CritMedic

We rejoin Brandon Oto and Tyler Christifulli for another episode of ICU Perspectives. We’ll talk about just what is stable enough for transport and many other patient care considerations. Be sure to check out Part 1 of the ICU Perspectives over at the Lifestar Podcast as well! Rapid-fire opinions on: How stable is stable enough for transfer? Sufficient Vascular Access Patient positioning (supine, head-up, prone) Tube securement Scenarios: Your approach if your patient suddenly develops… A-fib with RVR Agitation/vent dyssynchrony Hypoxia (on the vent) Hypotension Show Notes Tyler Christifulli – Lifestar EMS Podcast Brandon Oto – Critical Concepts Fuller, B. M., Ferguson, I. T., Mohr, N. M., Drewry, A. M., Palmer, C., Wessman, B. T., . . . Kollef, M. H. (2017). Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial. Annals of Emergency Medicine. doi:10.1016/j.annemergmed.2017.01.013 FlightBridgeED, LLC (2015). Prolonging LIFE! – Hypotensive Approach – High Vt Applicaiton & Discussion, YouTube.

Can you be allergic to work? In this episode, we’ll discuss the concept of Exercise Induced Anaphylaxis (EIA) and Food Dependent Exercise Induced Anaphylaxis (FDEIA).   Case Scenario: During a 5K race standby, you arrive to find a 24 YOF lying on the side of the track against a concrete barrier. She is conscious, but a little bit lethargic. She is complaining of a sudden onset difficulty breathing during the run that worsened. Now she feels like her throat is closing off and she feels like she can’t breathe. Only medical history is an amalgam based dental filling 2 months ago. Only medications include oral birth control pills and an NSAID last night and this morning due to some soreness from some pre-race workout and training. On physical exam, you note her skin is flush some itching. You hear expiratory wheezing on auscultation. Vital signs: Heart Rate – 137 Blood Pressure – 80/50 SpO2 – 90% She denies any allergies. Denies any new foods or medication. Last oral intake was corn on the cob at the pre-race BBQ along with chili (that’s chili WITH beans, for you Texans). No possibility of pregnancy — LMP is now. No new known exposures. No new clothing. No new laundry detergent. No insect bites or stings. In short, she’s had NO allergen exposure. What’s going on?   Show Notes Barg, W., Medrala, W., & Wolanczyk-Medrala, A. (2010). Exercise-Induced Anaphylaxis: An Update on Diagnosis and Treatment. Current Allergy and Asthma Reports, 11(1), 45-51. doi:10.1007/s11882-010-0150-y Pravettoni, V., & Incorvaia, C. (2016). Diagnosis of exercise-induced anaphylaxis: current insights. Journal of Asthma and Allergy, Volume 9, 191-198. doi:10.2147/jaa.s109105 Ansley, L., Bonini, M., Delgado, L., Giacco, S. D., Toit, G. D., Khaitov, M., . . . Robson-Ansley, P. J. (2015). Pathophysiological mechanisms of exercise-induced anaphylaxis: an EAACI position statement. Allergy, 70(10), 1212-1221. doi:10.1111/all.12677

What is a “Dry Land Drowning”? Acute Pulmonary Edema! We’ll cover the pathophysiology of pulmonary edema as well as the pulmonary lymphatic system. The focus of this podcast was originally primarily on high dose nitroglycerin administration as well as dissuade providers from using therapies known to significantly worsens outcomes.   High Dose Nitroglycerin Systolic BP > 120 mmHg – 1 tablet – 0.4 mg Systolic BP > 160 mmHg – 2 tablets – 0.8 mg Systolic BP > 200 mmHg – 3 tablets – 1.2 mg Repeat dosage every 5 minutes, titrated to current blood pressure.   Summary Nitroglycerin: Good High Dose Nitroglycerin: Best Late CPAP: Good Early CPAP: Best Furosemide: Bad Morphine: Bad   For a down to earth, simple, and visual presentation on Pulmonary Edema with renown Cardiologist, Dr. Amal Mattu, check out this video of his presentation at Resuscitation Conference in 2014…   Show Notes Featured Image Credit: Lars O., Flickr, Creative Commons Viau, D. M., Sala-Mercado, J. A., Spranger, M. D., O’leary, D. S., & Levy, P. D. (2015). The pathophysiology of hypertensive acute heart failure. Heart, 101(23), 1861-1867. doi:10.1136/heartjnl-2015-307461 Reeves JT, Linehan JH, Stenmark KR. Distensibility of the normal human lung circulation during exercise. Am J Physiol Lung Cell Mol Physiol. 2005;288(3):L419-25. Braunwald E, Kelly ER. The effects of exercise on central blood volume in man. J Clin Invest. 1960;39:413-9. Coates, G., O’Brodovich, H., Jefferies, A. L., & Gray, G. W. (1984). Effects of exercise on lung lymph flow in sheep and goats during normoxia and hypoxia. J Clin Invest, 74(1), 133-151. doi:10.1172/JCI111393 Gandhi, S. K., Powers, J. C., Nomeir, A., Fowle, K., Kitzman, D. W., Rankin, K. M., & Little, W. C. (2001). The Pathogenesis of Acute Pulmonary Edema Associated with Hypertension. New England Journal of Medicine, 344(1), 17-22. doi:10.1056/nejm200101043440103 Ford, L. E. (2010). Acute hypertensive pulmonary edema: a new paradigm. Canadian Journal of Physiology and Pharmacology, 88(1), 9-13. doi:10.1139/y09-113 Williams, T. A., Finn, J., Perkins, G. D., & Jacobs, I. G. (2013). Prehospital Continuous Positive Airway Pressure for Acute Respiratory Failure: A Systematic Review and Meta-Analysis. Prehospital Emergency Care, 17(2), 261-273. doi:10.3109/10903127.2012.749967 Plaisance, P., Pirracchio, R., Berton, C., Vicaut, E., & Payen, D. (2007). A randomized study of out-of-hospital continuous positive airway pressure for acute cardiogenic pulmonary oedema: physiological and clinical effects. European Heart Journal, 28(23), 2895-2901. doi:10.1093/eurheartj/ehm502 Weber, K. T. (2001). Aldosterone in Congestive Heart Failure. New England Journal of Medicine, 345(23), 1689-1697. doi:10.1056/nejmra000050 Andrew, P. (2002). Renin-Angiotensin-Aldosterone Activation in Heart Failure, Aldosterone Escape. Chest, 122(2), 755. doi:10.1378/chest.122.2.755 Haber, H, Simek, C, Bergin, JD. (1994) Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance. Journal of Cardiothoracic and Vascular Anesthesia, 8(1), 125. doi:10.1016/1053-0770(94)90028-0 Muirhead, G. (2008). Treat Acute Heart Failure With High-Dose Nitrates. American College of Emergency Physicians, Retrieved April 22, 2017. Cotter, G., Metzkor, E., Kaluski, E., Faigenberg, Z., Miller, R., Simovitz, A., . . . Golik, A. (1998). Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. The Lancet, 351(9100), 389-393. doi:10.1016/s0140-6736(97)08417-1 Guglina, M. E. (1997). [High-dose nitroglycerin in cardiogenic shock]. Klinicheskaia Meditsina, 75(6), 27-30. 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. doi:10.1016/j.annemergmed.2007.02.022 Lee, S. J., Sung, Y. K., & Zaragoza, A. J. (1970). Effects of nitroglycerin on left ventricular volumes and wall tension in patients with ischaemic heart disease. Heart, 32(6), 790-794. doi:10.1136/hrt.32.6.790 Wilson, S. S., Kwiatkowski, G. M., Millis, S. R., Purakal, J. D., Mahajan, A. P., & Levy, P. D. (2017). Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure. The American Journal of Emergency Medicine, 35(1), 126-131. doi:10.1016/j.ajem.2016.10.038 Clemency, B. M., Thompson, J. J., Tundo, G. N., & Lindstrom, H. A. (2013). Prehospital High-dose Sublingual Nitroglycerin Rarely Causes Hypotension. Prehospital and Disaster Medicine, 28(05), 477-481. doi:10.1017/s1049023x13008777 Noonan, P. K., & Benet, L. Z. (1985). Incomplete and delayed bioavailability of sublingual nitroglycerin. The American Journal of Cardiology, 55(1), 184-187. doi:10.1016/0002-9149(85)90325-x Feldman, R. L., Pepine, C. J., & Conti, C. R. (1981). Magnitude of dilatation of large and small coronary arteries of nitroglycerin. Circulation, 64(2), 324-333. doi:10.1161/01.cir.64.2.324 Bussmann, W. (1986). Acute and chronic heart failure: Diagnosis and therapy. Berlin: Springer-Verlag. Sharon, A., Shpirer, I., Kaluski, E., Moshkovitz, Y., Milovanov, O., Polak, R., . . . Cotter, G. (2000). High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. Journal of the American College of Cardiology, 36(3), 832-837. doi:10.1016/s0735-1097(00)00785-3 Furosemide in the Treatment of Acute Pulmonary Edema.Swaminathan, A. (2016, April 07). Retrieved April 22, 2017, emDocs.

You respond to the home of a 56 YOM for a 3rd party caller reporting their family member is confused. Upon arrival, you note that the patient has diabetic medications in the house as well as an IV pump with a medication you are not familiar with. Blood sugar on your glucometer is 148 mg/dl. You transport him to the hospital, where lab glucose determines that he is actually hypoglycemic. What happened? The patient was taking a medication called Extraneal, which contains Icodextrin and is used for peritoneal dialysis. This can affect certain types of glucometers, leading to false high readings. Do you know which type of glucometer you have? Find out here. Here are common types: Glucose Dehydrogenase Pyrroloquinoline Quinone (GDH-PQQ) Glucose Dehydrogenase Flavin-Adenine Dinucleotide (GDH-FAD) Glucose Dehydrogenase Nicotinamide-Adenine Dinucleotide (GDH-NAD) Show Notes FDA Public Health Notification: Potentially Fatal Errors with GDH-PQQ* Glucose Monitoring Technology. (2009, August 13). Retrieved January 10, 2017 de Lange, S., Fernández Cabrera, J., & Gomar Vidal, S. (2011). [Occult hypoglycemia in patient with chronic kidney failure and chronic ambulatory peritoneal dialysis]. Medicina intensiva, 2, 133–134. Floré, K. M., & Delanghe, J. R. (). Analytical interferences in point-of-care testing glucometers by icodextrin and its metabolites: an overview. Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis, 4, 377–383. Khouli, M. M. (2012). Masked hypoglycemia in the presence of icodextrin for peritoneal dialysis. The Journal of emergency medicine, 2, e191-3. Al-Dorzi, H. M., Al-Sum, H., Alqurashi, S., et al. (2011). Severe hypoglycemia in peritoneal dialysis patients due to overestimation of blood glucose by the point-of-care glucometer. Saudi journal of kidney diseases and transplantation, Saudi Arabia, 4, 764–768. Grassmann, A., Gioberge, S., Moeller, S., & Brown, G. (2005). ESRD patients in 2004: global overview of patient numbers, treatment modalities and associated trends. Nephrology, dialysis, transplantation, 12, 2587–2593.

Are we giving our patients a sweet chance at ROSC? Or consigning them to a sugary grave? We examine the evidence for and against Dextrose in Cardiac Arrest. Two renown EMS blogs, Rogue Medic and Mill Hill Avenue Command, have already covered the topic before. But let’s take a deeper look at the evidence for and against Dextrose as well as discuss the cardiac physiology pertaining to Glucose metabolism. We’ll also cover how patients who become hypoglycemic end up going into cardiac arrest in the first place and whether we can accurately detect hypoglycemia in cardiac arrest. Just like our Narcan podcast, we’re going to science and evidence the crap out of this one. Here’s a breakdown of the points in this podcast. Myocardial cells don’t use glucose as a primary source of fuel. As little as 4% of myocardial ATP is generated from glucose. Giving dextrose during periods of ischemia increases anaerobic metabolism, promotes the conversion of pyruvate into lactate, causes intracellular acidosis, and may decrease cerebral blood flow, exacerbating cerebral ischemic injury. We can’t accurately determine blood glucose in cardiac arrest using capillary blood glucose. Glucometry using a venous sample without a venous reagent strip is suspect and potentially inaccurate. The largest study to date (Peng, 2015) shows worse overall survival to discharge. The largest study to date (Peng, 2015) shows  worse neurologic outcome. The largest study to date (Peng, 2015) shows no association between dextrose administration and ROSC when propensity-matched analysis was used. Studies show even D5W can worsen outcomes in cardiac arrest. Here’s the total body of evidence for Dextrose in cardiac arrest resuscitation (click to enlarge)… The above data has been reproduced in accordance with the provisions of 17 U.S. Code § 107 “Fair Use” for the purposes of criticism, comment, and non-commercial educational purposes. Show Notes Featured Image by Alden Chadwick (Flickr, Creative Commons License) Atkin, S. H., Dasmahapatra, A., Jaker, M. A., Chorost, M. I., & Reddy, S. (1991). Fingerstick glucose determination in shock. Annals of internal medicine, 12, 1020–1024. Meaney, P. A., B. J. Bobrow, and M. E. Mancini, et al. “Cardiopulmonary Resuscitation Quality: Improving Cardiac Resuscitation Outcomes Both Inside And Outside The Hospital: A Consensus Statement From The American Heart Association”. Circulation 128.4 (2013): 417-435. Web. 10 July 2016. DOI: 10.1161/CIR.0b013e31829d8654 Boyd, R., Leigh, B., & Stuart, P. (2005). Capillary versus venous bedside blood glucose estimations. Emergency medicine journal : EMJ, 3, 177–179. Sylvain, H. F., Pokorny, M. E., English, S. M., Benson, N. H., Whitley, T. W., Ferenczy, C. J., & Harrison, J. G. (1995). Accuracy of fingerstick glucose values in shock patients. American journal of critical care : an official publication, American Association of Critical-Care Nurses, 1, 44–48. Thomas, S. H., Gough, J. E., Benson, N., Austin, P. E., & Stone, C. K. (1994). Accuracy of fingerstick glucose determination in patients receiving CPR.Southern medical journal, 11, 1072–1075. Kobayashi, K., & Neely, J. R. (1979). Control of maximum rates of glycolysis in rat cardiac muscle. Circulation research, 2, 166–175 Holmes, D. R. (2007). Cardiovascular medicine (Third ed.). United Kingdom: Springer-Verlag New York. Sperelakis, N. (Ed.). (2011). Physiology and Pathophysiology of the heart. United States: Springer-Verlag New York. Drake, K. J., Sidorov, V. Y., McGuinness, O. P., Wasserman, D. H., & Wikswo, J. P. (2012). Amino acids as metabolic substrates during cardiac ischemia. Experimental Biology and Medicine, 237(12), 1369–1378. doi:10.1258/ebm.2012.012025 Kammermeier, H., & Giesen, J. (1980). States of myocardial metabolism related to ischemia. Clinical Cardiology, 3(3), 197–199. doi:10.1002/clc.4960030308 Weiss, R., & Maslov, M. (2004). Normal Myocardial Metabolism: Fueling Cardiac Contraction. Advanced Studies in Medicine, 4(6B), S457–S463. Peng, T. J., Andersen, L. W., Saindon, B. Z., Giberson, T. A., Kim, W. Y., Berg, K., Novack, V., Donnino, M. W., & , . (2015). The administration of dextrose during in-hospital cardiac arrest is associated with increased mortality and neurologic morbidity. Critical care (London, England), , 160. Anderson, R. V., Siegman, M. G., Balaban, R. S., Ceckler, T. L., & Swain, J. A. (1992). Hyperglycemia increases cerebral intracellular acidosis during circulatory arrest. The Annals of thoracic surgery, 6, 1126–1130. Rehncrona S, Rosén I, Siesjö BK. (1981). Brain lactic acidosis and ischemic cell damage. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 3, 297–311. D’Alecy, L. G., Lundy, E. F., Barton, K. J., & Zelenock, G. B. (1986). Dextrose containing intravenous fluid impairs outcome and increases death after eight minutes of cardiac arrest and resuscitation in dogs. Surgery, 3, 505–511. Browning, R. G., Olson, D. W., Stueven, H. A., & Mateer, J. R. (1990). 50% dextrose: antidote or toxin? Annals of emergency medicine, 6, 683–687. Wass, C. T., & Lanier, W. L. (1996). Glucose modulation of ischemic brain injury: review and clinical recommendations. Mayo Clinic proceedings, 8, 801–812. Müllner, M., Sterz, F., Binder, M., Schreiber, W., Deimel, A., & Laggner, A. N. (1997). Blood glucose concentration after cardiopulmonary resuscitation influences functional neurological recovery in human cardiac arrest survivors. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 4, 430–436. Nakakimura, K., Fleischer, J. E., Drummond, J. C., Scheller, M. S., Zornow, M. H., Grafe, M. R., & Shapiro, H. M. (1990). Glucose administration before cardiac arrest worsens neurologic outcome in cats. Anesthesiology, 6, 1005–1011. American Heart Association. (2015). Part 12: Pediatric advanced life support – ECC guidelines 2015. Retrieved July 10, 2016. Losek, J. D. (2000). Hypoglycemia and the ABC’S (sugar) of pediatric resuscitation. Annals of emergency medicine, 1, 43–46. Chopra, S., & Kewal, A. (2012). Does hypoglycemia cause cardiovascular events? Indian Journal of Endocrinology and Metabolism, 16(1), 102. doi:10.4103/2230-8210.91203 Tattersall, R. B., & Gill, G. V. (1991). Unexplained deaths of type 1 diabetic patients. Diabetic medicine : a journal of the British Diabetic Association, 1,49–58. Beiser, D. G., Carr, G. E., Edelson, D. P., Peberdy, M. A., & Hoek, T. L. V. (2009). Derangements in blood glucose following initial resuscitation from in-hospital cardiac arrest: A report from the national registry of cardiopulmonary resuscitation. Resuscitation, 80(6), 624–630. doi:10.1016/j.resuscitation.2009.02.011 Longstreth, W. T., Diehr, P., Cobb, L. A., Hanson, R. W., & Blair, A. D. (1986). Neurologic outcome and blood glucose levels during out-of-hospital cardiopulmonary resuscitation. Neurology, 9, 1186–1191. Nolan, J. P., Neumar, R. W., Adrie, C., Aibiki, M., Berg, R. A., Böttiger, B. W., … Hoek, T. V. (2008). Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication. Resuscitation, 79(3), 350–379. doi:10.1016/j.resuscitation.2008.09.017 Walsh, B. (2012, March 14). Using Dextrose in Cardiac Arrest. Retrieved July 10, 2016, from Mill Hill Ave Command. Noonan, T. (2015, March 12). Dextrose in cardiac arrest – more kitchen sink medicine. Retrieved July 10, 2016, from Rogue Medic.

You respond to a rural ED for a 1 hour transfer to a tertiary facility MICU for higher level of care. Patient is a 44 YOF (5’5″, 100 kg ABW) with a history of IDDM with a current diagnosis of DKA. Laboratory blood glucose at 940 mg/dl (68.6 gr/pt). Patient’s GCS is 2/2/4. She is breathing 30 – 40 per minute and saturating 88% on a NRB. She has an 18 gauge IV in the Right AC and received 1000 ml of saline. She is being transferred with insulin running at 12 units/hr. She has vomited x4 since being admitted to the ED. Vitals and labs are as follows: BP – 94/40 HR – 118 bpm RR – 30 – 40 bpm SpO2 – 88% on 15 LPM GCS – 8 EKG – Sinus Tachycardia pH 7.06, PaCO2 25, PaO2 53, HCO3 11 RBC 7, HGB 21, HCT 63, WBC 10,000, Plt 350,000 Na 114, Cl 106 K 2.3, BGL 940, BUN 26, Cr 2 Medications: Paxil, Lantus, Humalog, Prolixin, Zyprexa, Lyrica, Hydrocodone History: Depression, Schizophrenia, Bipolar, Fibromyalgia, IDDM Allergies: Haldol, NSAIDs, Sulfa, PCN How do you manage this patient? In this episode we discuss: SBP vs MAP Compensatory Respiratory Alkalosis Hyperglycemia / DKA Effect of Glucose on Sodium Values Hypokalemia Effects of Insulin on Potassium Dangers of Intubation / RSI Ventilator settings Smothering patients with pillows   Show Notes Vucicevic, Z., Degoricija, V., Alfirevic, Z., & Vukicevic-Badouin, D. (2007). Fatal hyponatremia and other metabolic disturbances associated with psychotropic drug polypharmacy. International journal of clinical pharmacology and therapeutics, 5, 289–292. Westerberg, D. P. (2013). Diabetic ketoacidosis: evaluation and treatment. American family physician, 5, 337–346. Bauer, E. R. (2015). Ventilator management: A Pre-Hospital perspective.

Does Naloxone save lives? Does it help in cardiac arrest? Prehospital use of Naloxone is surrounded by misinformation. This week, we examine the history behind Naloxone as well as how it can provide benefit. One of the most common misconceptions is the Naloxone has some benefit in cardiac arrest. It does not. The Rogue Medic did an excellent write up of Naloxone in his blog (see Show Notes) years before, but it has not killed the mythos of Naloxone in cardiac arrest. My hope is that this episode may be enlightening to a few providers, who can then share the knowledge with their peers. But first, let’s put to rest the misconception of evidence for Naloxone in cardiac arrest. Many “Naloxone Apologists” will cite Saybolt, et al. as evidence of benefit, but fail to actually dig through the data. When we read through the “evidence” supplied in the study, it does not paint a picture that anyone could logically construe as providing benefit. But don’t take my word for it, here’s the very data from the study. Age & Gender Recorded response time Narrative Outcome 73 YOF Asystole?ventricular fibrillation4 min. Found in asystole. Over 22 min received epinephrine 3× and atropine 3× without effect. Subsequently administered naloxone 2 mg followed by epinephrine 1×. Pronounced in ED 49 YOF PEA?sinus tachycardia1 min. Found in asystole. Over 16 min received epinephrine 1× and atropine 1×. Rhythm changed to PEA (rate unknown). Naloxone 2 mg administered, rhythm changed to sinus tachycardia (118 bpm) Died in Hospital, Day 2. 37 YOM Asystole?accelerated junctional rhythm1 min. Found in asystole. Received epinephrine 2× and atropine 2× over 8 min. Naloxone 2 mg administered followed immediately by epinephrine at which point EKG converted to accelerated junctional rhythm (60 bpm). Pronounced in ED 24 YOM Asystole?PEA4 min. Found in ventricular fibrillation. Defibrillated at 200 J and converted to asystole. Administered epinephrine and atropine without rhythm change. Naloxone 2 mg administered, rhythm changed to PEA (rate unknown). Pronounced in ED 62 YOM PEA?ventricular fibrillation6 min. Found in PEA (rate 40 s). Over 6 min, received epinephrine 1× and atropine 1×. Remained in PEA (rate 90). Received naloxone 2 mg and epinephrine 1× and rhythm change to ventricular fibrillation. Died in Hospital, Day 1. 47 YOF Asystole?PEA3 min. Arrest witnessed by BLS with

In light of surging air medical demand, Dr. Bryan Bledsoe joins us for a discussion on whether HEMS is actually beneficial — and, if so, under what set of circumstances. As informed providers, we owe a duty to our patients not to unnecessarily straddle them with crippling debt and higher risk mode of transport if there is no justifiable benefit. What benefit does rotor wing air medical have? Speed: For transport distances of over 45 – 60 miles, HEMS is typically faster than ground transport. But this is only beneficial in patients who have a time sensitive emergency — STEMI, CVA within window, Penetrating Trauma, Severely Injured Trauma Patients. Advanced Medical Care: When patients need a higher level of care and treatment than is available on by ground EMS — ventilators, RSI, fibrinolytics, antibiotics, additional medications. Difficult to reach patients: HEMS is beneficial in extracting patients from difficult areas to reach or traverse by ground providers — gorges, large parks, isolated locations, natural disasters, inaccessibility due to construction or traffic. In this podcast, Dr. Bledsoe also tackles several myths associated with HEMS usage, including: HEMS is always faster the ground EMS. Time saved going by HEMS always benefits patient care. If we don’t support HEMS with business when we don’t need them, they won’t be around when we do need them. Critical care or advanced paramedic care is only available on HEMS. We should send patients who don’t need it by HEMS to save rural resources. HEMS transports are always smoother and more gentle than ground. I have been accused by some, over the years, of being “anti-HEMS”. That is not the case. As a certified Flight Paramedic with friends working for various flight services, I fully support air medical and view it as an invaluable resource in times of need. I am against excessive overutilization that saddles patients with unnecessary bills and exposes our peers to additional and needless risk.   Show Notes Guest material by Dr. Bryan Bledsoe. Bledsoe, B. E., Wesley, A. K., Eckstein, M., Dunn, T. M., & O’Keefe, M. F. (2006). Helicopter scene transport of trauma patients with nonlife-threatening injuries: a meta-analysis. The Journal of trauma, 6, 1257-65; discussion 1265-6. Diaz, M. A., Hendey, G. W., & Bivins, H. G. (2005). When is the helicopter faster? A comparison of helicopter and ground ambulance transport times. The Journal of trauma, 1, 148–153. Murphy, B. (2008, June 15). Crash rate raises med copter safety fears. Retrieved May 29, 2016

Are we a danger to our patients and partners? Are we too tired to care? This week, we discuss the ins and outs of fatigue and the effects it can have on us and our patients. We’ll draw on lessons learned from another mission critical profession where lives are in the balance. No matter how experienced or new the provider — no matter how highly trained — fatigue can effect ALL of us. We need knowledgeable people to take charge of the problem and help mitigate the risks — both from an individual standpoint and that of an agency.     Does your service have fatigue guidelines?   Mandatory Overtime Some EMS services (mine included) are using what’s called “Mandatory Overtime” to fill scheduling vacancies. This means that an EMT or Paramedic is called and told they MUST show up for work at a certain time and place of the company’s choosing IN ADDITION to the regularly scheduled work. For instance, my personal schedule is a permanent 52 hour week — equivalent to working 9 – 5 Monday to Friday, 9 – 5 on Saturday, and 9-1 on Sunday. My company then tells me I have to come in for 6 – 12 more hours on a day of their choosing or face employment consequences. EMTs and Paramedics work in a high stress, high risk field where the decisions and judgements they make can make an impact on the survival of the most acutely ill patients in our community. We work in often austere conditions with little direct supervision. Forcing those providers to work additional hours beyond what they feel they are capable of jeopardizes public health in by increasing the likelihood of committing a serious error. Furthermore, as EMS personnel have the responsibility to driving an emergency vehicle in hazardous conditions and an in a manner that does pose a measure of risk to the motorist public at large. We are expected to use due regard. And if we are fatigued due to overwork from involuntary mandatory overtime, our judgement may be impaired leading to a greater risk of accident. EMS providers also have above average divorce rates and above average rates of depression and suicide (see the Code Green Campaign). Mandatory overtime deprives hardworking emergency service providers of the little amount of time they get spend with their families. Coupled with the effects of fatigue induced depression and other deleterious mental health impacts, Mandatory Overtime has the potential to disrupt the family structure of our first responders.   >>> Sign The Petition <<< Providers in New York State are starting a push with the State Senators to end this practice. Nurses already have similar protections enacted that prohibit mandatory overtime except in the event of disasters. It’s time New York’s EMS personnel have the same protection. Nothing about this prohibits voluntary overtime — just mandatory overtime against the provider’s judgement and choice. If you’re in New York, please sign the petition!   Change.org Petition: Limitation on mandatory overtime for EMS providers Show Notes Dr. Samuel Strauss, Pilot Fatigue (LinkedIn). Watt, C. G., Lt. Col., USAF. (2009). Aircrew Fatigue Management (Unpublished dissertation). Air War College, Air War University. Retrieved May 22, 2016. Tittelbach, A. (2012). Barometer on Pilot Fatigue [Trade Publication]. Brussels: European Cockpit Association. Goode, J. H. (2003). Are pilots at risk of accidents due to fatigue? Journal of safety research, 3, 309–313. Powell DMC, Spencer MB, Petrie KJ. Fatigue in airline pilots after an additional day’s layover period. Aviat Space Environ Med 2010; 81:1-5 Folkard, S., & Tucker, P. (2003). Shift work, safety and productivity.Occupational medicine (Oxford, England), 2, 95–9101. Gundel, A., Drescher, J., Maas, H., Samel, A., & Vejvoda, M. (1995). Sleepiness of civil airline pilots during two consecutive night flights of extended duration. Biological psychology, 1-2, 131–141. Spencer MB, Robertson KA. 2005. Aircrew fatigue: A review of research undertaken on behalf of the UK Civil Aviation Authority. UK CAA Paper 2005/04 Belenky, G., Wesensten, N. J., Thorne, D. R., Thomas, M. L., Sing, H. C., Redmond, D. P., Russo, M. B., & Balkin, T. J. (2003). Patterns of performance degradation and restoration during sleep restriction and subsequent recovery: a sleep dose-response study. Journal of sleep research, 1, 1–12. Comperatore, C. A., Caldwell, J. A., & Caldwell, J. L. (1997). Leader’s Guide to Crew Endurance. Department of Defense. US Army Aeromedical Research Laboratory NYS Department of Labor. Mandatory Overtime for Nurses. Retrieved May 22, 2016.

Paramedic and Attorney Wes Ogilvie discusses what we DIDN’T learn on law in EMS education. Most providers are concerned about being sued. But a lawsuit wouldn’t cost you your certification and livelihood. It’s administrative law that has the power to strip providers of their certification — and providers must be aware of this field of law. Wes also discusses some misconceptions EMS providers have about the law as well as points out some of the most egregious EMS legal situations. Show Notes Guest Presentation by Wes Ogilvie The Ambulance Chaser – Wes Ogilvie’s Blog

Needle chest decompression has long been the standard of prehospital care. But what if we can do better? Klint Kloepping, Flight Paramedic from Nebraska, joins us for a discussion on finger thoracostomy. For those not familiar, a finger thoracostomy is performed by taking a scalpel to the tissues at the 5th rib at the midaxillary and bluntly dissecting down to the pleural space with a finger or, sometimes, a pair of hemostats or clamps. The issues surrounding standard needle thoracostomy for decompression and several fold. Many agencies do not have a special, dedicated extra-length angiocatheter for needle decompression. In a study the standard 4.6 cm angiocatheter was found to be long enough to reach the pleural space in only 52.7% of patients when done at the 2nd intercostal space, midclavicular line. In some cases, this location has also been shown to result in life threatening hemorrhage from lacerating the subclavian vessels, internal mammary artery and its medial branches. You know what really helps your patient with a life threatening pneumothorax? An iatrogenic life threatening hemothorax on top of it. The lateral or midaxillary position is not free from risk an adverse effects either. Using a proper 8 cm chest decompression needle (such as the Cook Pneumothorax Kit), providers have a significantly increased the risk of damaging the left ventricle, when using a left midaxillary approach. When you look at it, it’s a wonder that we considered plunging a long needle into the chest without knowing the underlying anatomy a good idea at all. Show Notes Guest discussion with Klint Kloepping FlightBridgeED Second Shift Podcast EMCrit: Podcast 62 – Needle vs. Knife II: Needle Thoracostomy? Carter TE, et al. Needle Decompression in Appalachia Do Obese Patients Need Longer Needles? West J Emerg Med, 2013; 14(6): 650–2. Ferrie EP, Collum N, McGovern S. The right place in the right space? Awareness of site for needle thoracocentesis. Emerg Med J, 2005 Nov; 22(11): 788–9. Rawlins R, et al. Life threatening haemorrhage after anterior needle aspiration of pneumothoraces. A role for lateral needle aspiration in emergency decompression of spontaneous pneumothorax. Emerg Med J, 2003 Jul; 20(4): 383–4.

Paramedic Point-Of-Care ultrasound (POCUS) is one of the few technologies on the horizon that promises to revolutionize prehospital care. Yet many people don’t see the advantages this technology presents. In this week’s special video podcast, Peter Bonadonna presents all the useful applications of point-of-care ultrasound and its advantages. If you’re a skeptic or non-believer, this video is especially for you. Ultrasound can diagnose: Abdominal Bleeding Pneumothorax Hemothorax Pericardial Effusion Cardiac Tamponade Pulmonary Embolus Heart Failure Pulmonary Edema Hypovolemia Liver Cirrhosis Gall Stones Neurogenic Bladder Hydronephrosis Ectopic Pregnancy Fetal Position Fetal Heartbeat Hyperthyroid / Thyroid Storm Carotid Plaque Carotid Stenosis Bone Fractures Intracranial Hemorrhage Retinal Detachment Increased Intracranial Pressure Cellulitis Gas Gangrene True PEA Death Myocardial Infarction Endotracheal Tube Placement (before a breath is even given) Abdominal Aortic Aneurysm Aortic Dissection Ludwig’s Angina Mean Arterial Pressure in VAD patients And more… The applications of EMS POCUS (Point Of Care Ultrasound) are limited only by provider imagination! With far more applications than a 12-lead and better diagnostic accuracy that physical exam alone – sometimes better than X-ray… why aren’t more of us excited for this technology? This technology is the linchpin of all future advances in medicine. Pericardiocentesis or drain? Guided Nerve Block? Central Lines? Chest tube? Resuscitative ECMO? You’ll never see those advances without the prior implementation of and proficiency in Ultrasound. So let’s get started! Additional Resources Paramedic Ultrasound EMS and Sonosite Ultrasound Show Notes Video Podcast material by Peter Bonadonna

We tackle the recently released Amiodarone, Lidocaine, or Placebo study. The study attempts to answer the question of which medication, if any, is better in out-of-hospital cardiac arrest with shock refractory VF or VT. Amiodarone and Lidocaine have been a core tenant of ACLS for quite some time. But do they actually work? Well, the evidence seems to say no. Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia. The details of the data are somewhat interesting. When you break down the data to various subgroups, you actually see where the Amiodarone and Lidocaine actually fair somewhat well. Does this mean we should start looking at our cardiac arrests a little differently? Show Notes Featured image copyright of Dom Pates (Flickr) Kudenchuk, P. J., Brown, S. P., Daya, M., …., (2016). Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. The New England journal of medicine. Antiarrhythmic drugs found beneficial when used by EMS treating cardiac arrest. National Heart, Lung, and Blood Institute, Retrieved from web 4/4/2016. Hagihara, A., Hasegawa, M., Abe, T., Nagata, T., Wakata, Y., & Miyazaki, S. (2012). Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA, 11, 1161–1168. PARAMEDIC2 Trial

I had the privilege of joining Kelly Grayson and Chris Cebollero on the Inside EMS podcast on EMS1 for a debate on the utility of EMS POCUS – Point Of Care Ultrasound. I enjoyed discussing ultrasound with them, though we only touched the tip of the iceberg. On April 17th, we will have our own CritMedic Ultrasound feature! In the meanwhile, here’s a quick list of what EMS POCUS can tell us: Abdominal bleeding Thoracic bleeding Aortic Aneurysm Aortic Dissection Myocardial Infarction Pericardial Effusion / Cardiac Tamponade Ejection Fraction and Heart Failure Pulmonary Embolism Pneumothorax Differentiate COPD vs Pulmonary Edema Carotid Stenosis Intubation confirmation Retinal Detachment Intracranial hemorrhage Deep Vein Thrombosis Kidney perfusion Hydration status Fetal position during labor Ectopic Pregnancy Urinary Retention Cholelithiasis Bone fractures Peripheral Bloodflow Thyroid Storm … and more! Show Notes It should be plainly obvious that this is not my Podcast. The Inside EMS Podcast is copyright EMS1. Inside EMS Podcast: Is prehospital ultrasound the next big thing in EMS care?

In recognition of International Transgender Day of Visibility (March 31st), we have Tyger Marie Gearheart on as a special guest to talk about gender identity and some of the specific health concerns in transgendered patients. Remember: No matter your personal feelings on the issues of gender identity, transsexuality, or sexual orientation, we owe a duty to our patients to provide them with compassionate care in a non-judgemental fashion. Show Notes World Professional Association for Transgender Health

The venerable non-rebreather mask has long been considered the gold standard for high flow oxygen delivery. But is that reputation deserved? We’ll discuss the science and benefits of the lowly nasal cannula and how it can help us oxygenate even apneic patients. Next time you see someone putting on a nasal cannula to a patient in respiratory arrest, they might not be crazy — they may just be practicing NODESAT and apneic oxygenation. We’ll also cover other tips and tricks, such as positioning, use of airway adjuncts, and the “Two Thumbs Down” mask seal technique. Why should we do 15-liters by nasal cannula? Evidence shows that it maintains or improves oxygen saturation, even in patients who are entirely apneic. How quickly do patients desaturate without supplemental oxygen during intubation? Too fast. Show Notes EMCrit – The Laryngoscope as a Murder Weapon Series *** RECOMMENDED *** EMCrit – A Primer on BVM Ventilation with Dr. Strayer *** RECOMMENDED *** EMCrit – Preoxygenation, Reoxygenation, and Deoxygenation Weingart, S. D., & Levitan, R. M. (2011). Preoxygenation and prevention of desaturation during emergency airway management. Annals of emergency medicine, 3, 165-75.e1. FRUMIN, M. J., EPSTEIN, R. M., & COHEN, G. (). Apneic oxygenation in man. Anesthesiology, , 789–798. Ramachandran, S. K., Cosnowski, A., Shanks, A., & Turner, C. R. (2010). Apneic oxygenation during prolonged laryngoscopy in obese patients: a randomized, controlled trial of nasal oxygen administration. Journal of clinical anesthesia, 3, 164–168.

“Learn why you’re doing what you’re doing.” Dr. Smertka rejoins us for some follow up questions and answers after last week’s show. Some of the questions answered this week are: Do you foresee any changes occurring with the definition of shock in the context of trauma? What are some common errors providers make when assessing GCS? Do you foresee any changes that could effect the benefit of ALS in trauma? What are your thoughts on TXA? Do you foresee a time, perhaps with Ultrasound, when patients bypass the ED for immediate surgery? Is there anything that EMS does that complicates or worsens your management of trauma patients? Is there anything that EMS does (or can do) that greatly improves patient outcomes? If you had to give EMS one bit of advice that you feel would save the most amount of lives, what would that be? Show Notes Podcast featured image copyright Paul Kehrer (Creative Commons)

Dr. Mike Smertka, M.D., Ph.D. joins us for a guest presentation on the outline of trauma care. He discusses how our initial care in the field impact the patient long after they’ve been moved to the Trauma ICU and addresses some myths and misinformation associated with trauma.   About Dr. Smertka Mike started off as a Paramedic in a fire-based EMS service, but has also worked third service, private, industrial, and as an ED tech in a major trauma facility prior to going to medical school. He’s treated patients and taught in 7 countries on 3 continents – in every environment from warzones to major urban trauma centers. He hopes to create his own surgical intensivist specialty that combines surgery, anesthesia, and emergency medicine.   Show Notes Podcast featured image copyright of Ben Grimmnitz (Creative Commons)

Whether you’re bringing a patient in that you intubated in the field or a critical transfer between hospitals, keeping your patient comfortable and sedate is not just a matter of being nice – it’s a matter of quality care that can impact patient outcomes. We discuss the “ICU Triad” of Pain, Agitation, and Delirium and how we can do our part to avoid it. Anyone can provide sedation and analgesia to the stable patient. But providing it to the critical, hypotensive patient is a delicate art. We discuss dosing concerns for hemodynamics and discuss ways we can still provide compassionate, quality care. Show Notes:

We’ve covered pain physiology. Now it’s time to get into the good stuff – what we can do to actually treat pain. In this episode, we talk about some of the common prehospital pain options as well as one that may be less common. Have you considered what medications you can use to improve your care alongside your standard pain management regimen? We also mention some cautions and pitfalls associated with the different medications as well. Acute pain protocol for moderate/severe pain by Ed Gentile, MD (Sourced from EMCrit, see link in Show Notes) Administer morphine 0.1 mg/kg IVP (If pt is > 55 y/o, substitute morphine 0.05 mg/kg IVP for this 1st dose) + diphenhydramine 0.5 mg/kg IVP 7 minutes later the patient is asked, “Would you like more pain medicine?” If the answer is yes, give a 2nd dose of morphine 0.05 mg/kg IVP 7 minutes later, the patient is asked again, “Would you like more pain medicine?” If the answer is yes, give a 3rd dose of morphine 0.05 mg/kg IVP This continues every 7 minutes until the patient answers “no” to the question or the patient is asleep. Show Notes: EMCrit Podcast 26 – Patient Controlled Analgesia by Edward Gentile *** RECOMMENDED *** International Narcotics Control Board – 2011 Report Blogspot – Opiophilia: How Heroin is Made O’Connor, A. B., Lang, V. J., & Quill, T. E. (2006). Underdosing of morphine in comparison with other parenteral opioids in an acute hospital: a quality of care challenge. Pain medicine (Malden, Mass.), 4, 299–307. Larijani, G. E., Goldberg, M. E., Gratz, I., & Warshal, D. P. (2004). Analgesic and hemodynamic effects of a single 7.5-mg intravenous dose of morphine in patients with moderate-to-severe postoperative pain. Pharmacotherapy, 12, 1675–1680. Aubrun, F., Mazoit, J. X., & Riou, B. (2012). Postoperative intravenous morphine titration. British Journal of Anaesthesia, 2, 193–201. Carr, K. D., Hiller, J. M., & Simon, E. J. (1985). Diphenhydramine potentiates narcotic but not endogenous opioid analgesia. Neuropeptides, 4-6, 411–414. Chang, A. K., Bijur, P. E., Holden, L., & Gallagher, E. J. (2015). Efficacy of an Acute Pain Titration Protocol Driven by Patient Response to a Simple Query: Do You Want More Pain Medication? Annals of emergency medicine, doi: 10.1016/j.annemergmed.2015.04.035 Strayer, R. (2015, December). Ketamine: How to use it fearlessly for all its indications. Retrieved from http://www.smacc.net.au/2015/12/ketamine-how-to-use-it-fearlessly-for-all-its-indications-by-reuben-strayer/