Critical Care

The Poor Man's Tox Screen: ECG Findings in the Acute Overdose

Case

In the middle of a busy ED shift the tech runs up to you with an ECG. Just prior to signing the top “No STEMI” you think: “wait, why do the QRS complexes look like that?”

Figure 1 EKG.png

You walk back to triage with the tech to see a 86 year old male patient who looks unwell. Dry mucus membranes, mumbling to himself and not making sense, not responding to your questions, febrile, diaphoretic. You know something is wrong, and a quick review of his nursing home paper work gives you the answer: digoxin toxicity.

Figuring out what medication is causing problem for an altered patient can be challenging for any physician. Luckily, there are some classic ECG changes that will help clue to into what a patient may have overdosed on.

Beta Blocker

Beta blockers (such as metoprolol, propranolol, carvedilol) interfere with catecholamine effect on beta adrenergic receptors (principally Beta-1 on heart muscle cells) leading to a decreased heart rate and contractility (Yates & Manini 2012). This leads to low heart rate and blood pressure, as well as an increased probability of sinus bradycardia on ECG.

There are a few main-stays of treatment, all of which try to counteract the drugs activity at the cell. High dose insulin therapy (1U/kg/hr) with high dose glucose (0.5g/kg/hr) is thought by some to be first line for beta blocker overdose (Nelson et al. 2016). Hypoglycemia is coming in these patients, so make sure that highly concentrated (≥5% dextrose solutions) glucose is given before the insulin. If this fails to correct the hypotension, beta-selective pressers such as dobutamine and isoproterenol may help, but carry the risk of paroxysmal hypotension due to the high doses that are often required (Nelson et al. 2016). Glucagon is the classic first line treatment for beta blocker overdose, but has high rates of vomiting and requires large doses, so most hospitals will exhaust their supply before the beta blocker has time to wear off (Nelson et al. 2016). Additionally, phosphodiesterase inhibitors (inamrinone, milrinone, enoximone) can help prevent cAMP breakdown and thereby increase calcium activity within the cell to increase frequency and strength of contract (Nelson et al. 2016). Vasopressin (Holger et al. 2007), levosimendan (Archan & Toller 2008), pyruvate (Hermann et al. 2004), and fat emulsion are also possible treatment options, but only have animal trials or case reports to support their use, so it is unclear if these actually work.

Calcium channel blocker

Calcium channel blockers (such as amlodipine, nifedipine, diltiazem, verapamil) have similar effects to beta blockers (lower heart rate), but calcium channel also usually block sodium channels, causing conduction delays and QRS widening. This key difference may clue you to a calcium channel blocker overdose in a bradycardia patient.

Common treatment for both beta blockers are calcium channel blockers include high dose insulin and glucose, pressors, glucagon, and phosphodiesterase inhibitors. Calcium channel blockers toxicity can also be treated with calcium itself (3mg/kg/min of CaCl2) (Reikeras et al. 1985)

Sodium Channel Blockers

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Sodium channels are responsible for depolarization of myocytes in the atria and ventricles, so blockade of these channels will lead to prolong depolarization and widen the QRS complex (Nelson et al. 2016). There is also a classic ECG finding of a prominent r-wave and a rightward axis of the terminal deflection of the r-wave that is seen in lead aVR of a 12-lead ECG.

This finding is a result of sodium channel blocker’s preference for blocking the right bundle of the bundle of Hiss (Yates & Manini 2012). Drugs that block this channel include lidocaine, procainamide, and flecainide.

Overdose treatment for sodium channel blockade may vary slightly depending upon the specific xenobiotic that is causing toxicity. In general, a prolonged QRS from a drug known to cause sodium channel blockade is treated with sodium bicarbonate at a rate of 1-2meq/kg as an initial bolus, followed by a drop of 150 met in 1L D5W at twice maintenance. Keep the ECG attached while doing this so a quick ECG can be done to assess for narrowing of QRS. Any overdose with a QRS longer than 100ms (Nelson et al. 2016) should be treated because of the risk of arrhythmia and death (Boehnert & Lovejoy 1985).

Potassium Channel Blockers

Potassium channels mediate cardiac repolarization, so cause lengthening of the QT interval on ECG (Barrett et al. 2016). This QT prolongation is thought to increase the risk of developing a polymorphic wide complex tachycardia known as Torsades de Pointes (Kurita et al. 1992). Many drugs can have this affect, though few use this effect therapeutically. Some examples include anti-nausea medication, anti-psychotic medication, macrolide and fluoroquinolone antibiotics, and antihistamines.

The mainstay of treatment for most potassium channel blocker xenobiotic overdoses is observation and symptomatic care. While there are not many specific treatments known for potassium channel blockade, IV magnesium (2mg) is used for treatment of prevention of Torsade’s de Pointes (Brady 2016). Electrical cardioversion and overdrive pacing are also treatment options for unstable patient in Torsades (Brady 2016).

Na/K/ATPase Blockers

Digoxin and other cardiac glycoside plants exert both therapeutic and toxic effects by blocking the action of Na/K/ATPase pump. By increasing the intracellular concentration of calcium, contractions of the heart are stronger and occur at a faster rate (Nelson et al. 2016). All this extra calcium causes makes the gives the heart cells a lower activation energy, and makes they more prone to random contraction. Blocking this pump also causes AV nodal blockade by lowering the gradient for calcium influx and thus AV nodal depolarization. These combined effects lead to the classic ECG findings of digoxin toxicity: increased automaticity with block and rhythms such as bi-directional VT (Nelson et al. 2016), atrial flutter with ventricular bradycardia, and the “scooped out” t-wave (the QRS terminates into a depressed and down-sloping ST segment with a short QT interval) known as Salvador Dali’s mustache (Ma et al. 2001).

 Image caption: Life in the Fast Lane: Digoxin Effect. https://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2012/01/Digoxin-reverse-tick-salvador-dali-moustache.jpg?ssl=1

Image caption: Life in the Fast Lane: Digoxin Effect. https://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2012/01/Digoxin-reverse-tick-salvador-dali-moustache.jpg?ssl=1

Treatment includes digoxin-specific antibody fragment (DSFab) (acute toxicity dose = (mg ingested / 0.5mg/vial * 80% bioavailability; chronic toxicity dose = (serum digoxin concentration in ng/L) x (weight in kg) ÷ 100), usually 10-20 vials for acute poison and 3-6 vials for chronic poisoning in adults, 1-2 vials in children). This antidote is effective for cardiac glycosides other than digoxin (such as oleander) (Nelson et al. 2016). Atropine, phenytoin, and lidocaine have also been used, but are often not needed due to DSFab efficacy (Nelson et al. 2016).

Xenobiotic ECG Findings ECG Image Physiology Treatment
Beta-blocker (e.g. propranolol, labetalol) Sinus bradycardia Blockage of cardiac beta receptors Glucagon, high dose insulin and glucose, Pressors
Ca2+ Channel Blocker (e.g. diltiazem, verapamil) Sinus bradycardia, wide QRS Prolongation of phase 0 of nodal action potential, slowing rate of depolarization and thus heart rate High dose insulin, Pressors, glucagon, and phosphodiesterase inhibitors, calcium
Na+ Channel Blocker (e.g. TCA, local anesthetics) Wide QRS, negative deflection of terminal R wave in aVR Prolongation of phase 0 of myocyte action potential, prolonging depolarization phase of cardiac myocytes Sodium bicarbonate to pH <7.55 if QRS > than 100ms, pressors, lidocaine
K+ Channel Blocker (e.g. antipsychotics) Long QT Prolongation of phase 3 of action potential, prolonging time for repolarization Magnesium to treat or prevent Torsades de pointes
Na/K/ATPase Blocker (e.g. cardiac glycoside, digoxin) Biphasic QRS, Increased automaticity with AV block Increased calcium in cardiac myocytes increasing sensitivity to multiple signals and increasing automaticity Digoxin Immune Fab

Table 1: Summary of xenobiotic effects and associated ECG findings. 

These ECG tracings were use with the permission of Dr. Mike Cadogan, and additional images, summary, and description of ECG changes seen in overdose can be seen on his website www.lifeinthefastlane.com.

Faculty Reviewer: Dr. Jason Hack

References

Archan S, Toller W. “Levosimendan: current status and future prospect.” Current Opinions in Anesthesiology. 21:78-84. 2008.

Barrett K, Barman S, Boitano S, Brooks H. Ganong’s Review of Medical Physiology, 25th Edition. 2016

Boehnert MT, Lovejoy FH Jr. “Value of the QRS duration verses the serum drug level in predicting seizures and ventricular arrhythmias after an acute overdose of tricyclic antidepressant.” NEJM. 313:474-479. 1985.

Brady WJ, Laughrey TS, Ghaemmaghami CA. Cardiac Rhythm Disturbances. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds.Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016. 

Graudins, A., Lee, H. M., and Druda, D. (2016) Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. Br J Clin Pharmacol, 81: 453–461.

Hermann HP, Arp J, Pieske B, et. al. “Improved systolic and diastolic myocardial function with intracoronary pyruvate in patients with congestive heart failure.” Cardiovascular Drugs and Therapies. 15:405-411. 2004.

Holger JS, Engebreten KM, Fritzlar SJ, Patten LC, Harris CR, Flottemesch TJ. “Insulin vs vasopressin and epinephrine to treat beta-blocker toxicity.” Clinical Toxicology. 45:396-401. 2007.

Holstege C, Eldridge D, Rowden A. “ECG Manifestations: The Poisoned Patient.” Emergency Medicine Clinics of North America. 24:159-177. 2006.

Kurita T, Ohe T, Marui N, Aihara N, et al. “Bradycardia-induced abnormal QT prolongation in patients with complete atrioventricular block with torsades de pointes.” American Journal of Cardiology. 69(6):628-33. 1992.

Ma G, Brady W, Pollack M, Chan T. “Electrocardiographic manifestations: Digitalis toxicity.” Journal of Emergency Medicine. 20:145-152. 2001.

Nelson L, Lewin N, Howland M, Hoffman R, Goldfrank L, Flomenbaum N. Goldfrank’s Toxicologic Emergencies. 9th Edition. McGraw-Hill Companies Inc. 2011.

Reikeras O, Gunnes P, Sorlie D, Ekroth R, Jorde R, Mjos OD. Metabolic effects of high doses of insulin during acute left ventricular failure in dogs. European Heart Journal. 6:451-457. 1985.

Image Credit

Images Courtesy of Life in the Fast Lane blog and are used with permission: www.lifeinthefastlane.com

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https://i1.wp.com/lifeinthefastlane.com/wp-content/uploads/2012/01/flecainide-overdose.jpg

https://i2.wp.com/lifeinthefastlane.com/wp-content/uploads/2010/12/ECG90503-Subarachnoid-haemorrhage.jpg

https://i2.wp.com/lifeinthefastlane.com/wp-content/uploads/2011/04/ECG-1-BVT.jpg

"High Quality CPR" and You!

CPR as we know it was “invented” by numerous resuscitation scientists working in competing labs during the 1950s.  Since then, CPR has gone through a number of changes, from compression-to-ventilation rates, training programs and even the manner in which it is delivered.  In the 1990s, pubic defibrillators became mainstream.  In the mid 2000s, external CPR devices became more common and in 2010 “hands-only” CPR was the predominant layperson resuscitation method.  The latest iteration of CPR and resuscitation science is the focus on “high quality” CPR, “team-focused” CPR and “cardiocerebral resuscitation” (CCR).

When discussing CPR and the holy grail of evidence-based practice, there are a number of caveats to acknowledge.  Firstly, there have been a very limited number of prospective, randomized and controlled trials on CPR and resuscitation due to many inherent barriers to performing such a study – cost, the infrequency of out-of-hospital cardiac arrest (OHCA), and the difficulty and ethical concerns inherent in studying something which is thought to be efficacious (CPR) against something else which may not be.  Fortunately, there have been a number of trials conducted that can inform our practice, and large, curated resuscitation outcomes databases exist for retrospective studies.  In this article, we’ll discuss CPR, Rhode Island State EMS protocols, and the evidence for and against them.

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In March of 2017, the Rhode Island Department of Health instituted new protocols requiring EMS providers to stay on the scene of an atraumatic cardiac arrest for up to 30-minutes, or until return of spontaneous circulation (ROSC) is achieved[i].  Pre-hospital medicine policies and protocols vary according to the region, state, resources, distance from definitive care, and culture.  When treating trauma patients, for example, EMS providers are instructed to transport as quickly as possible to a hospital.  Traditionally, EMS providers have also been taught to transport OHCA patients to hospitals quickly as well, so asking them to remain on-scene for up to 30-minutes is controversial.  According to the American Heart Association (AHA), approximately 355,000 people each year suffer an OHCA event (110 events per 100,000 population).  Studies vary, but the overall survival rate for OHCA is anywhere from 6-12%[ii],[iii] nationally.  Extrapolating these statistics to Rhode Island’s population of 1 million, we can estimate that approximately 1100 Rhode Islanders are having OHCA each year, or 3 people every day.  Clearly, OHCA is an important topic and is worth exerting considerable effort to improve outcomes.

Historically, we know that certain factors in OHCA have prognostic importance and are associated with better outcomes, including witnessed arrest, time to CPR and defibrillation, initial shockable rhythm (VT/VF), AED use, and patient ageiii,[iv].  Although there are a myriad of factors that play into treating OHCA patients – airway use, mechanical or manual CPR, ACLS drugs, etc., the idea behind emphasizing on-scene CPR is that it gives EMS agencies the opportunity to defibrillate as soon as possible, perform great CPR and increase a patient’s chance of ROSC by re-establishing myocardial perfusion, instead of focusing on patient packaging and transport.  In other words, the theory is that you can run a code in the field, in the ER, or in the back of an ambulance, but the sooner you run it well, the better odds a patient has of a good outcome.  Below, we’ll review some of the key concepts of high-quality CPR.

Continuous Chest Compressions

Chest compressions.JPG

Many simulation, animal and observational studies have been performed on all manner of aspects of CPR, including compression depth, recoil, and speed.  Recently, focus has been drawn to cardiocerebral resuscitation (CCR), or minimally interrupted, continuous CPR.  The concept behind this mode of CPR delivery is that of coronary perfusion pressure – that it takes time giving compressions to reach the threshold at which the heart has enough coronary blood flow to possibly begin beating again, and each pause in CPR resets the pressure to 0. In the 3-phase model of VF arrest, the first 5 minutes are the “electrical phase”, in which defibrillation can result in ROSC. After this is the “hemodynamic phase”, during which restoration of “adequate arterial pressure” by CPR can increase odds of ROSC.  Importantly, it can take up to 45 seconds to establish adequate arterial pressure.  Lastly is the “metabolic phase”, during which outcomes are poor[v],[vi].  According to this theory, the sooner patients get defibrillation and CPR, and the better the CPR is, the higher odds they have of ROSC.  To date, several registry-based studies seem to agree with this idea, and have demonstrated improved outcomes among both VF and non-VF arrests with high chest compression fraction (i.e., less CPR interruptions)[vii].  Assuming that continuous CPR, or high chest compression fraction is beneficial, it also follows that any interruptions during CPR can result in worse outcomes – for example, pauses around defibrillation, intubation and transport, and research has borne this out[viii].  It’s worth noting, however, that although many of these concepts have become resuscitation truths, not all research agrees.  In one of the few RCTs on CPR, published in the New England Journal in 2015, Nichol et al. compared continuous to interrupted chest compressions, and found no statistically-significant difference in favorable neurologic function at discharge, although the protocol compliance was low, and many variables were similar between both groups[ix].  Both groups, for example, had CPR fractions higher than typical, so both study groups may not be representative of the real world.

Passive Oxygenation and Delayed Intubation

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One of the key exposures in the NEJM study by Nichol et al., was the mode of ventilation.  In comparing continuous to interrupted chest compressions, the “interruption” was providing rescue breaths in the traditional 30:2 ratio.  If we subscribe to the idea that it takes up to 45 seconds to develop enough coronary perfusion pressure that defibrillation might be successful, stopping CPR every 30 compressions begins to seem like a bad idea.  We also know that a provider’s focus on airway management can detract from compression quality.  One observational study found that pre-hospital providers caring for OHCA patients paused CPR a median of 109 seconds for airway placement[x].  Coupling this finding with other studies showing that CPR pause duration is associated with increased mortality[xi] leads us to consider forgetting about the airway completely (at least initially).  Other literature seems to support this idea.  McMullan et al published a paper in 2013 on data from the Cardiac Arrest Registry to Enhance Survival (CARES), evaluating different airway management techniques and their association with neurologically intact survival.  The authors found that of 10,691 OHCA patients, survival was highest among those who received neither endotracheal intubation nor supraglottic airways (OR of 1.31)[xii].  Although this appears damning for any types of airway management at face value, it’s worth noting that patients with the best outcome often will have no opportunity for airway management – in other words, they are shocked out of VF, then wake up!  More information is coming soon, with an RCT due to be published in 2020 comparing airway management methods prospectively.

CPR During Transport

Another significant factor in deciding whether to work a code on scene or transport rapidly is the quality of CPR possible.  On scene, with a team of prepared EMS personnel, it seems a reasonable assumption that CPR metrics would be superior.  Prior literature seems to support this conclusion, with a number of simulation studies demonstrating worse or more variable CPR metrics in patients during transport, such as compression depth and rate[xiii].  In a small study published by Olasveengen et al., non-traumatic OHCA patients had increased time without compressions during transport compared with when on scene (27% vs. 19%).  However, in one 2017 registry-based study in Canada, the proportion of OHCA patients receiving “high-quality” CPR, defined as depth >5cm, rate >100/min, and chest compression fraction of >0.7 was similar between on-scene and transported groups[xiv].  Even if EMS providers are able to provide high-quality CPR in the back of a moving ambulance, consideration must be made of the danger to EMS personnel, who are then required to stand and perform a physically demanding task in a moving vehicle.  The science is not completely clear on which method is superior – on-scene or in transport, though clearly these studies have implications for proponents of running on-scene codes.

Team-Focused CPR

Eager to implement these cutting-edge techniques, some EMS systems have published their results with high-quality, “pit-crew style” and “team-focused” CPR.  Stopyra published data from a prospectively collected pre and post-intervention cohort study in rural North Carolina.  Data was collected on OHCA from 1-year prior to the intervention and 1-year after the intervention implementation.  All OHCA of presumed cardiac etiology was included.  The intervention included training of all providers, including police and EMS.  They were instructed to fulfill a choreographed position based on the timing of their arrival to the code.  The first rescuer would begin CPR, the second would place defibrillation pads and insert a blind airway, the third would be the team leader.  After arrival of the third provider, parenteral access could be attempted.  Rescuers continued with resuscitation until ROSC or end tidal <10mm for 20 minutes.  They found that after protocol implementation, there was a significant increase in number of patients achieving ROSC (65.7% vs. 28.4%, p<0.001), though there was no statistically significant change in survival to discharge.  Some of the limitations of this study include the small n (105 total resuscitations), and the lack of ability to control for in-hospital care (with regards to the lack of difference in survival to discharge)[xv].

A second North Carolina was undertaken by Pearson et al, and published in Resuscitation, detailing OHCA outcomes before and after an intervention of “team-focused CPR”[xvi].  Researchers evaluated arrest characteristics of nearly 15,000 OHCA patients using CARES registry data.  EMS agencies self-reports compliance with “team-focused CPR”, which emphasized early defibrillation, high quality CPR, and airway management with BVM over advanced airways.  Authors used a logistic regression to control for arrest characteristics, such as CPR device used, witnessed or unwitnessed, race, comorbidities and hypothermia, and found that team-focused CPR had a better odds of good neurologic outcome as measured by cerebral performance category score (OR 1.5) compared with traditional CPR.

A similar effort was undertaken in Salt Lake City in 2011.  The results from SLC Fire Department’s “pit crew approach” were published in 2015 in the Journal of the American Heart Association.  This study had significantly larger numbers (737 attempted resuscitations), and was based in an urban department with 11 ALS units and 8 BLS units.   The intervention in SLC included use of defibrillator real-time feedback to rescuers, strong medical direction and QA of all OHCA calls, rhythm-filtering technology that allowed rescuers to see the rhythm during CPR prior to stopping for pulse-check, limited peri-shock pauses, and encouraged on-scene resuscitation (vs. early transport) to reduce interruptions inherent in transfer and transport.  Additionally, passive oxygen was applied via facemask for the first 6-8 minutes, and asynchronous BVM for all unwitnessed, pediatric and respiratory arrests. 

After the intervention, SLC Fire Department saw more field ROSC (44% vs. 30%, p<0.0001).  Among patients who survived to admission, there was more survival to discharge (50% vs. 37%, p=0.0005), and more patients with favorable neurologic function, defined as Cerebral Performance Category 1 or 2 (46% vs. 26%, p=0.0005), although there was no statistically significant change in survival to hospital admission.  Although these numbers are promising for high-quality CPR, several confounders are present, including improved medical control, and preferential triage of OHCA patients with ROSC to PCI-capable centers, which was not the practice in the pre-intervention period[xvii]

Rhode Island is among the first states to institute a protocol mandating 30-minutes of on-scene CPR. While some have demonstrated improved outcomes with the implementation of similar interventions, bundled together with CPR training, use of novel technology (such as real-time feedback, end-tidal CO2, and rhythm filtration programs), strong medical direction and QA, it remains to be seen whether a statewide intervention can lead to more ROSC in the field, and, more importantly, more neurologically intact survival to discharge.  Reviewing the resuscitation literature, we see the trend toward decreased initial advanced airway use, higher focus on continuous CPR and minimal interruptions, such as the peri-shock pause and, to delay transport of the patient until ROSC is achieved.  While local news reports have highlighted anecdotal success stories[xviii], the full impact of the Rhode Island intervention have yet to be described.

Faculty Reviewer: Nick Asselin, DO

References

[i] Rhode Island Statewide Emergency Medical Services Protocols.” Rhode Island Department of Health, p. 3.03a., health.ri.gov/publications/protocols/StatewideEmergencyMedicalServices.pdf.

[ii] Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., … Turner, M. B. (2015). Heart Disease and Stroke Statistics—2016 Update. Circulation, 133(4), e38–e360. https://doi.org/10.1161/cir.0000000000000350

[iii] Becker, L. B., Aufderheide, T. P., & Graham, R. (2015). Strategies to Improve Survival From Cardiac Arrest. JAMA, 314(3), 223. https://doi.org/10.1001/jama.2015.8454

[iv] Haukoos, J. S., Lewis, R. J., & Niemann, J. T. (2004). Prediction rules for estimating neurologic outcome following out-of-hospital cardiac arrest. Resuscitation, 63(2), 145–155. https://doi.org/10.1016/j.resuscitation.2004.04.014

[v] Weisfeldt, M. L., & Becker, L. B. (2002). Resuscitation After Cardiac Arrest. JAMA, 288(23), 3035. https://doi.org/10.1001/jama.288.23.3035

[vi] Berg, R. A., Sanders, A. B., Kern, K. B., Hilwig, R. W., Heidenreich, J. W., Porter, M. E., & Ewy, G. A. (2001). Adverse Hemodynamic Effects of Interrupting Chest Compressions for Rescue Breathing During Cardiopulmonary Resuscitation for Ventricular Fibrillation Cardiac Arrest. Circulation, 104(20), 2465–2470. https://doi.org/10.1161/hc4501.098926

[vii] Vaillancourt, C., Everson-Stewart, S., Christenson, J., Andrusiek, D., Powell, J., Nichol, G., … Stiell, I. G. (2011). The impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation. Resuscitation, 82(12), 1501–1507. https://doi.org/10.1016/j.resuscitation.2011.07.011

[viii] Cheskes, S., Schmicker, R. H., Christenson, J., Salcido, D. D., Rea, T., … Powell, J. (2011). Perishock Pause: An Independent Predictor of Survival From Out-of-Hospital Shockable Cardiac Arrest. Circulation, 124(1), 58–66. https://doi.org/10.1161/circulationaha.110.010736

[ix] Nichol, G., Leroux, B., Wang, H., Callaway, C. W., Sopko, G., Weisfeldt, M., … Ornato, J. P. (2015). Trial of Continuous or Interrupted Chest Compressions during CPR. New England Journal of Medicine, 373(23), 2203–2214. https://doi.org/10.1056/nejmoa1509139

[x] Wang, H. E., Simeone, S. J., Weaver, M. D., & Callaway, C. W. (2009). Interruptions in Cardiopulmonary Resuscitation From Paramedic Endotracheal Intubation. Annals of Emergency Medicine, 54(5), 645–652.e1. https://doi.org/10.1016/j.annemergmed.2009.05.024

[xi] Brouwer, T. F., Walker, R. G., Chapman, F. W., & Koster, R. W. (2015). Association Between Chest Compression Interruptions and Clinical Outcomes of Ventricular Fibrillation Out-of-Hospital Cardiac ArrestCLINICAL PERSPECTIVE. Circulation, 132(11), 1030–1037. https://doi.org/10.1161/circulationaha.115.014016

[xii] McMullan, J., Gerecht, R., Bonomo, J., Robb, R., McNally, B., Donnelly, J., & Wang, H. E. (2014). Airway management and out-of-hospital cardiac arrest outcome in the CARES registry. Resuscitation, 85(5), 617–622. https://doi.org/10.1016/j.resuscitation.2014.02.007

[xiii] Roosa, J. R., Vadeboncoeur, T. F., Dommer, P. B., Panchal, A. R., Venuti, M., Smith, G., … Bobrow, B. J. (2013). CPR variability during ground ambulance transport of patients in cardiac arrest. Resuscitation, 84(5), 592–595. https://doi.org/10.1016/j.resuscitation.2012.07.042

[xiv] Cheskes, S., Byers, A., Zhan, C., Verbeek, P. R., Ko, D., Drennan, I. R., … Morrison, L. J. (2017). CPR quality during out-of-hospital cardiac arrest transport. Resuscitation, 114, 34–39. https://doi.org/10.1016/j.resuscitation.2017.02.016

[xv] Stopyra, J. P., Courage, C., Davis, C. A., Hiestand, B. C., Nelson, R. D., & Winslow, J. E. (2016). Impact of a “Team-focused CPR” Protocol on Out-of-hospital Cardiac Arrest Survival in a Rural EMS System. Critical Pathways in Cardiology, 15(3), 98–102. https://doi.org/10.1097/hpc.0000000000000080

[xvi] Pearson, D. A., Darrell Nelson, R., Monk, L., Tyson, C., Jollis, J. G., Granger, C. B., … Runyon, M. S. (2016). Comparison of team-focused CPR vs standard CPR in resuscitation from out-of-hospital cardiac arrest: Results from a statewide quality improvement initiative. Resuscitation, 105, 165–172. https://doi.org/10.1016/j.resuscitation.2016.04.008

[xvii] Hopkins, C. L., Burk, C., Moser, S., Meersman, J., Baldwin, C., & Youngquist, S. T. (2016). Implementation of Pit Crew Approach and Cardiopulmonary Resuscitation Metrics for Out‐of‐Hospital Cardiac Arrest Improves Patient Survival and Neurological Outcome. Journal of the American Heart Association, 5(1), e002892. https://doi.org/10.1161/jaha.115.002892

[xviii] http://wpri.com/2017/02/16/new-rule-cpr-for-30-minutes-before-taking-cardiac-arrest-victims-to-hospital/

AEM Early Access 05: The Role of Prehospital ACLS for Potential E-CPR Candidates

Welcome to the fifth episode of AEM Early Access, a FOAMed podcast collaboration between the Academic Emergency Medicine Journal and Brown Emergency Medicine. Each month, we'll give you digital open access to an AEM Article in Press, with an author interview podcast and links to curated FOAMed supportive educational materials for EM learners.

Find previous podcasts and subscribe to this series on I tunes here.

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  Dr. Alexis Cournoyer, MD   Universite de Montreal, Montreal, Quebec, Canada Hospital du Sacre-Coeur de Montreal, Montreal, Quebec, Canada Institut de Cardiologie de Montreal, Montreal, Quebec, Canada

Dr. Alexis Cournoyer, MD

Universite de Montreal, Montreal, Quebec, Canada
Hospital du Sacre-Coeur de Montreal, Montreal, Quebec, Canada
Institut de Cardiologie de Montreal, Montreal, Quebec, Canada

 

 

 

Listen now: Interview with Dr. Alexis Cournoyer, lead author, interviewed by Dr. Thomas Ross

Open Access Through September 30th. Click below:

Prehospital Advanced Cardiac Life Support for Out-of-Hospital Cardiac Arrest: A Cohort Study. Cournoyer A, et. al

Article Summary:

Objectives: Out-of-hospital advanced cardiac life support (ACLS) has not consistently shown a positive impact on survival. Extracorporeal cardiopulmonary resuscitation (E-CPR) could render prolonged on-site resuscitation (ACLS or basic cardiac life support [BCLS]) undesirable in selected cases. The objectives of this study were to evaluate, in patients suffering from out-of-hospital cardiac arrest (OHCA) and in a subgroup of potential E-CPR candidates, the association between the addition of prehospital ACLS to BCLS and survival to hospital discharge, prehospital return of spontaneous circulation (ROSC) and delay from call to hospital arrival. 

Methods: This cohort study targets adult patients treated for OHCA between April 1010 and December 2015 in the city of Montreal, Canada. We defined potential E-CPR candidates using clinical criteria previously described in the literature (65 years of age or younger, initial shockable rhythm, absence of return of spontaneous circulation after 15 minutes of prehospital resuscitation and emergency medical services witnessed collapse or witnessed collapse with bystander cardiopulmonary resuscitation). Associations were evaluated using multivariate regression models.

Results: A total of 7134 patients with OHCA were included, 761 (10.7%) of whom survived to discharge. No independent association between survival to hospital discharge and the addition of prehospital ACLS to BCLS was found in either the entire cohort [adjusted odds ratio (AOR) 1.05 (95% confidence interval 0.84-1.32), p=0.68] or amongst the 246 potential E-CPR candidates [AOR 0.82 (95% confidence interval 0.36-1.84), p=0.63]. The addition of prehospital ACLS to BCLS was associated with a significant increase in the rate of prehospital ROSC in all patients experiencing OHCA (AOR 3.92 [95% CI 3.38-4.55], p<0.001) and in potential E-CPR candidates (AOR 3.48 [95% CI 1.76-6.88], p<0.001) as compared to isolated prehospital BCLS. Delay from call to hospital arrival was longer in the ACLS group than in the BCLS group (difference=16 min [95% CI 15-16], p<0.001). 

Conclusions:  In a tiered-response  urban emergency medical service setting, prehospital ACLS is not associated with an improvement in survival to hospital discharge in patients suffering from OHCA and in potential E-CPR candidates, but with an improvement in prehospital ROSC and with longer delay to hospital arrival. 

Suggestions for Further Reading: 

Open Access:

RAGE Podcast: E-CPR by Vincent Pellegrino

EM Docs: ECMO in the ED

Subscriptions/Abstracts:

Sanghavi P, Jena AB, Newhouse JP, Zaslavsky AM. Outcomes after out-of-hospital cardiac arrest treated by basic vs advanced life support. JAMA Intern Med 2015;175:196-204. 

Ma MH, Chiang WC, Ko PC, et al. Outcomes from out-of-hospital cardiac arrest in Metropolitan Taipei: does an advanced life support service make a difference? Resuscitation 2007;74:461-9.

Bakalos G, Mamali M, Komninos C, et. al. Advanced life support versus basic life support in the pre-hospital setting: a meta analysis. Resuscitation 2011;82:1130-7.

Stub D, Bernard S, Pellegrino V, et. al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation 2014. 

Siao FY, Chiu CC, Chiu CW, et al. Managing cardiac arrest with refractory ventricular fibrillation in the emergency department: Conventional cardiopulmonary resuscitation versus extracorporeal cardiopulmonary resuscitation. Resuscitation 2015;92:70-6. 

Faculty Editors/Reviewers: Dr. Gita Pensa and Dr. Kristy McAteer 

Podcast credits: Used under creative commons license: intro music by freemusicarchive.org , sound effect from freesound.org, exit music by bensound.com