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Prevalence of Pulmonary Embolism among Patients Hospitalized for Syncope

21/10/2016

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Look at the below link to NEJMs “Quick Take” and article. The results of this study seem practice changing, but probably are not (see analysis below).

Article:
http://www.nejm.org/doi/full/10.1056/NEJMoa1602172?query=TOC


Quick Take:
​http://www.nejm.org/do/10.1056/NEJMdo005093/full/?query=TOC


Prospective study. 11 Italian hospitals, 560 patients presenting with first syncope. All underwent CXR, ECG, Well’s Score assessment and D-Dimer testing (not age adjusted, as far as I can see). 

A total of 560 patients (mean age, 76 years) were included in the study. 
  • Pulmonary embolism was ruled out in 330 of the 560 patients (58.9%) on the basis of the combination of a low pretest clinical probability of pulmonary embolism and negative d-dimer assay. 
  • Among the remaining 230 patients, pulmonary embolism was identified in 97 (42.2%). 
  • In the entire cohort, the prevalence of pulmonary embolism was 17.3%.
  • Evidence of an embolus in a main pulmonary or lobar artery or evidence of perfusion defects larger than 25% of the total area of both lungs was found in 61 patients.
  • Pulmonary embolism was identified in 45 of the 355 patients (12.7%) who had an alternative explanation for syncope and in 52 of the 205 patients (25.4%) who did not.
  • Of the 97 patients with pulmonary embolism, 24 (24.7%) had no clinical manifestations of the diagnosis, including tachypnea, tachycardia, hypotension, or clinical signs or symptoms of deep-vein thrombosis.

Conclusion:
Pulmonary embolism was identified in nearly one of every six patients hospitalized for a first episode of syncope.

Analysis (based on blog by Rory Spiegel​ on EMCrit):
  • This is not a cohort of 97 pulmonary embolisms in 560 patients as it has been portrayed. Rather this was 97 (3.8%) radiographic pulmonary embolisms in 2584 patients presenting to the Emergency Department for a syncopal event. 
  • Only the patients admitted to the hospital after an Emergency Department workup for syncope were enrolled into the PESIT cohort.
  • The majority of patients presenting to the Emergency Department were discharged home without further workup. 
  • This means 1 in 26 patients presenting to the Emergency Department will have a pulmonary embolism found on imaging. The large majority of these will be incidental findings and the remainder will be clinically obvious.

To quote the conclusion of Rory Spiegel’s blog on EMCRit:
"There are times when our clinical experience is misleading. When empiric evidence should call into question our long standing practice patterns. But there are times when the evidence is in such conflict with our shared experience, there is nothing to be done but to questions its validity. There is no doubt that these results will be misinterpreted over the next few days, weeks and years. We will now be tasked with performing invasive diagnostic workups in patients with no clinical signs or symptoms of pulmonary embolisms. Any Emergency Physician will tell you not to order a CTPA on a patient in whom you do not wish to know the results. Likewise, do not order a D-dimer in a patient who you have no intention of acquiring further imaging. Prandoni et al have perpetrated the systematic equivalent of this diagnostic absurdity. To translate these results into meaning that all patients presenting to the Emergency Department after a syncopal event require a work-up for pulmonary embolism is not only statistical hoodwinkery, but is just bad medicine. These patients will be exposed to needless and harmful downstream workups, radiation and anticoagulation. We have chased the ghost of Pulmonary Embolism far beyond the reaches of good clinical practice. And this quixotic quest has left a path of over-diagnosis and unnecessary treatments in its wake. At some point someone has to stop this madness. I offer that time is here and now”.

Maybe not so practice changing after all. 
​
Danny Ben-Eli

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Amal Mattu: IV Amiodarone for WCT: Time to Say Goodbye?

12/10/2016

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Amal Mattu, MD | October 05, 2016
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Emerging Doubt About Amiodarone

Intravenous amiodarone was introduced to mainstream acute care providers in the resuscitation guidelines released in 2000.[1] It was touted as the drug of choice for treating wide complex tachycardia (WCT) of various types, especially for monomorphic ventricular tachycardia (VT). Because it suppresses ventricular conduction and also has atrioventricular nodal blocking effects, it was presumed effective for other types of WCT as well, and it quickly became the preferred therapy for all undifferentiated WCT. However, in recent years, studies have cast some doubt on the effectiveness of this drug. The most recent study[2] of amiodarone vs the older drug procainamide has perhaps added one more nail in amiodarone's coffin.

Amiodarone vs Procainamide

Ortiz and colleagues[2] sought to compare the efficacy of amiodarone vs procainamide in patients with hemodynamically stable, regular WCT. The exact diagnosis (eg, VT vs supraventricular tachycardia with aberrant conduction) was not the focus of the study, given that in real-world scenarios the real diagnosis is typically uncertain, and no ECG criteria have been found to be reliable in this distinction. The authors performed a multicenter, randomized, open-label study in which a total of 29 patients received amiodarone (5 mg/kg over 20 minutes) and 33 patients received procainamide (10 mg/kg over 20 minutes). The primary endpoint was the incidence of major cardiac adverse events (clinical signs of peripheral hypoperfusion, signs of acute heart failure, development of severe hypotension, tachycardia acceleration of >20 beats/min, or appearance of fast polymorphic VT) within 40 minutes after beginning the infusion. Response to treatment was defined by conversion of the WCT to the patient's known or presumed usual heart rhythm within the study period.

The primary endpoint occurred in 12/29 (41%) in the amiodarone group vs 3/33 (9%) in the procainamide group. Tachycardia termination occurred in 11 (38%) in the amiodarone group and 22 (67%) in the procainamide group. In the following 24 hours, adverse events occurred in 31% of the amiodarone group vs 18% of the procainamide group. Among 49 patients with structural heart disease, adverse events occurred more commonly in the amiodarone group as well (43% vs 11%).

Viewpoint

This study demonstrated that procainamide was more effective and safer than amiodarone for patients with WCT, including those with structural heart disease. Although this is the first controlled prospective trial comparing procainamide vs amiodarone, this is not the first study that has cast doubt on the effectiveness of amiodarone in WCTs. Previous studies by Marill and colleagues[3] and Tomlinson and colleagues[4] demonstrated that amiodarone was only effective in 29% of cases of stable VT. In 2006, the American College of Cardiology, the American Heart Association, and the European Society of Cardiology endorsed procainamide as the preferred drug for stable monomorphic ventricular tachycardia[5]; and in 2010, the American Heart Association resuscitation guidelines followed suit.[6] With respect to irregular WCT, amiodarone is contraindicated when there is concern for atrial fibrillation with pre-excitation.[7] For treatment and conversion of stable narrow complex atrial fibrillation as well, procainamide has received strong support and is commonly used in Canada.[8]

Admittedly, procainamide is not a perfect drug either. Rapid administration can induce hypotension or prolongation of the QRS or QT intervals, leading to (rarely) torsades de pointes. However, the habitual use of amiodarone in patients with undifferentiated WCTs is not well-supported by the literature. Amiodarone is poorly effective in VT; and it is dangerous in pregnancy (class D), in prolonged QT conditions, and in patients with atrial fibrillation plus pre-excitation. Safer drugs are available; and, when in doubt, acute care providers should not hesitate to sedate and cardiovert patients with WCTs. It's time to let amiodarone rest in peace and, if available to you, get reacquainted with an old friend, procainamide.

​
References
  1. [No authors listed]. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 5: pharmacology I: agents for arrhythmias. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation. 2000;102(8 Suppl):I112-I128.
  2. Ortiz M, Martin A, Arribas F, et al; PROCAMIO Study Investigators. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2016 Jun 28. [Epub ahead of print]
  3. Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med. 2006;47:217-224. Abstract
  4. Tomlinson DR, Cherian P, Betts TR, Bashir Y. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J. 2008;25:15-18. Abstract
  5. Zipes DP, Camm AJ, Borggrefe M, et al; American College of Cardiology/American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society. ACC/AHA/ESC 2006 Guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114:e385-e484. Abstract
  6. Field JM, Hazinski MF, Sayre MR, et al. Part I: executive summary: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 Suppl 3):S640-S656.
  7. January CT, Wann LS, Alpert JS, et al; ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014;130:2071-2104.7.
  8. Stiell IG, Clement CM, Perry JJ, et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM. 2010;12:181-191. Abstract

Medscape Emergency Medicine © 2016  WebMD, LLC 
Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this article: IV Amiodarone for WCT: Time to Say Goodbye?. Medscape. Oct 05, 2016.
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Does intubation during paediatric cardiac arrest save lives?

5/10/2016

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Brand new article published in JAMA - looks at the association between intubation and outcome during in-hospital paediatric cardiac arrest. Sure, it's not an RCT but being such a rare event, will we ever have one?

Go to the website to download the (non-paywalled) article.
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Come learn Thoracic Ultrasound!

5/10/2016

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Guys the next EMUG Victoria (Emergency Medicine Ultrasound Group) meeting is fast approaching on Thursday November 10. It is FREE for trainees and is being organised by some local experts including Dr. Pourya Pouryahya, Carolynne Cormack and myself. Check out the website (www.emugs.org) and register on the website ASAP, and bring some non-Monash friends!
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