COMMENTARY

Three Must-Read Emergency Medicine Articles From 2017

Amal Mattu, MD

Disclosures

January 19, 2018

The 2017 calendar year had many outstanding articles focused on high-risk topics that directly relate to emergency medicine clinical practice. As in past years, I solicited my colleagues for their opinions on the best and most useful journal publications of the year. I received dozens of selections to consider that ranged from deadly conditions, such as myocardial infarction and stroke, to more benign everyday conditions, such as pharyngitis.

I narrowed the selections to articles that provided (1) practical, immediately useful recommendations and (2) would help critically ill patients in the emergency department (ED). Given the space limitations, I again have chosen only three articles.

I'll make the usual disclaimer that these are not necessarily the best articles from a methodological standpoint, but they are practice-changing and focus on high-risk conditions where lives are at stake. This year, I also chose articles that have not received much fanfare at conferences I've attended or on social media. My summaries will be brief, and I encourage readers to seek further details from the articles themselves to learn best how to incorporate the information into your clinical practice.

What were your favorite articles from 2017? Please tell us in the comments section.

Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial

We in emergency medicine no longer work in an environment where our intubated patients are whisked up to the intensive care unit (ICU) within minutes. Instead, we commonly find ourselves responsible for caring for these intubated patients in the ED for longer and longer periods.

As a result of this boarding, we have to come to learn that the provision of lung-protective strategies for mechanically ventilated patients is vitally important. Failure to provide appropriate ventilator management leads to increased in-hospital development of acute respiratory distress syndrome (ARDS), aspiration, and other ventilator-associated lung injury. This article, published in Annals of Emergency Medicine, nicely demonstrates just how important it is for emergency physicians to initiate lung-protective ventilation as early as possible.[1]

In this trial, Fuller and colleagues[1] incorporated a four-part protocol of postintubation interventions, including low tidal volumes (6-8 mL/kg predicted body weight), appropriate setting of positive end-expiratory pressure (generally 8-10 cm H2O, on the basis of body mass index), rapid oxygen weaning (while maintaining SpO2 ~ 90%-95% or PaO2 55-60 mm Hg), and head-of-bed elevation > 30 degrees. Plateau pressures were maintained to a goal of < 30 cm H2O. Patients who had the intervention were compared with a preintervention control group.

The result of the protocol was dramatic: Patients who received the lung-protective protocol had a reduction in development of ARDS and other ventilator-associated complications from 14.5% to 7.4%, and in-hospital mortality decreased from 34.1% to 19.6%. The protocol was also associated with a reduction in ventilator-free days, ICU-free dates, and hospital length of stay.

The study validates the critical importance of all emergency physicians practicing lung-protective ventilator management, and it once again demonstrates the influence that ED-initiated care has on subsequent hospital outcome.

Severe Hyperkalemia: Can the Electrocardiogram Risk-Stratify for Short-Term Adverse Events?

The obvious answer to the question posed in the title is "yes," but the actual ECG findings that predict adverse events are apparently not well known to many physicians. I was reminded of this fact repeatedly this past year, when I was sent three different cases to review in which patients had cardiac arrest due to hyperkalemia, and in none of the cases was hyperkalemia recognized on the initial ECG. The reason was simple: We all have been taught a myth that peaked T-waves are the most common and important finding on the ECG of a patient with hyperkalemia. In none of the three cases were prominent peaked T-waves present. Instead, all three cases had bradycardia that failed to respond to atropine or (in one case) pacing before arrest.

In this study, published in the Western Journal of Emergency Medicine, Durfey and colleagues[2] evaluated the ECGs of patients with hyperkalemia (potassium levels ≥ 6.5 mEq/L) over a 5-year period and correlated the findings with the occurrence of short-term adverse events (development of symptomatic arrhythmias, cardiac arrest, or death within 6 hours).[2] Short-term adverse outcomes occurred in 15% of patients, all of whom had abnormalities on the initial ECG, but the most common ECG finding of hyperkalemia in these patients was not peaked T-waves. In fact, peaked T-waves were found to have no correlation with short-term adverse effects. In contrast, the finding that was associated with the highest relative risk for an adverse outcome by far was bradycardia (heart rate < 50 beats/min) (relative risk [RR], 12.29), followed by junctional rhythm (RR, 7.46) and QRS prolongation (RR, 4.74).

Anecdotally, we have also repeatedly found that bradycardia is a very common finding in patients with critical hyperkalemia, and the presence of peaked T-waves is quite variable. These bradycardias are often irregular, lack P-waves, and appear somewhat bizarre. Furthermore, typical advanced cardiac life support (ACLS) recommendations for bradycardia (atropine and pacing) will frequently be ineffective in these patients.

The key point here is that physicians must remember hyperkalemia as a potential cause of bradycardia, and when ACLS is not working for these patients, remember to give calcium or sodium bicarbonate.

Use of Nitroglycerin by Bolus Prevents ICU Admission in Patients With Acute Hypertensive Heart Failure

My final choice of articles will probably be a source of controversy among some readers, because it is far from being outstanding from a methodological standpoint. However, the reason I chose this article is because it reaffirms a critically important treatment point in caring for the sickest of patients with acute hypertensive heart failure in the ED: very high-dose nitroglycerin is safe, well tolerated, and effective, but typically underused.

Traditional treatment of acute heart failure (AHF) includes intravenous diuretics and low-dose nitroglycerin either in topical or sublingual form. Even when nitroglycerin is used intravenously, it is often used as a very low-dose, essentially subtherapeutic infusion. At a recent international emergency medicine conference in Lisbon, I informally surveyed the audience and found that the majority of physicians were hesitant to use nitroglycerin infusions > 50 µg/min, and many of the physicians were even using nitropaste for preload reduction. Consider for comparison that sublingual nitroglycerin given every 3-5 minutes provides the equivalent of a nitroglycerin infusion of 60-80 µg/min. In other words, a nitroglycerin infusion < 60 µg/min is less effective than simply giving sublingual tablets. Topical nitrates provide erratic absorption and are even less effective.

In this study, published in the American Journal of Emergency Medicine, Wilson and colleagues[3] evaluated hypertensive patients presenting with AHF who were treated by traditional continuous infusion (which was generally 20-60 µg/min) versus very high-dose nitroglycerin, given as intravenous bolus doses of 2000 µg, repeated at the discretion of the treating physician every 3-5 minutes.[3] The majority (79%) of patients in this group received only a single bolus dose, although 14.6% received two doses and 4% received three or more doses. A third group of patients received the continuous infusion with additional intermittent high-dose boluses of nitroglycerin. The use of other heart failure therapies, such as diuretics, was similar between the groups.

The authors found that compared with low-dose nitroglycerin infusion therapy, patients receiving the intermittent bolus dosing of nitroglycerin had lower rates of ICU admission, a shorter hospital stay, and no difference in the risk for hypotension or any other adverse events. A reduction in 30-day readmission was noted as well.

Prior studies on this use of very high-dose nitroglycerin have also demonstrated reduced ICU utilization as well as lower rates of endotracheal intubation and myocardial injury.[4,5,6] This should come as no surprise when you consider that these very high doses of nitroglycerin not only provide extremely effective preload reduction but also afterload reduction and renal perfusion, thus allowing early improvement in cardiac output as well as diuresis.

In our practice at the University of Maryland's ED, we have not taken to using the bolus dosing of intravenous nitroglycerin, but instead we consider studies such as this as validating the safety and efficacy of being aggressive with nitroglycerin in hypertensive patients with AHF. Typical contraindications must also be considered (eg, recent use of sildenafil, critical aortic stenosis). Our typical starting dose of nitroglycerin infusions for these patients is 200 µg/min, and we feel comfortable titrating upward with a goal of 400-500 µg/min. Using this protocol, it has become extremely rare for even the sickest of our AHF patients to need intubation, and only the minority of them ever need an ICU admission. For others out there who give this a try, you too will find that your patients respond quickly and tolerate the medication well.

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