, R. (2007). Treatment of Severe Decompensated Heart Failure With High-Dose Intravenous Nitroglycerin: A Feasibility and Outcome Analysis. Annals of Emergency Medicine, 50(2), 144–152. https://doi.org/10.1016/j.annemergmed.2007.02.022 Mebazaa, A., Gheorghiade, M., Piña, I. L., Harjola, V.-P., Hollenberg, S. M., Follath, F., … Filippatos, G. (2008). Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Critical Care Medicine, 36(Suppl), S129–S139. https://doi.org/10.1097/01.CCM.0000296274.51933.4C Agrawal, N., Kumar, A., Aggarwal, P., &amp; Jamshed, N. (2016). Sympathetic crashing acute pulmonary edema. Indian Journal of Critical Care Medicine, 20(12), 719. https://doi.org/10.4103/0972-5229.195710 Mattu, A., Martinez, J. P., &amp; Kelly, B. S. (2005). Modern management of cardiogenic pulmonary edema. Emergency Medicine Clinics of North America. https://doi.org/10.1016/j.emc.2005.07.005 Scott Weingart. EMCrit Podcast 1 – Sympathetic Crashing Acute Pulmonary Edema (SCAPE). EMCrit Blog. Published on April 25, 2009. Accessed on September 11th 2018. Available at [https://emcrit.org/emcrit/scape/ ].

What is SCAPE? For this podcast, we're discussing the acute pulmonary edema presentation. This patient is hypertensive (SBP &gt;140mmHg), severely dyspneic, with diffuse rales and clearly anxious. The "no-shitter, drowning-before-your-very-eyes" type of pulmonary edema.  This is the SCAPE patient. SCAPE = Sympathetic Crashing Acute Pulmonary Edema. Patho Quick Hits The core causative factor in the SCAPE patient is an acute increase in left ventricular filling pressure. There are a myriad of causes for a sudden increase in LV pressure, but the end result is a redistribution of fluid into the lungs. 1) Acute increase in LV filling pressure. 2) Fluid redistribution into the lungs and alveolar space. 3) Hypoxia ensues. 4) Catecholamine production and increase in SVR. 5) Activation of the RAAS. It's important to remember that the majority of these patients are not volume overloaded. This is a fluid distribution problem due to increased LV pressure. As the RV continues to pump fluid into the pulmonary circulation, the LV cannot move that fluid forward because of the increased afterload. This creates a pressure gradient that transmits that pressure back into the pulmonary capillaries. 5 Major Causes of SCAPE - Exacerbation of chronic LV failure - Acute myocardial ischemia or infarction involving 25% or more of the myocardial mass - Severe systemic hypertension - Left sided valvular disorders - Acute tachydysrhythmias and bradysrhythmias Treatment In the out of hospital realm, the core treatments are Non Invasive Positive Pressure Ventilation (NIPPV) via CPAP or BiPAP, coupled with nitroglycerine as a first-line medication. For the "regular guy" toolbox, the treatment pathway looks a little like this: 1) Treating the underlying cause if evident. 2) NIPPV 3) NTG 4) More NTG 5) More NTG 6) More NTG  Do not delay NIPPV to see if other therapies (like a NRB) will work first. In the awake patient maintaining their own airway presenting with SCAPE, have a low threshold to apply your NIPPV mode of choice. These patients need PEEP: they generally have an oxygenation problem, and not a ventilation problem. To that point, most prehospital disposable CPAP systems do not deliver 100% FiO2. The O_two and Pulmodyne O2-MAX systems we generally use are either fixed FiO2 or provide a titration of FiO2 based on oxygen flow. The O_two system will provide between 59% and 77% FiO2 at oxygen flow rates between 8L/min and 25 L/min respectively. The Pulmodyne O2-MAX system provides 30% FiO2 regardless of PEEP, or with an additional adapter may provide 30%, 60%, or 90% FiO2 independent of the set PEEP. Nitrogylcerin If sublingual NTG is all you have, give it. Often, too. Lifting up the CPAP mask for 20 seconds is highly unlikely to cause clinically relevant harm. If you have the option of IV NTG, that should be your go-to. Standard dosing strategies for IV NTG of 5-40mcg/min are likely ineffective, and there is literature to support higher dosing strategies. Consider that we bolus 400mcg of SL NTG, and that the bioequivalence of SL NTG is comparable to around an IV NTG dose of 60-80mcg/min, so rapid titration of IV NTG even up to 100mcg/min is not entirely unreasonable and largely supported by current literature. Bibliography Dec, G. W. (2007). Management of Acute Decompensated Heart Failure. Current Problems in Cardiology, 32(6), 321–366. <a href="https://doi.org/10.1016/j.cpcardiol.2007.02.002" rel="nofollow" target="_blank">https://doi.org/10.1016/j.cpcardiol.2007.02.002</a> Mosesso, V. N. J., Dunford, J., Blackwell, T., &amp; Griswell, J. K. (2003). Prehospital therapy for acute congestive heart failure: state of the art. Prehospital Emergency Care : Official Journal of the National Association of EMS Physicians and the National Association of State EMS Directors, 7(1), 13–23. Retrieved from <a href="http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=reference&amp;D=med4&amp;NEWS=N&amp;AN=12540139" rel="nofollow" target="_blank">http://ovidsp.ovid.com/ovidweb.cgi?T=JS&amp;PAGE=reference&amp;D=med4&amp;NEWS=N&amp;AN=12540139</a> Aguilar, S., Lee, J., Castillo, E., Lam, B., Choy, J., Patel, E., … Serra, J. (2013). Assessment of the addition of prehospital continuous positive airway pressure (CPAP) to an urban emergency medical services (EMS) system in persons with severe respiratory distress. The Journal of Emergency Medicine, 45(2), 210–9. <a href="https://doi.org/10.1016/j.jemermed.2013.01.044" rel="nofollow" target="_blank">https://doi.org/10.1016/j.jemermed.2013.01.044</a> Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., … Zalenski, R. (2007). Treatment of Severe Decompensated Heart Failure With High-Dose Intravenous Nitroglycerin: A Feasibility and Outcome Analysis. Annals of Emergency Medicine, 50(2), 144–152. <a href="https://doi.org/10.1016/j.annemergmed.2007.02.022" rel="nofollow" target="_blank">https://doi.org/10.1016/j.annemergmed.2007.02.022</a> Mebazaa, A., Gheorghiade, M., Piña, I. L., Harjola, V.-P., Hollenberg, S. M., Follath, F., … Filippatos, G. (2008). Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Critical Care Medicine, 36(Suppl), S129–S139. <a href="https://doi.org/10.1097/01.CCM.0000296274.51933.4C" rel="nofollow" target="_blank">https://doi.org/10.1097/01.CCM.0000296274.51933.4C</a> Agrawal, N., Kumar, A., Aggarwal, P., &amp; Jamshed, N. (2016). Sympathetic crashing acute pulmonary edema. Indian Journal of Critical Care Medicine, 20(12), 719. <a href="https://doi.org/10.4103/0972-5229.195710" rel="nofollow" target="_blank">https://doi.org/10.4103/0972-5229.195710</a> Mattu, A., Martinez, J. P., &amp; Kelly, B. S. (2005). Modern management of cardiogenic pulmonary edema. Emergency Medicine Clinics of North America. <a href="https://doi.org/10.1016/j.emc.2005.07.005" rel="nofollow" target="_blank">https://doi.org/10.1016/j.emc.2005.07.005</a> Scott Weingart. EMCrit Podcast 1 – Sympathetic Crashing Acute Pulmonary Edema (SCAPE). EMCrit Blog. Published on April 25, 2009. Accessed on September 11th 2018. Available at [<a href="https://emcrit.org/emcrit/scape/" rel="nofollow" target="_blank">https://emcrit.org/emcrit/scape/</a> ].

Acute Pulmonary Edema 

Walt Lubbers

This podcast is based on the Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients (FEEL) Study, and inferences made from it. The study was to determine the feasibility of prehospital ultrasound, but there were more astonishing results:  74.5% of patients in (pseudo) PEA had cardiac activity. 35% of patients in (suspected) asystole had cardiac activity.   We brought on EMS Physician Walt Lubbers to answer whether or not ultrasound would inform our decision making or alter how we manage a patient in cardiac arrest.   What we really wanted to know is 1) should we shock asystole "just in case" it could be very fine VF, and 2) would the presence of cardiac activity on ultrasound change how we manage a patient in cardiac arrest.  We discussed in detail some cardiac arrest physiology and referenced a video lecture and studies cited by Dr. Peter Kudenchuk from the Resuscitation Academy.

This podcast is based on the Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients (FEEL) <a href="https://www.ncbi.nlm.nih.gov/pubmed/20801576" rel="nofollow" target="_blank">Study</a>, and inferences made from it. The study was to determine the feasibility of prehospital ultrasound, but there were more astonishing results: <ul> <li>74.5% of patients in (pseudo) PEA had cardiac activity.</li> <li>35% of patients in (suspected) asystole had cardiac activity. </li> </ul> We brought on EMS Physician Walt Lubbers to answer whether or not ultrasound would inform our decision making or alter how we manage a patient in cardiac arrest.   What we really wanted to know is 1) should we shock asystole "just in case" it could be very fine VF, and 2) would the presence of cardiac activity on ultrasound change how we manage a patient in cardiac arrest.  We discussed in detail some cardiac arrest physiology and referenced a <a href="https://youtu.be/44142bQp1sY" rel="nofollow" target="_blank">video</a> lecture and studies cited by Dr. Peter Kudenchuk from the Resuscitation Academy.

FEELing for a Pulse and Shocking Asystole with Walt Lubbers

Terminology Wet, dry, or near drowning are not medically accepted terms and should not be used. There is nothing “near” about drowning. It happened or it didn’t. Drowning is: “the process of experiencing respiratory impairment due to submersion or immersion in liquid.”   Drowning has three outcomes. This is a uniform way of reporting data after a drowning event is using the Utstein template: 1) Morbidity 2) No morbidity 3) Mortality Submersion or immersion incident without evidence of respiratory impairment is considered a water rescue and not a drowning.  Pathophysiology  A person holds their breath until water enters the mouth. This water is voluntarily spat out or swallowed. The next conscious response is breath holding which lasts around one minute. The inspiratory drive becomes to strong and some water is aspirated into the airways (reflexive swallowing). Laryngospasm occurs, but is rapidly terminated by the onset of brain hypoxia. Aspiration continues, and hypoxemia leads to the loss of consciousness and apnea. The initial cardiac rhythm is tachycardia, then bradycardia, then asystole.  - Adapted from Szpilman et. al.  On average, less than 30 mL of fluid or NO fluid enters the lungs.   Clinical presentation  Water washes out surfactant = frothy pulmonary edema Cellular Injury – alveolar collapse leads to atelectasis Hypoxic vasoconstriction due to V/Q mismatch Bronchospasm Inflamation  The main problem is NO OXYGEN TO THE BRAIN. This is a hypoxic cardiac arrest and should be treated as such.   In-water Rescue (If properly trained) “Reach, Throw, Row, Don’t GO” – Don’t become a victim If properly trained, and the patient HAS A PULSE, mouth to mouth resuscitation can result and a 3 times greater likelihood of surviving as compared with taking the person first to land.  CPR will be ineffective  Cervical Spine Immobilization  Incidence of cervical spine injuries is 0.5%-5% Without obvious signs of trauma or a known fall or diving event, routine cervical spine immobilization is unnecessary and can delay providing oxygen to the brain. If the patient is awake, follow standard spinal clearance algorithms.  Land Resuscitation  Airway, Airway, Airway   Start with basics: Mouth to mouth, mouth to mask, BVM, Etc. Delay placing an advanced airway – restoring oxygenation is more important. Cardiac arrest in drowning is due to hypoxia. There is no place for “hands only CPR” CPR only will only circulate blood with a severe oxygen debt that won’t be restored without positive pressure ventilation. Beware of Acute Pulmonary Edema  Water + Soap = Foam. Possibly lots of it. You don’t need to suction unless vomit or frank water is present. Suctioning foam will keep coming. Bag it down. Use PEEP  The Heimlich maneuver No. Little water is aspirated into the lungs, and it only delays the administration of oxygen.  If patient is awake and/or has a pulse and is intubated CPAP if not at risk for vomiting If managed via an advanced airway, use an ARDS approach  Low tidal volumes: 6-8 cc/kg of ideal body weight Respiratory rate to maintain eucapnea: 16-18 Increase PEEP and FiO2 in tandem to achieve and adequate SpO2   Who should be resuscitated?  Per WMS Practice Guidelines: “Minimal chance of neurologically intact survival with submersion time greater than 30 minutes in water greater than 43 degrees F.” “Minimal chance of Minimal chance of neurologically intact survival with submersion time greater than 90 minutes in water less than 43 degrees F.”   When should resuscitative efforts cease?  WMS Recommendation: After 25 minutes continuous CPR  What about cold water drowning? A Dutch prospective of children who drowned in cold water showed that no child in asystole, who was resuscitated for more than 30 min survived without being neurologically devastated. Another large study conducted by Quan et. al. involving adults who drowned in cold or very cold waters showed that of 1094 victims, the majority had bad outcomes. Those with good outcomes were likely to be submerged for less than 11 minutes. Brown et. al found that there is a neuroprotective effect in avalanche victims, but not in those who asphyxiated first, then became hypothermic. The mantra “they’re not dead until they’re warm and dead” appears to be overhyped, and more and more data suggests there’s not as much of a neuroprotective effect of cold water drowning as once thought, and that mantra is probably only applicable to the patient who becomes hypothermic before going into cardiac arrest or becoming hypoxic.  Disposition of an awake patient Most patients who experienced a drowning incident requiring the need for EMS to be contacted should be transported for evaluation. Depending on where you practice, you may have to make a mission critical decision of whether or not to evacuate or continue with close monitoring of the patient.  Statistically, a person without a severe cough, frothy sputum or a foamy airway, and a normal cardiac examination has a mortality rate of 0%.  The more severe the symptoms, the higher the mortality:  

Terminology Wet, dry, or near drowning are not medically accepted terms and should not be used. There is nothing “near” about drowning. It happened or it didn’t. Drowning is: “the process of experiencing respiratory impairment due to submersion or immersion in liquid.” Drowning has three outcomes. This is a uniform way of reporting data after a drowning event is using the Utstein template: 1) Morbidity 2) No morbidity 3) Mortality Submersion or immersion incident without evidence of respiratory impairment is considered a water rescue and not a drowning. Pathophysiology <ol> <li>A person holds their breath until water enters the mouth.</li> <li>This water is voluntarily spat out or swallowed.</li> <li>The next conscious response is breath holding which lasts around one minute.</li> <li>The inspiratory drive becomes to strong and some water is aspirated into the airways (reflexive swallowing).</li> <li>Laryngospasm occurs, but is rapidly terminated by the onset of brain hypoxia.</li> <li>Aspiration continues, and hypoxemia leads to the loss of consciousness and apnea.</li> <li>The initial cardiac rhythm is tachycardia, then bradycardia, then asystole.</li> </ol> - Adapted from Szpilman et. al.  On average, less than 30 mL of fluid or NO fluid enters the lungs.  Clinical presentation <ol> <li>Water washes out surfactant = frothy pulmonary edema</li> <li>Cellular Injury – alveolar collapse leads to atelectasis</li> <li>Hypoxic vasoconstriction due to V/Q mismatch</li> <li>Bronchospasm</li> <li>Inflamation</li> </ol> The main problem is NO OXYGEN TO THE BRAIN. This is a hypoxic cardiac arrest and should be treated as such.  In-water Rescue (If properly trained) “Reach, Throw, Row, Don’t GO” – Don’t become a victim If properly trained, and the patient HAS A PULSE, mouth to mouth resuscitation can result and a 3 times greater likelihood of surviving as compared with taking the person first to land.  CPR will be ineffective Cervical Spine Immobilization  Incidence of cervical spine injuries is 0.5%-5% Without obvious signs of trauma or a known fall or diving event, routine cervical spine immobilization is unnecessary and can delay providing oxygen to the brain. If the patient is awake, follow standard spinal clearance algorithms. Land Resuscitation  Airway, Airway, Airway  Start with basics: Mouth to mouth, mouth to mask, BVM, Etc. Delay placing an advanced airway – restoring oxygenation is more important. Cardiac arrest in drowning is due to hypoxia. There is no place for “hands only CPR” CPR only will only circulate blood with a severe oxygen debt that won’t be restored without positive pressure ventilation. Beware of Acute Pulmonary Edema  Water + Soap = Foam. Possibly lots of it. You don’t need to suction unless vomit or frank water is present. Suctioning foam will keep coming. Bag it down. Use PEEP The Heimlich maneuver No. Little water is aspirated into the lungs, and it only delays the administration of oxygen. If patient is awake and/or has a pulse and is intubated CPAP if not at risk for vomiting If managed via an advanced airway, use an ARDS approach <ul> <li>Low tidal volumes: 6-8 cc/kg of ideal body weight</li> <li>Respiratory rate to maintain eucapnea: 16-18</li> <li>Increase PEEP and FiO2 in tandem to achieve and adequate SpO2</li> </ul> Who should be resuscitated?  Per WMS Practice Guidelines: “Minimal chance of neurologically intact survival with submersion time greater than 30 minutes in water greater than 43 degrees F.” “Minimal chance of Minimal chance of neurologically intact survival with submersion time greater than 90 minutes in water less than 43 degrees F.” When should resuscitative efforts cease?  WMS Recommendation: After 25 minutes continuous CPR What about cold water drowning? A Dutch prospective of children who drowned in cold water showed that no child in asystole, who was resuscitated for more than 30 min survived without being neurologically devastated. Another large study conducted by Quan et. al. involving adults who drowned in cold or very cold waters showed that of 1094 victims, the majority had bad outcomes. Those with good outcomes were likely to be submerged for less than 11 minutes. Brown et. al found that there is a neuroprotective effect in avalanche victims, but not in those who asphyxiated first, then became hypothermic. The mantra “they’re not dead until they’re warm and dead” appears to be overhyped, and more and more data suggests there’s not as much of a neuroprotective effect of cold water drowning as once thought, and that mantra is probably only applicable to the patient who becomes hypothermic before going into cardiac arrest or becoming hypoxic. Disposition of an awake patient Most patients who experienced a drowning incident requiring the need for EMS to be contacted should be transported for evaluation. Depending on where you practice, you may have to make a mission critical decision of whether or not to evacuate or continue with close monitoring of the patient.  Statistically, a person without a severe cough, frothy sputum or a foamy airway, and a normal cardiac examination has a mortality rate of 0%.  The more severe the symptoms, the higher the mortality:

Drowning

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Curbside to Bedside

Patients DO NOT have to present with integumentary involvement to be in anaphylaxis - up to 20% of patients experiencing anaphylaxis will have absent or unrecognized skin signs. Patients DO NOT have to exhibit hypotension to diagnose ongoing anaphylaxis. Anaphylaxis is unpredictable in time to onset, and the severity of presenting signs and symptoms exist on a spectrum. Stay ahead of the curve and give epi early.  World Allergy Organization's Clinical Criteria for Anaphylaxis [1]:  Anaphylaxis is highly likely when any one of the following three criteria is fulfilled: 1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized urticaria, itching or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING:  Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) Reduced blood pressure or associated symptoms of end-organ dysfunction (eg. hypotonia collapse, syncope, incontinence)  2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours):  Involvement of the skin-mucosal tissue (eg, generalized urticaria, itch-flush, swollen lips-tongue-uvula) Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) Reduced blood pressure or associated symptoms (eg, hypotonia collapse, syncope, incontinence) Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting)  3. Reduced blood pressure after exposure to known allergen for that patient (minutes to several hours):  Infants and children: low systolic blood pressure (age-specific) or greater than 30% decrease in systolic blood pressure. Adults: systolic blood pressure of less than 90 mm Hg or greater than 30% decrease from that person’s baseline.  1st Line:  IM Epi -&gt; IV Fluids -&gt; IV epi PRN. IM epi should be administered in the lateral thigh If the patient is know to be on beta blockers, give glucagon 1mg IVP if available  2nd Line:  Inhaled beta agonists, antihistamines, and glucocorticoids.  Refractory anaphylaxis  Methylene Blue Transport to an ECMO-capable facility 

Patients DO NOT have to present with integumentary involvement to be in anaphylaxis - up to 20% of patients experiencing anaphylaxis will have absent or unrecognized skin signs. Patients DO NOT have to exhibit hypotension to diagnose ongoing anaphylaxis. Anaphylaxis is unpredictable in time to onset, and the severity of presenting signs and symptoms exist on a spectrum. Stay ahead of the curve and give epi early. World Allergy Organization's Clinical Criteria for Anaphylaxis [1]: Anaphylaxis is highly likely when any one of the following three criteria is fulfilled: 1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized urticaria, itching or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING: <ol> <li>Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)</li> <li>Reduced blood pressure or associated symptoms of end-organ dysfunction (eg. hypotonia collapse, syncope, incontinence)</li> </ol> 2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours): <ol> <li>Involvement of the skin-mucosal tissue (eg, generalized urticaria, itch-flush, swollen lips-tongue-uvula)</li> <li>Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)</li> <li>Reduced blood pressure or associated symptoms (eg, hypotonia collapse, syncope, incontinence)</li> <li>Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting)</li> </ol> 3. Reduced blood pressure after exposure to known allergen for that patient (minutes to several hours): <ol> <li>Infants and children: low systolic blood pressure (age-specific) or greater than 30% decrease in systolic blood pressure.</li> <li>Adults: systolic blood pressure of less than 90 mm Hg or greater than 30% decrease from that person’s baseline.</li> </ol> 1st Line: <ul> <li>IM Epi -&gt; IV Fluids -&gt; IV epi PRN.</li> <li>IM epi should be administered in the lateral thigh</li> <li>If the patient is know to be on beta blockers, give glucagon 1mg IVP if available</li> </ul> 2nd Line: <ul> <li>Inhaled beta agonists, antihistamines, and glucocorticoids.</li> </ul> Refractory anaphylaxis <ul> <li>Methylene Blue</li> <li>Transport to an ECMO-capable facility</li> </ul>

Anaphylaxis

For this episode, we bring in an expert and an esteemed guest to answer all of your burning questions about resuscitation of cardiac arrest. Part man, part mystery, but wholly dedicated to furthering excellence in out of hospital care: Dr. Walt Lubbers, MD. Some background: Walt is an Emergency and Prehospital Medicine physician who holds board certification in both EM and EMS. He's also an Assistant Professor of Emergency Medicine and Attending Physician at University of Kentucky Medical Center. If that wasn't enough, he's also the Medical Director of several EMS agencies throughout Central and Eastern Kentucky.

For this episode, we bring in an expert and an esteemed guest to answer all of your burning questions about resuscitation of cardiac arrest. Part man, part mystery, but wholly dedicated to furthering excellence in out of hospital care: Dr. Walt Lubbers, MD. Some background: Walt is an Emergency and Prehospital Medicine physician who holds board certification in both EM and EMS. He's also an Assistant Professor of Emergency Medicine and Attending Physician at University of Kentucky Medical Center. If that wasn't enough, he's also the Medical Director of several EMS agencies throughout Central and Eastern Kentucky.

Prehospital Cardiac Arrest with Walt Lubbers

Know what a normal LBBB “looks” like:  1) QRS duration greater than 120 ms 2) Negative QRS Complex in V1 3) Positive QRS Complex in lateral leads (I, aVL, V5-V6)  LBBB causes a repolarization abnormality:  Consider a “repol” abnormality when there is a “general pattern of ST discordance”, meaning the ST segment opposite the QRS in nearly every lead (can be caused by LVH, LBBB, WPW, etc.).  In a LBBB there is normally ST elevation in some leads at baseline. 2013 AHA STEMI Guidelines:  “New or presumably new LBBB has been considered a STEMI equivalent. Most cases of LBBB at time of presentation, however, are “not known to be old” because of prior electrocardiogram (ECG) is not available for comparison. New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation”.  New or presumed new LBBB does not predict an MI.  MI occurs at similar frequencies between patients with a new LBBB, an old LBBB, and patients without a LBBB.  Patients with a LBBB frequently have an unequivocal STEMI diagnosis go unrecognized because clinicians aren’t familiar with how to diagnose an MI in this setting.  Criteria for diagnosing STEMI in a LBBB  Standard Sgarbossa Criteria 1) ST-segment elevation ≥1 mm concordant with the QRS complex in any lead (5 points) 2) ST-segment depression ≥1 mm in lead V1, V2, or V3 (3 points) 3) ST-segment elevation ≥5 mm discordant with the QRS complex in any lead (2 points) Smith Modified Sgarbossa  ≥ 1 lead with ≥1 mm of concordant ST elevation ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave. 

Know what a normal LBBB “looks” like: 1) QRS duration greater than 120 ms 2) Negative QRS Complex in V1 3) Positive QRS Complex in lateral leads (I, aVL, V5-V6) LBBB causes a repolarization abnormality: Consider a “repol” abnormality when there is a “general pattern of ST discordance”, meaning the ST segment opposite the QRS in nearly every lead (can be caused by LVH, LBBB, WPW, etc.). In a LBBB there is normally ST elevation in some leads at baseline. 2013 AHA STEMI Guidelines: “New or presumably new LBBB has been considered a STEMI equivalent. Most cases of LBBB at time of presentation, however, are “not known to be old” because of prior electrocardiogram (ECG) is not available for comparison. New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation”. New or presumed new LBBB does not predict an MI. MI occurs at similar frequencies between patients with a new LBBB, an old LBBB, and patients without a LBBB. Patients with a LBBB frequently have an unequivocal STEMI diagnosis go unrecognized because clinicians aren’t familiar with how to diagnose an MI in this setting. Criteria for diagnosing STEMI in a LBBB Standard Sgarbossa Criteria 1) ST-segment elevation ≥1 mm concordant with the QRS complex in any lead (5 points) 2) ST-segment depression ≥1 mm in lead V1, V2, or V3 (3 points) 3) ST-segment elevation ≥5 mm discordant with the QRS complex in any lead (2 points) Smith Modified Sgarbossa <ul> <li>≥ 1 lead with ≥1 mm of concordant ST elevation</li> <li>≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression</li> <li>≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave.</li> </ul>

Diagnosing STEMI in Left Bundle Branch Block

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