"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.


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

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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


[i] Rhode Island Statewide Emergency Medical Services Protocols.” Rhode Island Department of Health, p. 3.03a.,

[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.

[iii] Becker, L. B., Aufderheide, T. P., & Graham, R. (2015). Strategies to Improve Survival From Cardiac Arrest. JAMA, 314(3), 223.

[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.

[v] Weisfeldt, M. L., & Becker, L. B. (2002). Resuscitation After Cardiac Arrest. 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.

[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.

[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.

[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.

[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.

[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.

[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.

[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.

[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.

[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.

[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.

[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.


AEM Early Access 13: Syncope Prognosis Based on ED Diagnosis

Welcome to the thirteenth 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 recent AEM Article or Article in Press, with an author interview podcast and suggested supportive educational materials for EM learners.

Find this podcast series on iTunes here.

A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

A FOAM Collaboration: Academic Emergency Medicine Journal and Brown EM

DISCUSSING:(Click for Open Access Through 4/30/18)

Syncope Prognosis Based on Emergency Department Diagnosis: A Prospective Cohort Study. Cristian Toarta, MD, Muhammad Mukarram, MBBS, MPH, Kirtana Arcot, MSc, Soo-Min Kim, BScH, Sarah Gaudet, RN, Marco L. A. Sivilotti, MD, MSc, Brian H. Rowe, MD, MSc, and Venkatesh Thiruganasambandamoorthy, MBBS, MSc. Academic Emergency Medicine 2018



Christian Toarta, M.D.

PGY-3, Emergency Medicine

University of Toronto

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Venkatesh Thiruganasambandamoorthy CCFP-EM, M.Sc
Associate Professor, Dept. of Emergency Medicine, and

School of Epidemiology and Public Health

Scientist, Ottawa Hospital Research Institute

New Investigator, Heart and Stroke Foundation Canada
Staff Attending Physician,The Ottawa Hospital

Twitter: @TeamVenk



Objectives: Patients presenting to emergency departments (EDs) with syncope are given various diagnoses for cause including: vasovagal, orthostatic hypotension, cardiac and unknown. This study aims to determine short-term outcomes in each diagnostic group up to 30 days following the initial ED visit for syncope.

Methods: Adult syncope patients were prospectively enrolled from six Canadian EDs by treating physicians. Syncope was defined as a transient loss of consciousness followed by complete recovery and those with presyncope, persistent mental status changes, seizures, alcohol or drug intoxication or patients with major trauma were excluded. Additionally, patients with serious conditions identified during the initial ED visit were excluded as the study aimed to prognosticate after diagnosis. Patient demographics, ED management, presumed diagnosis at the end of visit and physician confidence in that diagnosis were collected at the time of visit. Serious outcomes, including death, arrhythmias, myocardial infarction, structural heart disease, pulmonary embolism, subarachnoid hemorrhage, serious hemorrhage or other conditions that would require a return visit or intervention were assessed 30 days following the initial visit.

Results: A total of 5,010 patients were included in the final analysis, of whom the cause of syncope was found to be vasovagal in 2,671 (53.3%) unknown in 1,615 (32.2%), orthostatic in 456 (9.1%) and cardiac in 268 (5.4%) of patients. Of all patients, 177 (3.5%) suffered serious outcomes including 15 deaths (0.3%), 115 cardiac (2.3%) and 47 non-cardiac (0.9%) outcomes. No deaths occurred in the vasovagal syncope group. The proportion of serious outcomes was significantly higher in all groups other than vasovagal, increasing in the following order: vasovagal, orthostatic hypotension, unknown and cardiac (p< 0.01). The proportion of patients among whom diagnostic testing was performed also increased in the same order with least in vasovagal and most in cardiac syncope (p< 0.001), with 42.9% of those with cardiac syncope hospitalized compared to 9.4% overall. The physician confidence in assigning a diagnosis was highest in the vasovagal syncope group and lowest in the unknown syncope group. 

Conclusions: Physician diagnosis strongly correlated with probability of serious outcomes in patients with syncope. This initial diagnosis with physician clinical judgment could be factored into future scores for risk stratification and management of patients with syncope.



 1. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2016;188(12):E289-298

 2. Thiruganasambandamoorthy V, Stiell IG, Sivilotti ML, et al. Risk stratification of adult emergency department syncope patients to predict short-term serious outcomes after discharge (RiSEDS) study. BMC Emergency Medicine. 2014;14:8.

3. Costantino G, Casazza G, Reed M, et al. Syncope risk stratification tools vs clinical judgment: an individual patient data meta-analysis. The American Journal of Medicine. 2014;127(11):1126.e1113-1125.

4. Quinn JV, Stiell IG, McDermott DA, Sellers KL, Kohn MA, Wells GA. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Annals of Emergency Medicine. 2004;43(2):224-232.


Community Case: Not Your Average Fainting Spell

A 36-year-old woman came into the ED by EMS with multiple ‘fainting spells’ throughout the day (her family thought it was because her blood sugar was low at 83 when they checked at home and treated with glucagon and candy).  I was handed this EKG by the receiving nurse:

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I walk into the Trauma Room to find a woman who is awake, alert, diaphoretic, and talking. I get handed this next EKG:

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Moments later the patient becomes suddenly unresponsive and this is what we see:

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Torsades de Pointes (TdP) = Polymorphic V Tach (PVT) + Long QT

So then what did we do?

*   Gave Magnesium 2 mg IV bolus x 2 immediately

*   iSTAT showed K 2.6 so started aggressive repletion, placed central venous access to increase rate of safe repletion

*   Started Magnesium drip, gave magnesium bolus PRN anytime there were prolonged runs of TdP

*   Gave lidocaine bolus 100 mg (dose can range from 0.5 to 0.75 up to 1 to 1.5mg/kg)

*   Shocked patient three times (during prolonged runs of TdP associated with unresponsiveness):

Blue arrow indicates defibrillation; return of NSR afterward

Blue arrow indicates defibrillation; return of NSR afterward

*   Gave isoproterenol after confirming no history LQTS or prior prolonged QTc on prior EKGs (initial dose 0.05 to 0.1 mcg/kg/min in children and 2 mcg/min in adults)

*   She was transferred to the cardiology service in good condition, awake and alert

Torsades de Pointes ECG Pearls:

·      Long QT + PVT with characteristic morphology that seems to twist around isoelectric line

·      QT interval is inversely proportional to heart rate (HR)

o   The QT shortens at faster HR

o   The QT lengthens at shorter HR

o   There are formulas to calculate the QT interval (

·      TdP with HR >220 more likely to degenerate into VF

·      Bigeminy in a patient with known LQTS may herald imminent TdP:

This was the prehospital EKG

This was the prehospital EKG

Presence of abnormal giant T-U waves may also precede TdP.

Pathophysiology of TdP:

·      A prolonged QT reflects prolonged myocyte repolarization due to ion channel malfunction

·      This prolonged repolarization period also gives rise to early-after-depolarizations (EADs)

·      EADs may manifest on ECG as tall u waves; if these reach threshold amplitude, they may manifest as PVCs

·      TdP is initiated when a PVC occurs during a preceding T wave, known as ‘R-on-T’ phenomena

·      The onset of TdP is often preceded by a sequence of short-long-short PR intervals, so called ‘pause-dependent’ TdP with longer pauses associated with faster runs of VT

Clinical Significance:

·      TdP is often short lived and self-terminating, however can be associated with hemodynamic instability and ultimately may degenerate into ventricular fibrillation

·      If it does not spontaneously convert and the patient is unstable, it will need defibrillation

·      QT prolongation may be acquired and occur secondary to multiple drug effects, electrolyte abnormalities, medical conditions, or congenital long-QT syndrome (LQTS)

·      Recognizing the cause of TdP (acquired vs. congenital) allows initiation of specific treatment strategies

*   Defibrillation if unstable

*   Give magnesium (Mg 2-4 grams IV push followed by Mg drip of 3-10 mg/minute)

*   Removal of offending agent in acquired long QT

*   Correct any electrolyte abnormalities (especially hypoMg, hypoK, hypoCa)

*   Correct contributing factors such as respiratory alkalosis (which can worsen hypoK, etc)

*   Remove any offending agents (such as certain anti-arrhythmics, antibiotics, anti-emetics, psychotropics, or methadone)

*   Lidocaine may help because it can suppress PVCs, and therefore stop the R-on-T phenomena

*   Overdrive Pacing (usually at a rate of 100 bpm due to heart rate dependent effects of QT)

*   Only in acquired long QT: beta-adrenergic stimulation with isoproterenol

*   Only in LQTS: give beta-blockade (start with esmolol, then propranolol if not effective)

*   Patients with LQTS may require permanent pacing and ICD

*   Amiodarone may be harmful because it lengthens the QT interval and can possibly cause PVCs (although amiodarone has never been specifically shown to cause Torsades)

ACC/AHA/ESC Guidelines:

The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines for the management of ventricular arrhythmias and the prevention of SCD addressed the management of TdP in the setting of acquired LQTS:

*   Intravenous magnesium

*   Temporary pacing

*   Isoproterenol


· Up To Date:

· Life In the Fast Lane:

· HQMedEd:

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Faculty Reviewer: Dr. Kristina McAteer