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Tuesday, May 21, 2019

Successful Cardiac Arrest Resuscitation?
Congratulations, but You're Not Done


The goal of cardiac arrest resuscitation is to minimize downtime and obtain and support the return of spontaneous circulation. Once the heart is beating and the patient has at least a palpable blood pressure, most emergency physicians think their clinical tasks are essentially finished, congratulating themselves on a successful resuscitation.

But the next step should be an attempt to ferret out the cause of the cardiac arrest, obtain basic blood work, repeat the electrocardiogram, perhaps initiate hypothermia, consult cardiology, and expedite transfer to the coronary care unit. Other interventions, such as IV fluids, vasopressors, and antiarrhythmics, are occasionally required, but unfortunately, the long-term survival rate for out-of-hospital cardiac arrest patients with normal neurologic function is quite poor.

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Approximately 350,000 patients experience out-of-hospital cardiac arrest (OHCA) in the United States each year. (Circulation. 2018;137[12]: e67; They have a plethora of causes, some directly related to the heart but others with the heart as a target of other dysfunctions, such as cardiac arrest after pulmonary arrest. It may not be possible to determine the cause of cardiac arrest in the ED. Acute myocardial infarction is one common cause of OHCA, and this is more common in patients who have post-arrest cardiac arrhythmias, a new left bundle branch block, or an obviously abnormal ECG suggesting acute MI. Coronary angiography and revascularization are the standard of care for an acute MI, but the efficacy of these interventions is uncertain when performed in the absence of hard data confirming acute MI as the cause of arrest. Even when the cardiac arrest is due to myocardial infarction, it is not uncommon for the initial post-resuscitation ECG to lack obvious or classic findings.

A number of studies have attempted to clarify the role of acute cardiac angiography after out-of-hospital cardiac arrest, but this is a difficult concept to study with rigor. Data on pre-arrest symptoms or even a medical history and accurate downtime are difficult to obtain. Some studies of post-arrest cardiac catheterization have included in-hospital cardiac arrest or patients without definite evidence of acute MI on a post-resuscitation ECG. Another confounding variable is that an ECG suggestive of an acute MI post-arrest does not necessarily mean coronary occlusion, and a nonspecific ECG can initially be seen after a bona fide MI. Suffice it to say that acute coronary artery occlusion is poorly predicted by clinical and ECG findings in the immediate post-arrest scenario. Some studies have also considered an intervention within 24 hours similar to one performed immediately after resuscitation.

Read a fantastic recent article discussing these concepts in detail: Circulation. 2019;139[12]:e530;

Early Coronary Angiography and Survival after Out-of-Hospital Cardiac Arrest: A Systematic Review and Meta-Analysis
Khera R, CarlLee S, et al.
Open Heart.

This recent review addresses immediate cardiac catheterization to evaluate patients who have been resuscitated from OHCA. This intervention has been studied in some depth in the past, and it has generally been concluded that such early intervention is worthwhile and associated with improved long-term survival in those with an acute MI. Data and consensus on non-STEMI arrest are less robust, so the role of cardiac catheterization remains uncertain, though numerous articles of varying quality deal with the subject. These authors searched electronic databases from 1990 to 2017 that included early coronary angiography, defined as within one day of cardiac arrest, compared with a control group that did not have this intervention. The goal was to evaluate rapid cardiac catheterization with survival outcome. More than 8,000 studies were identified, but only 17 were selected for meta-analysis because of various exclusions.

The use of this early invasive strategy for patients with OHCA is a particularly difficult subject in resuscitated patients who are without obvious signs of ischemia on a post-resuscitation ECG. In fact, an immediate 12-lead ECG is unreliable in diagnosing AMI in resuscitated patients. False-positive and false-negative ECGs may be seen. And merely restoring myocardial perfusion does not necessarily mean better neurological outcome. Subjects were those resuscitated from OHCA who received cardiac catheterization within 24 hours of onset, particularly evaluating final neurological outcome. The control group did not undergo early cardiac catheterization, but they could have had the procedure more than 24 hours after cardiac arrest. The authors looked at in-hospital survival, 30-day survival, and in-hospital survival with favorable neurological outcome. Neurological outcome was evaluated via a modified Rankin scale and a cerebral performance category score, which are commonly used to assess neurological outcome at discharge.

Cardiac catheterization was obtained in 44 percent of the 14,972 patients with OHCA; 66 percent of patients did not undergo the procedure. The age range was 57 to 67, with a median age of 62. Patients with an initial shockable rhythm ranged from 26 percent to 100 percent. The rate of STEMI was 32 percent, but it ranged from zero to 100 percent. Cardiac catheterization was performed in about 18 percent of patients who did not have a STEMI on their presenting ECG.

The analysis demonstrated a statistically significant positive association from the use of early cardiac catheterization and survival to discharge, as well as survival with a favorable neurological outcome, though a wide range of variables were noted. Early cardiac catheterization in studies that only included patients with an initial shockable rhythm was associated with a twofold increase in the odds of survival to discharge and a 50 percent increase in the odds of a favorable neurological outcome.

The authors stated that patients with OHCA caused by an initial shockable rhythm, such as ventricular fibrillation, were more likely to have an MI as the underlying ideology and would have a greater benefit from cardiac catheterization. Likewise, they felt that patients with STEMI would also have a better outcome because this would include only those with treatable coronary lesions. This was not a randomized study, but the authors said their findings support early cardiac catheterization to improve survival in patients with OHCA.

Comment: I could not ascertain in this study if a stent or angioplasty was performed whenever angiography identified a discrete coronary lesion. I would assume so. I also could not figure out how patients were chosen to include only those with a presumed cardiac cause for their cardiac arrest, how many patients with non-STEMI were included, and whether post-cardiac arrest hypothermia was a concomitant intervention. The time from cardiac arrest to intervention was not discussed either. Nonetheless, it is the largest analysis to date, and it showed a favorable outcome for post-cardiac arrest.

Using cardiac catheterization immediately or within 24 hours for survivors of OHCA has been evolving since the 1990s. It does not seem that waiting 24 hours v. immediate cardiac catheterization makes much of a difference. Spaulding, et al., performed angiography on 84 consecutive patients who had no obvious noncardiac cause for the arrest; 48 percent had coronary artery occlusion. These authors treated all comers, and found that clinical evaluation and ECG findings were poor indicators of significant coronary artery occlusion. Twenty-eight percent of patients in this study had normal coronary arteries or clinically insignificant lesions. (New Engl J Med. 1997;336[23]:1629;

Cardiac catheterization following cardiac arrest for all subjects except those with obvious noncardiac causes (trauma, respiratory arrest) is an increasingly common intervention that is not reserved only for patients with obvious STEMI on post-arrest ECG. Some facilities perform catheterization for all patients with ROSC. Studies have shown that about 70 percent of patients with VF have significant coronary lesions upon catheterization regardless of post-arrest ECG. Some centers do angiography even for comatose patients when a cardiovascular etiology is suspected, performing cardiac catheterization in patients who are hemodynamically unstable.

It should be noted, however, that the results of cardiac catheterization in those without obvious acute MI on ECG have not been so impressive. (Intensive Care Med. 2015;41[5]:856, New Engl J Med. 2019;380[15]:1397; Dumas, et al., in the widening PROCAT registry found a culprit coronary lesion requiring angioplasty in nearly one-third of patients with OHCA without STEMI on ECG. In patients with no STEMI on post-resuscitation ECG, cardiac catheterization was associated with a nearly twofold increase in favorable outcomes. Note that a shockable rhythm was more highly associated with a culprit lesion that could be fixed by stenting. (JACC Cardiovasc Interv. 2016;9[10]:1011;

The role of cardiac catheterization post-recovery from OHCA is quickly evolving to the point where it is reasonably supported in all patients except those with an obvious noncardiac cause. The benefit of immediate cardiac catheterization rather than within 24 hours of arrest is unclear, but it appears reasonable that the emergency clinician should initiate contact with cardiology and the cardiac catheterization laboratory following resuscitation of all eligible patients.

This protocol is not widely disseminated and often not even considered in the ED once ROSC has been established. It is also unclear what to do in hospitals without cardiac catheterization capability, but immediate cardiac catheterization after ROSC has significant support in the medical literature, and organizing this may become yet another new task for first-line providers. Why not do it directly from the ED as we do with acute MI?

Dr. Roberts is a professor of emergency medicine and toxicology at the Drexel University College of Medicine in Philadelphia. Read the Procedural Pause, a blog by Dr. Roberts and his daughter, Martha Roberts, ACNP, PNP, at, and read his past columns at

Read InFocus and Earn CME!
Earn CME by completing a quiz about this article. You may read the article here, on our website, or in our iPad app, and then complete the quiz, answering at least 70 percent of the questions correctly to earn CME credit. The cost of the CME exam is $10. The payment covers processing and certificate fees.

Visit for more information about this educational offering and to complete the CME activity. This enduring material is available to physicians in all specialties, nurses, and other allied health professionals. Lippincott Continuing Medical Education Institute, Inc., is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Lippincott Continuing Medical Education Institute, Inc., designates this enduring material for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity. This activity expires May 31, 2021.

Learning Objectives for This Month's CME Activity: After participating in this CME activity, readers should be better able to identify which patients with out-of-hospital cardiac arrest should have cardiac catheterization.

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Friday, May 17, 2019

The Quixotic Quest to Control Atrial Fibrillation


Very little about the management of atrial fibrillation is an emergency, yet we in emergency medicine have embraced it as one. We gleefully bring to bear the full technological powers available to us to tame its irregular irregularity. Using this aggressive approach has proven that we are quite adept at controlling atrial fibrillation, discharging the majority of patients home in sinus rhythm. (Ann Emerg Med. 2017;69[5]:562;

But to what end?

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The recent publication of the RACE-7 trial by Pluymaekers, et al., highlights just how absurd and wasted our struggles toward sinus normalcy are. (N Engl J Med. March 18, 2019; doi: 10.1056/NEJMoa1900353.) The authors enrolled adults presenting to 15 EDs in the Netherlands with stable, recent-onset, symptomatic atrial fibrillation (defined as starting within 36 hours of presentation).

Patients were randomized to immediate cardioversion in the ED or a delayed approach. Those in the delayed strategy group received rate-controlling medication in the ED and were then discharged with a plan to follow up in 48 hours. Patients were assessed at 48 hours to determine if they remained in atrial fibrillation, and if so, they were sent back to the ED for immediate cardioversion.

The researchers randomized 437 patients over a four-year period, 218 to the delayed cardioversion group and 219 to the early cardioversion group. The cohort overall was fairly representative of patients who typically present to the ED for symptomatic atrial fibrillation. The mean age was 65, 40 percent were female, 44 percent presented with their first episode of atrial fibrillation, 64 percent had a CHA2DS2-VASc score of 2 or higher, and 40 percent were taking oral anticoagulants at the time of presentation.

Reversion to sinus rhythm occurred in 94 percent of the patients randomized to the immediate cardioversion strategy; 16 percent experienced spontaneous cardioversion and 78 percent underwent chemical or electrical cardioversion (37.9% and 40.2%, respectively). Ninety-eight percent of the patients in the delayed group achieved rate control in the ED: 71 percent with a beta-blocker, 2.3 percent with a non-dihydropyridine calcium-channel blocker, and six percent with digoxin. Rate control was achieved in 19 percent without the assistance of any medication.

Despite their almost-universal success in the early cardioversion group at achieving sinus rhythm prior to discharge, the authors observed no difference in their primary endpoint, the presence of sinus rhythm on the ECG recorded at the four-week visit, which was observed in 91 percent in the delayed cardioversion group and 94 percent in the early cardioversion group. This 2.9 percent difference met the authors' noninferiority margin of 10% (95% CI−8.2 to 2.2; P=0.005 for noninferiority).

The authors also did not find any difference in any of their secondary endpoints. Almost all the patients in both groups were discharged following the index ED visit. ED revisits for atrial fibrillation was seven percent in both groups. No differences were observed in the rate of cardiovascular complications, 10 in the delayed cardioversion group (including one with ischemic stroke and three with acute coronary syndrome or unstable angina), and eight in the early cardioversion group (including one with transient ischemic attack and three with acute coronary syndrome or unstable angina). Total median duration of the index visit was 120 minutes in the delayed cardioversion group and 158 minutes in the early cardioversion group.

Flaws and Insights
This trial is far from ideal. It compared an immediate approach to a slightly less emergent one, leaving us all wondering what they would have found if they had not attempted to control the rhythm at all. The primary endpoint—the number of patients in sinus rhythm at one month—holds no clinical meaning because, as we have known for some time, a rhythm control strategy does not lead to better outcomes.

Flaws aside, this trial does give us some insight into the true futility of our emergency endeavors for early rhythm control. Sixty-nine percent of the patients at the 48-hour follow-up visit had spontaneously converted without active cardioversion. This number would likely have been even higher if the authors had foregone delayed cardioversion in favor of a simple rate control strategy. The number of patients who experienced repeated bouts of atrial fibrillation over the first 28 days was also similar between the two groups, 30 percent and 29 percent in the delayed and immediate strategies, respectively.

No difference was seen in patients' quality-of-life scores, often cited as one of the major advantages of an immediate defibrillation strategy. Simply put, the majority of patients evaluated in the ED for stable, symptomatic atrial fibrillation will spontaneously revert to sinus rhythm by 48 hours. Immediate cardioversion had no effect on how often patients experience bouts of atrial fibrillation in the following 28 days, the number of patients in sinus rhythm at one month, and any patient-important outcomes.

Atrial fibrillation is a chronic disease with outcomes measured in years. Constraining its irregularities for the fleeting moments the patient is before us in the emergency department has minimal effect on patient outcomes or well-being. An immediate cardioversion strategy is a quixotic attempt to check a symptom that is not only incredibly difficult to control, but whose regulation has never been found to improve patient-important outcomes.

When viewed from this perspective, the futility of ED cardioversion seems obvious. It serves only as a distractor, diverting our attention from rate control and the appropriate use of anticoagulants, interventions that have proven benefits for patients' downstream health and well-being.

Dr. Spiegel is a clinical instructor in emergency medicine and a critical care fellow in the division of pulmonary and critical care medicine at the University of Maryland Medical Center. Visit his blog at, follow him on Twitter @emnerd_, and read his past articles at

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Tuesday, May 14, 2019

The Dumbing Down of Respiratory Support


Noninvasive ventilation and positive-pressure strategies for routine emergency management of patients with respiratory failure have revolutionized ED practice. The ability to provide effective and life-saving respiratory support without the need for endotracheal intubation stands as one of the most incredible technological advances in modern emergency medicine, but the brief and bastardized deployment of these devices has left room for refinement.

First described in 1936 when an intrepid English physician strapped an Electrolux vacuum to a patient with pulmonary edema (have no worry—he advised that "the machine should be run for a few minutes first of all to get rid of dust"), noninvasive ventilation (NIV) quickly evolved into widely available and portable continuous and bi-level positive airway pressure (CPAP or BiPAP) units placed in EDs and bedrooms across the country. (Lancet. 1936;231[5904]:981;

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Uptake was brisk, and NIV found routine use in the spectrum of respiratory failure in less than a generation. Unfortunately, the systematic and scholastic method with which we typically introduce new interventions was eclipsed by the ability to simplify and streamline NIV, and early reflective respiratory support quickly gave way to what is now a bromidic and benighted practice, a rush to BiPAP and a troublesome evasion of nuance in critical ventilatory support.

CPAP use in patients presenting with cardiogenic pulmonary edema saves lives. (Lancet. 2006;367[9517]:1155.) The positive end-expiratory pressure induced by CPAP reduces right and left ventricular preload, afterload, and cardiac transmural pressure without negatively affecting myocardial contractility, driving an increase in ejection fraction without increasing cardiac myocyte workload. (J Accid Emerg Med. 2000;17[2]:79; Contrary to the somewhat common misconception that NIV blows the water out of the lungs, the benefit of CPAP in patients with heart failure is largely from its actions on the Frank-Starling mechanisms, long forgotten and rarely considered in bedside practice.

The escalation to BiPAP involves oscillation between an inspiratory positive airway pressure (IPAP) triggered by the patient with a lower expiratory positive airway pressure (EPAP). The difference between IPAP and EPAP drives ventilation, and is responsible for relieving the work of breathing while decreasing elevated PCO2 in patients with hypercarbic respiratory failure. BiPAP is a critical intervention in patients with COPD, decreasing the need for endotracheal intubation in one of three patients and saving nearly as many from death or long-term morbidity. (Crit Care Med. 1997;25[10]:1685.)

The problem—and my objection—comes when the forest of ED respiratory support is lost for the trees of familiarity and simplification. The fundamental benefits of NIV modes have been seemingly forgotten, and patients with respiratory failure secondary to pulmonary edema are placed on BiPAP without hesitation in departments across the country. Sometimes the EMS-applied CPAP unit is even ripped off in favor of the ostensibly superior bi-level ventilation brought to the bedside. This practice, however, represents a dumbing down of respiratory support at a minimum, and might lead to worse outcomes for some of our most critical patients.

Small Benefits
One of the earliest trials comparing CPAP with BiPAP in patients with acute pulmonary edema was terminated early because of a higher rate of myocardial infarction in the BiPAP group. (Crit Care Med. 1997;25[4]:620.) A subsequent investigation suggested a trend toward higher mortality and organ failure rates in patients receiving BiPAP (Chest. 1998;113[5]:1339), and a trial nearly a decade later again hinted at higher rates of myocardial infarction in patients placed on BiPAP compared with CPAP. (Lancet. 2006;367[9517]:1155.)

The authors of a large and extremely well done systematic review and meta-analysis, however, reported no significant difference in patient-oriented outcomes between CPAP and BiPAP in patients with acute cardiogenic pulmonary edema. (Am J Emerg Med. 2013;31[9]:1322.) Close examination of the data, including visual inspection of forest plots and (an admittedly liberal) interpretation of the reported data, shows an undeniable pattern of CPAP outperforming BiPAP in nearly every category. At some point, statistical snobbery and cries of non-significance have to give way to a sober admission that CPAP likely holds small but difficult-to-parse benefits over BiPAP in patients presenting with acute exacerbations of heart failure and pulmonary edema.

But even if these benefits are vanishingly small—or so minute that they are all but insignificant in the dynamic clinical environment of the emergency department—the routine use of BiPAP in patients with pulmonary edema lacks face validity and data of efficacy. These patients simply don't need assistance in ventilation and elimination of PCO2, and the addition of IPAP/EPAP oscillations adds complexity without benefit amid recurrent signals of harm. Claims of improved patient comfort and tolerance lack any true supporting data, and the oversimplification of NIV in the ED to BiPAP for all comers represents an abdication of rational respiratory support, a devaluation and distortion of a technological marvel and bulwark of emergency medicine.

We are fortunate to be equipped with readily available tools that help us save lives. These powerful interventions are flexible and forgiving, but settling for a one-size-fits-all deployment of NIV ignores the subtlety and nuance that underlies its strength. The use of CPAP in patients with respiratory failure due to pulmonary edema represents a rational return to considered and individualized use of noninvasive ventilation, a refined approach with the potential for better outcomes for our patients.

Dr. Pescatore is the director of emergency medicine research for the Crozer-Keystone Health System in Chester, PA. He is also the host with Ali Raja, MD, of the podcast EMN Live, which focuses on hot topics in emergency medicine: Follow him on Twitter @Rick_Pescatore, and read his past columns at

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Tuesday, April 30, 2019

​Early Norepinephrine Has Potential in Septic Shock


Standard sepsis algorithms have suggested completing a fluid bolus before starting vasopressors in patients with septic shock, but multiple observational trials have shown an association between early vasopressor use and improved outcomes. (Resuscitation. 2004;62[2]:249;; Crit Care. 2014;18[5]:532;

CENSER was the first randomized controlled trial to examine this. (Am J Respir Crit Care Med. 2019 Feb 1. doi: 10.1164/rccm.201806-1034OC.) The researchers enrolled adults 18 and older with a mean arterial blood pressure lower than 65 mm Hg with infection as the suspected cause. Patients were excluded if they were in septic shock for more than one hour or had a stroke, an acute coronary syndrome, acute pulmonary edema, status asthmaticus, active arrhythmias, active GI hemorrhage, pregnancy, seizure, drug overdose, trauma, need for immediate surgery, or advanced staged cancer.


Patients were given norepinephrine (0.05 mcg/kg/min or about 3.5 mcg/min for a 70 kg adult) without titration for 24 hours or placebo (D5W). Both groups received protocol-driven sepsis management according to the 2012 surviving sepsis campaign guidelines, including antibiotics, crystalloid bolus, and source control. Fluid therapy was at the discretion of the treating physician. Open label vasopressors were added in both groups if a MAP >65 was not achieved after a 30 mL/kg fluid bolus.

The primary outcome was shock control by six hours, defined as a MAP >65 on two consecutive blood pressures 15 minutes apart plus adequate tissue perfusion, as evidenced by a urine output of 0.5 mL/kg/hr or a 10 percent decrease in lactate. The researchers included 310 patients.

These were sick patients, with an APACHE-II score of 20, a mean arterial blood pressure of 56, and a lactate of 2.8. The groups looked similar at the outset of the trial, but the norepinephrine group ultimately looked much better (76.1% vs. 48.4%; odds ratio: 3.4; 95% CI: 2.09–5.53; P<0.001). Their target MAP was achieved in 3.5 hours compared with 4.75 hours with placebo. Shock control was achieved at 4.75 hours compared with six hours with placebo.

Mortality was 15.5 percent with norepinephrine v. 21.9 percent with placebo (relative risk [RR]: 0.79, 95%CI: 0.53-1.11; P=0.15). There was less cardiogenic edema (14.4% vs 27.7%, p=0.004) and fewer new onset arrhythmias (11% vs 20%, p=0.03) in the norepinephrine group. All other adverse events, including gut and limb ischemia, were similar between the groups. Renal replacement therapy was required in 12 percent of the norepinephrine group and 14 percent of the placebo group (p=0.51).

Strengths and Problems
CENSER was an important trial. Current guidelines continue to emphasize relatively large volumes of crystalloid resuscitation before starting vasopressors, but fluids can cause harm. (Intensive Care Medicine. 2018;44[6]:925;; Anaesthesiol Intensive Ther. 2017;49[5]:323;

Two observational trials demonstrated an association between early vasopressor use and improved outcomes, including improved mortality, but observational trials are inherently limited by their various intrinsic biases. (Resuscitation. 2004;62[2]:249;; Crit Care. 2014;18[5]:532;

This trial had a number of strengths, including appropriate blinding and allocation concealment, the use of an intention-to-treat analysis, and complete follow-up of their patients. On the other hand, it was a single-center trial, and there were hints that practices are somewhat different in Thailand, potentially limiting external validity. The exclusions were also broad and might eliminate a large number of the patients I see with septic shock. Unblinding was likely because it is difficult to mask the jump in blood pressure when starting norepinephrine. They also used lactate clearance as a marker of shock resolution, but recent evidence showed this is not a great marker to guide sepsis resuscitation. (JAMA. 2019;321[7]:654; "Sepsis Update 2019." Feb. 21, 2019;

The biggest problem was that the primary outcome is not a patient-oriented outcome. Raising blood pressure is a monitor-oriented outcome that doesn't necessarily equate to patient-important outcomes. (Raising the blood pressure doesn't matter much if it comes at the expense of tissue perfusion.) They added markers of tissue perfusion, but it wasn't clear how important lactate clearance is. I can buy urine output as a reasonable surrogate, but at the end of the day, it doesn't matter at all to patients how much they are urinating in the ICU if it doesn't lead to better outcomes after they leave the ICU.

In this case, patient-oriented outcomes might have been better. The mortality number certainly looked better, although the trial wasn't powered for mortality, and the result wasn't statistically significant. It is reassuring that there weren't any of the serious side effects we worry about with vasopressors, but the trial was too small to be sure about potential harms.

One interesting note is that norepinephrine was run peripherally if a central line wasn't placed (which was the case in almost 60 percent of the cohort). One case of skin necrosis was found in each group, which is clearly not different. So we effectively have a small RCT of norepinephrine used through a peripheral IV to bolster the data we already had indicating that this is a relatively safe practice. (First10EM. May21, 2018;

It is also interesting to note the destination of these patients. Only half were treated in the ICU despite being in septic shock and each potentially being on a vasopressor. The rest were sent to the ward. Criteria for ICU admission were endotracheal intubation, need for renal replacement therapy, or need for invasive hemodynamic monitoring. We could be overusing ICU resources in Western settings, but this is an important difference that could limit external validity.

It isn't time to change sepsis protocols yet, but this was a promising trial. Early norepinephrine improved some disease-oriented outcomes in this RCT, and there were hints that this might result in important patient benefit. I will probably change my practice somewhat, reaching for norepinephrine a little earlier than I have been, but I will wait for the necessary large, multicenter RCT before suggesting this routinely.

Dr. Morgenstern is a community emergency physician currently practicing at Taranaki Base Hospital in New Plymouth, New Zealand. His blog,, is dedicated to resuscitation and evidence-based medicine and encourages skepticism and a mindset of constant questioning, humility, and scientific reasoning in medicine. Follow him on Twitter @First10EM.

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Tuesday, April 23, 2019

A Practice Changer for Cardioversion in Obesity


An emergency physician we know recently had a challenge. A very big challenge. Under the care of Akhila Pamula, MD, was a large man—6'5" and 500 pounds—who presented with palpitations. And diaphoresis. And a heart rate higher than 200 bpm, which surely contributed to him feeling a bit winded.

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Dr. Pamula was not quite sure of the rhythm, but knew it was fast and labile with runs of what could be ventricular tachycardia. She knew that this gentleman needed emergent cardioversion and that sedation would be a significant risk. She also knew that cardioversion can be difficult in obese patients, with historical failure rates of 10 percent and higher. (Europace. 2018. doi: 10.1093/europace/euy285; Europace. 2012;14[5]:666; Heart 2008;94[7]:884.)

The Evidence
What is the best approach to electrical cardioversion of atrial dysrhythmias in the obese patient? This is a growing and evolving area in the literature. Ramirez, et al., reported tremendous success across all body habitus of a four-step approach to cardioversion for atrial fibrillation (AF). (Europace. 2018. doi: 10.1093/europace/euy285.) Step 1: 200 J biphasic shock delivered using anteroposterior self-adhesive electrodes; step 2: 200 J shock with anterolateral configuration while applying pressure over the electrodes with disconnected standard handheld paddles; step 3: 360 J biphasic shock delivered using the same technique as in step 2; step 4, wild type: at the treating physician's discretion.

This protocol—the Ottawa AF cardioversion protocol, or OAFCP—was associated with a 99 percent (386/389) cardioversion rate, which was sustained in 91.4 percent and remained significantly improved compared with prior practice even when adjusted for confounding factors such as body mass index (BMI) and transthoracic impedance. Of note, a stunning 50 percent of their enrolled patients met the criteria for obesity with a mean BMI of 31.1 (+/- 7.5). The OAFCP protocol would seem to be a reasonable choice for morbidly obese cardioversion, but what about evidence specifically tailored to this demographic? You are in luck!

Voskoboinik, et al., compared shock success in obese patients (BMI ≥30) with persistent AF randomized to receive transthoracic synchronized biphasic direct-current cardioversion by handheld paddles or by adhesive patches. (J Cardiovasc Electrophysiol. 2019;30[2]:155; The superiority of paddles over patches after the initial shock of 100 J, then 200 J if needed, was remarkable—90 percent (56/62) v. 68 percent (43/63), respectively. The authors drew a sensible conclusion: "Routine use of adhesive patches at 200 J is inadequate in obesity."

Interestingly, the success in this study was unaffected by electrode location and vector (anteroapical v. anteroposterior), which contradicts other studies. This investigation included a substudy of manual pressure augmentation (MPA), where they found MPA to be 80 percent effective in 20 patients who had failed to respond to 200 J with patches and paddles. The MPA technique seems simple enough—apply manual force to the adhesive patches with gloved hands for cardioversion during end-exhalation. Furthermore, it was safe and caused no injury to the physician. The trial did not directly compare initial augmented patch use with initial paddle use, but one could reasonably argue that physicians who lack handheld paddles should start with patches and MPA at 200 J. This, however, awaits formal evaluation.

The Verdict
Back to Dr. Pamula's diaphoretic and tachycardic challenge. Given the uncertainty of the rhythm, she gave 12 mg adenosine, which briefly slowed his heart rate and demonstrated atrial tachycardia—P waves, some with different morphologies. Before long, his heart rate ramped back up, and he became more diaphoretic and, though his blood pressure was stable, it seemed unlikely that it would hold.

Sedation seemed risky, given his size and difficult airway assessment. After a brief shared decision-making discussion, the patient opted for cardioversion with light midazolam and a variation of manual pressure augmentation. Using 15 pounds of Zimmer sand bag weights rather than manual pressure to augment 200 J, Dr. Pamula brought the patient around to normal sinus rhythm with one quick shock. He was then loaded with amiodarone and sent off to the telemetry ward.

Immediate application of this clinical anecdote and recent evidence to practice is straightforward: With increasing BMI, anticipate increasing resistance to electrical cardioversion. Start with maximal biphasic joules and pressure augmentation to the adhesive pads, be it with paddles or gloved hands. One could consider weights as Dr. Pamula did, but be aware that this alternative technique has not been well studied and one may need upward of 80 newtons (20 pounds) to achieve an 80 percent reduction in transthoracic impedance. (Pacing Clin Electrophysiol. 2016;39[10]:1141;

It is worth knowing if your ED has paddle electrodes available. Unfortunately, the increasing use of adhesive patches has led to a reduction of accessory paddle purchases. The results of this trial, however, attest to the importance of retaining access to paddles for use in obese patients and those with other dysrhythmias refractory to patch electrodes. If the dysrhythmia proves refractory, consider adjusting the electrode placement and pretreatment with an antidysrhythmic medication before repeating direct-current countershock.

Intravenous ibutilide, for example, lowers the energy requirements for transthoracic cardioversion, assuming there are no contraindications. (CJHP. 2006;59[4]:201; Pretreatment ibutilide is a Class I recommendation with the support of level B evidence in the 2014 Guideline for the Management of Patients with Atrial Fibrillation by the American Heart Association, the American College of Cardiology, and Heart Rhythm Society. (J Am Coll Cardiol. 2014;64[21]:e1;

Dr. Vinson is an emergency physician at Kaiser Permanente Sacramento Medical Center, a chair of the KP CREST (Clinical Research on Emergency Services and Treatment) Network, and an adjunct investigator at the Kaiser Permanente Division of Research. He also hosts Lit Bits, a blog that follows the medical literature at Dr. Ballard is an emergency physician at San Rafael Kaiser, a chair of the KP CREST Network, and the medical director for Marin County Emergency Medical Services. He is also the creator of the Medically Clear podcast on iTunes. Read his past articles at Follow him on Twitter @dballard30.

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