cardiac literature 2008″>American Journal of Emergency Medicine (2009) 27, 481-491

Reviews

The cardiac literature 2008

Amal Mattu MD ^a,?, Michael C. Bond MD ^a, William J. Brady MD^b,?

^aDepartment of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA

^bDepartment of Emergency Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908, USA

Received 23 January 2009; revised 27 January 2009; accepted 28 January 2009

1. Acute coronary syndrome: evaluation

Body R, McDowell G, Carley S, et al. Do risk factors for chronic coronary heart disease help diagnose acute myocardial infarction in the emergency department? Resuscitation 2008;79:41-45.

The authors of this study evaluated 796 patients who presented to the emergency department (ED) with suspected cardiac chest pain. The patients were assessed for the presence of hypertension, hyperlipidemia, diabetes mellitus, tobacco smoking, and family history of early coronary artery disease. The patients were then evaluated in the hospital (primary end point) and at 6 months (secondary end point) for acute myocardial infarction (MI). Overall, 148 (18.6%) patients ruled in for acute MI at the time of admission.

The authors found that coronary atherosclerosis risk factor (CRF) burden was not useful in the diagnosis or exclusion of acute MI. Of the patients with no CRFs, 12.2% ruled in for acute MI. Furthermore, when patients did have CRFs, increasing number of CRFs did not predict an increased risk of acute MI. The authors did find that an increasing number of CRFs predicted an increased risk of 6-month death, MI, or need for urgent revascularization; but even this association was noted to be only a weak trend.

These results are similar those in a study published in the emergency medicine literature last year [1] and are further support for what has been stated in the 2007 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for the management of non-ST-segment elevation (non-STEMI) ACS [2]: in the ED evaluation of patients with possible ACS, the most important historical predictor that a patient will rule in for ACS is the history of present illness not the CRF assessment.

1. Acute coronary syndromes: electrocardiography

Tabas JA, Rodriguez RM, Seligman HK, et al. electrocardiographic criteria for detecting acute myocardial infarction in patients with Left bundle branch block: a meta-analysis. Ann Emerg Med 2008;52:329-336.

* Corresponding authors.

E-mail addresses: [email protected] (A. Mattu), [email protected] (W.J. Brady).

Traditional teaching in medicine had been that the electrocardiogram (ECG) was an unreliable tool in diagnosing acute MI in the presence of a Left bundle-branch block (LBBB). In 1996, however, Sgarbossa and colleagues

[3] published a set of 3 ECG findings that were predictors for acute MI in patients with LBBB. The sensitivity of these findings was low, but the specificity was sufficiently high that these “Sgarbossa criteria” were incorporated into a clinical policy for emergency reperfusion by the American College of Emergency Physicians (ACEP) as a level B recommendation [4]. The 3 Sgarbossa criteria [3] are:

ST-segment elevation greater than 1 mm concordant with the QRS complex (ie, the QRS complex points upward and there is STE) in 2 contiguous leads;

ST depression greater than 1 mm concordant with the QRS complex in leads V₁, V₂, or V₃ (ie, the QRS points downward in these leads, and there is also ST depression in any of these leads) in 2 contiguous leads; and

Excessive discordant STE greater than 5 mm (ie, the QRS complex points downward but rather than just a few millimeters of STE, there is greater than 5 mm of STE in those leads) in 2 contiguous leads.

Sgarbossa and colleagues found that the first 2 criteria had the greatest specificity, although the ACEP Clinical Policy included any of the 3 as sufficient to reasonably justify the decision to initiate Emergent reperfusion therapy. In fact, the ACEP Clinical Policy expands the second Sgarbossa criteria and suggests applicability when concordant ST depression is present in any lead, and expands the third Sgarbossa criteria and suggests applicability when discordant ST-segment deviation greater than 5 mm is present, regardless of ST elevation or depression. However, when other authors have studied these criteria, their conclusions have been variable. Therefore, Tabas et al decided to reevaluate the published studies pertaining to ECG findings in ACS and LBBB to come to their own conclusion regarding the utility of the Sgarbossa criteria.

The authors identified 11 studies with 2100 patients who met at least one of the 3 Sgarbossa criteria. The studies as a whole demonstrated that when one of the first two criteria were present, the specificity for acute MI was extremely high (98%) as was the positive likelihood ratio (7.9), but if only the third criteria was present, the range of reported specificities in the published studies was too variable to reliably rule in acute MI. Tabas et al also comment that the lack of any Sgarbossa criteria is insufficient to rule out acute MI.

0735-6757/$ – see front matter doi:10.1016/j.ajem.2009.01.038

Tabas et al also comment on a disparity regarding exactly where ST- segment deviation should be measured. In patients with narrow QRS complexes and exercise treadmill testing, ST-segment deviation is measured 80 milliseconds after the J point. However, the Sgarbossa criteria are based on measurement of the ST-segment deviation at the J point itself. Many of the studies do not standardize the location of measurement of the ST-segment deviation, and this itself can produce Interobserver variability [5]. To deal with this disparity, we propose the following as a reasonable summary or guideline to follow, based on the ACEP Clinical Policy and the Tabas study:

1. Emergent reperfusion is still indicated for a new LBBB (despite a

common as the degree of TWA grew more pronounced: 8.2% of patients with T-wave flattening, 13.2% of patients with TWIs 1 to 5 mm, and 19.4% of patients with TWIs greater than 5 mm had the adverse outcomes. Overall, 10.8% of patients with any TWA had the adverse end point. All of these numbers were statistically significant, and the associations persisted regardless of initial troponin values and also regardless of whether the patients had a prior history of known CAD. Interestingly, TWAs were predictive of adverse outcomes even when the TWAs were known to be old. The bottom line here is very simple–TWAs are positive predictors of adverse events at 30 days.

positive likelihood ratio reported in the literature of only 1.4) [6].

This recommendation remains a part of the ACEP Clinical Policy.

1. Emergent reperfusion appears to be indicated for patients with either of the first 2 Sgarbossa criteria. This remains a part of the ACEP Clinical Policy and is supported by the Tabas study. Given that the Sgarbossa criteria were established based on measurement of the ST- segment deviation at the J point, we suggest that this location for measurement continue to be used in patients with LBBB.
2. Emergent reperfusion for the third Sgarbossa criteria or for the ACEP Clinical Policy’s “expanded” Sgarbossa criteria 2 and 3 (see above) warrants strong consideration in patients presenting with a reasonably good story for ACS. Although this is not necessarily supported by the Tabas study, this does remain a part of the ACEP Clinical Policy.
3. The Tabas study’s discussion appropriately suggests that patients with previous LBBB should receive consideration for emergent reperfusion therapy based on high pre-ECG likelihood of acute MI (ie, medical interpretation of the presentation), whereas patients with intermediate or low pre-ECG likelihood “should undergo further ED testing such as serial or Continuous ECG monitoring, rapid troponin or other specific biomarker assay tests, or noninvasive testing such as echocardiography to further clarify their appropriateness for emergency reperfusion.”

Lin KB, Shofer FS, McCusker C, et al. Predictive value of T-wave abnormalities at the time of emergency department presentation in patients with potential acute coronary syndromes. Acad Emerg Med 2008;15:537-543.

Much literature and teaching in electrocardiography focuses on ST- segment changes and its predictive value for adverse outcomes in patients with possible ACS. T-wave abnormalities (TWAs), however, are often discounted as nonspecific or poorly predictive of prognosis. The authors of this study sought to evaluate whether TWAs could, in fact, predict adverse outcomes in patients presenting with chest pain or possible anginal equivalent presentations. Electrocardiograms were obtained as part of the standard initial evaluation of patients older than 30 years presenting with such symptoms. Patients were excluded if ST-segment changes, significant Q waves, prior MI, or bundle branch blocks were present on the ECG. The authors evaluated 5582 patient visits. T-wave abnormalities were recorded based on the presence of T-wave inversions (TWIs) or flattening in at least 2 contiguous leads. The researchers also evaluated whether the inversions were new vs old, and whether the TWIs were 1 to 5 mm in depth or greater than 5 mm. The primary outcome measure was the rate of Composite end points of death, MI, reperfusion (Coronary artery bypass grafting [CABG] or percutaneous coronary intervention [PCI]), or diagnostic testing consistent with coronary artery disease (CAD) (catheterization with at least 1 vessel demonstrating at least 50% stenosis or stress test showing reversible ischemia) within 30 days of initial presentation. When patients presented more than once, each visit was counted separately, but when multiple studies were performed, the outcome was only counted once.

The researchers found that 74.6% of patients had no TWAs, 12.9% had T- wave flattening, 11.8% had TWIs of 1 to 5 mm, and 0.64% had TWIs of greater than 5 mm. The composite end point was found in 5.7% of patients with no TWAs (which essentially served as a baseline for comparison). In patients with TWAs, the composite end point was progressively more

Szymanski FM, Grabowski M, Filipiak KJ, et al. Admission ST-segment elevation in Lead aVR as the factor improving complex risk stratification in acute coronary syndromes. Am J Emerg Med 2008;26:408-412.

In the appropriate clinical setting, the literature has indicated that abnormalities in lead aVR, when used in isolation [7] or in conjunction with other leads [8], are a strong predictor of left main coronary artery (LMCA) occlusion. Studies have shown the presence of simultaneous STE in leads aVR and aVL [9] or the presence of STE in lead aVR that exceeds the amount of STE in lead V₁ [10,11] is highly specific for LMCA occlusion in patients with ACS. Other literature has discussed STE in lead aVR in less specific terms, simply citing that this finding is indicative of either LMCA occlusion or left anterior artery occlusion [12,13], or indicative of either LMCA occlusion or triple-vessel disease [14]. The articles are not consistent with each other in terms of the magnitude of STE in lead aVR, which is considered significant. This difference may account for the varying specificities for LMCA involvement. Regardless, STE in lead aVR in patients with ACS is associated with more significant coronary occlusions. Patients with LMCA occlusions, left anterior artery occlusions, or triple- vessel occlusions have a worse prognosis, requiring more aggressive immediate therapy and often bypass surgery. Because many of these patients will require CABG, it may be advisable to consider withholding clopidogrel when STE is seen in aVR [10].

Szymanski and colleagues evaluated the association of STE in lead aVR with mortality. The investigators assessed 205 consecutive patients with non-STEMI ACS for STE in lead aVR of at least 0.5 mm. Patients were divided into 3 risk groups (low, intermediate, and high) based on their TIMI risk. One hundred fourteen patients (55.6%) had STE in lead aVR. The researchers found that the presence of STE in lead aVR was a strong and independent predictor of 30-day mortality (odds ratio, 7.8). During this 30- day period, 18 (8.8%) patients died. Of those who died, 16 (88.9%) of 18 had STE in lead aVR vs 98 (52.4%) of 187 of the survivors who had STE in lead aVR. They also found that the mortality increased with the severity of STE in this lead: 2 (2.2%) of 91 for patients without STE in lead aVR, 8 (10.8%) of 74 for patients with STE of 0.5 mm, 4 (13.8%) of 29 for patients with STE of 1 mm, 2 (22.2%) of 9 for patients with STE of 1.5 to 2.5 mm, and 2 (50%) of 4 for patients with STE of greater than 3 mm. This trend was statistically significant.

When taking into account the TIMI Risk stratification scores, the researchers discovered that patients with STE in lead aVR, as compared to patients without STE in this lead, had higher Death rates in the low-risk (5/27 [18.5%] vs 0/40 [0%]) and intermediate-risk (9/58 [15.5%] vs 1/39 [2.6%]) groups. The authors concluded that STE in lead aVR in patients with ACS was a strong predictor of short-term mortality and could be used synergistically with TIMI scores for early stratification of risk. Patients with ACS (including non-STE ACS) who demonstrate STE in lead aVR have more complex coronary lesions and will generally benefit from aggressive management and earlier invasive therapy.

1. Acute coronary syndromes: management

Melloni C, Alexander KP, Chen AY, et al. unfractionated heparin dosing and risk of major bleeding in non–ST-segment elevation acute coronary syndromes. Am Heart J 2008;156:209-215.

Heparin is not a benign drug–such a statement is not a secret. In fact, heparin is one of the most common drugs associated with in-patient complications. However, because we in the ED rarely see the in-patient complications, we may have a tendency to be less precise in the initial dosing, and this may lead to subsequent complications.

The authors of this study wanted to evaluate the incidence of complications associated with inaccurate initial dosing of unfractionated heparin in patients with non-ST-segment elevation ACS (NSTE ACS). They focused on the initial bolus and infusion rates in patients who were enrolled in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA Guidelines (CRUSADE) registry [15], a 420-hospital registry consisting of more than 30,000 patients with high-risk NSTE ACS. They included only patients who received UFH, had documented weights, and were not transferred out of the system, leaving 24 021 patients. At the time of admission of these patients (between January 1, 2004, through June 30, 2006), the standard recommenda- tions for dosing of UFH in NSTE ACS [16,17]) was 60 to 70 U/kg as an Intravenous bolus and 12 to 15 U/kg per hour as a maintenance infusion. Excessive dosing was defined as either an initial bolus dose greater than 70 U/kg or infusion rate greater than 15 U/kg per hour.

The authors found that 35% of the patients received excessive dosing of UFH. Of these patients, 25.7% of patients received an excess bolus dose only, 25.4% received an excess infusion dose only, and 48.9% received an excess bolus and infusion dose. There was an overall preference by many of the treating physicians to use the simple dosing of 5000 U bolus (given to 42.7% of patients) and 1000 U/kg per hour (given to 46% of patients), which are often regarded as maximum doses. However, even when these maximum doses were used, 19% of patients were excessively dosed. The 2 groups of patients who stood out as most frequent recipients of excess dosing were women and elderly patients. But one may ask, given that the inpatient physicians later adjust the UFH dosing based on partial thromboplastin times, does excess initial dosing really make a difference on subsequent complications? The answer, unfortunately, was “yes.”

The authors defined major bleeding as an absolute hematocrit drop of greater than 12% from baseline, Intracranial bleeding, retroperitoneal bleeding, or any bleeding that required red blood cell transfusion. Using this definition, patients who received initial excess UFH dosing had major bleeding 27.2% more often than patients who did not receive excess dosing (13.1% vs 10.3%), and they also had 35.5% higher in-hospital mortality (4.2% vs 3.1%). The increased complications held true regardless of whether or not patients received PCI or glycoprotein IIb/IIIa receptor antagonists. Excess bolus dose and excess infusion dose were both individually predictive of increased complications.

Any physician that is considering early administration of clopidogrel must consider the risks and benefits in a given patient and also understand the paradox in using this medication: (1) if you give it to low-risk patients, they are at risk for Bleeding complications but derive practically no benefit; (2) if you give it to moderate-to-high-risk patients, they seem to benefit but only if they do not require an urgent CABG within 5 days.

In 2005, Mehta and colleagues [21] performed an analysis of the 62 000- patient Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA Guidelines (CRUSADE) registry (a multicenter Registry of patients admitted for non- STE ACS in the United States) in an attempt to determine a set of characteristics present at the time admission that would reliably predict which patients would and would not end up needing CABG. Such a prediction rule would allow physicians to reliably know which patients could receive clopidogrel early without worry about CABG vs which patients should avoid early clopidogrel. In the end, the investigators were unable to reliably identify which patients would and would not need CABG based on admission characteristics.

The authors of this new trial attempted to do the same thing that Mehta and colleagues attempted to do. To do this, they evaluated the Superior Yield of the New Strategy of Enoxaparin, Revascularization, and glycoprotein IIb/IIIa inhibitors (SYNERGY) trial database. The SYNERGY trial was a large multicenter project including 9902 patients who were being evaluated for enoxaparin vs UFH; the patients received early invasive management and were all moderate-to high-risk non-STE ACS patients [22]. A total of 9053 patients were available for analysis, of which 19.1% (1728) underwent CABG. Of these, 56.3% (972, or 10.7% of all patients) received CABG within 72 hours of angiography. Overall, the investigators found no reliable way of predicting which high-risk patients with ACS would need early CABG based on presenting characteristics.

The question, then, still remains, “Which patients in the ED should an emergency physician treat with clopidogrel?” It would seem most prudent to use clopidogrel only in settings in which noninvasive management is the norm (eg, very rural or international settings). If you work at a center that performs rapid frequent cardiac catheterizations, it makes sense to defer the use of clopidogrel to the cardiologist performing the catheterization. Once they visualize the patient’s anatomy, they can make the decision to either give the clopidogrel or to consult the cardiac surgeons for CABG. In addition, the ACC/AHA guidelines [2] do not provide any clarity to this question so it is best to discuss this issue with your admitting cardiologist because they often have their own preference.

1. Dysrhythmias

Emergency physicians should heed the following takeaway points.

First, although UFH dosing is certainly more convenient for us when we use the simple 5000-U dose, this common practice is dangerous to our patients. We need to dose UFH based on the patient’s weight. In addition, we all should be aware of the most recent ACC/AHA guidelines for NSTE ACS, which now recommend dosing of UFH at 60 U/kg (maximum, 4000 U) as an intravenous bolus and 12 U/kg per hour (maximum, 1000 U/h) as a maintenance infusion [2]. Second, be especially meticulous about dosing with women and with elderly patients. And finally, we should realize that the initial dose of UFH that we administer in the ED does have a significant bearing on the patient’s In-hospital prognosis.

Chew DP, Mahaffey KW, White HD, et al. Coronary artery bypass surgery in patients with acute coronary syndromes is difficult to predict. Am Heart J 2008;155:841-847.

Recent national guidelines for the early management of patients with both non-STE ACS as well as STEMI have emphasized the use of the potent antiplatelet medication clopidogrel [2]. Those guidelines, however, also indicate that clopidogrel should be withheld if CABG is anticipated to occur within 5 days because this therapy is associated with an increased risk of perioperative bleeding, increased need for transfusions, increased need for reoperation for hemostasis, and increased postoperative mortality [18-20].

Decker WW, Smars PA, Vaidyanathan L. A prospective, randomized trial of an emergency department observation unit for acute onset atrial fibrillation. Ann Emerg Med 2008;52:322-328.

As the population ages, the number of patients with Atrial fibrillation , including those with new-onset AF, will continue to increase. The traditional practice for patients with new-onset rapid AF has been to rate- control patients and admit them for further evaluation. Emergency department overcrowding and pressures to control costs, however, have been forcing physicians to consider ways of safely avoiding admission of such patients. Last year in this series, we discussed a protocol used in Ottawa to safely cardiovert patients with new-onset AF using procainamide [23,24]. The authors of this new study from Mayo Clinic propose the use of an observation unit protocol using electrical cardioversion (ECV) to safely cardiovert and discharge patients with new-onset AF.

Patients included in the study were adults presenting with AF of less than 48 hours duration without hemodynamic instability. The duration of the AF was determined by history (onset of symptoms). If there was any uncertainty regarding the duration, the patients were excluded. Other exclusion criteria included hemodynamic instability (systolic blood pressure [SBP] less than 90 mm Hg or heart rate greater than 130 beats/ min after attempts to Rate control), known intracardiac thrombus, class IV CHF, ejection fraction less than 30%, chest pain consistent with class IV

angina, acute MI within 4 weeks before AF onset, stroke or transient neurologic ischemic attack in the past 3 months, previous unsuccessful ECV of AF, or active medical problems other than AF (eg, unstable angina, pneumonia, transient neurologic ischemic attack, and stroke).

The authors randomized 153 patients (average age, 58 years) with new- onset AF to either the ED observation unit (75 patients) or routine in- hospital care (78 patients). Observation unit care consisted of ECG and continuous cardiac monitoring, chest x-ray, routine laboratory studies, and rate control with either a calcium channel blocker or ?-blocker. Rate control was defined as ventricular rate less than 100 beats/min at rest. Patient were then reassessed after 6 hours and if they were still in AF, they were sedated and electrically cardioverted and observed for 2 more hours. Those patients in sinus rhythm (SR) after the 2-hour observation period were discharged home with cardiology follow-up arranged within 3 days. They were given NO antidysrhythmic or anticoagulant therapy upon discharge. If patients were not successfully cardioverted or if they reverted back to AF during the 2-hour observation period, they were admitted to the hospital.

Patients receiving routine in-hospital care underwent similar initial ECG, x-ray, and laboratory investigations in the ED; they were rate-controlled with calcium channel blockers or ?-blockers; they were given anticoagulant treatment with a heparin infusion; and then they were admitted to a monitored bed. Further in-patient care was at the discretion of the treating physicians. Patients were followed up at 30 days and again at 6 months, and no patients were lost to follow-up. Of the 2 groups, 85% of the patients in the ED observation group converted to SR (and were discharged) compared to 73% of the routine care group. Among the ED observation group, 32% reverted to SR after rate-control and 51% ended up requiring ECV. Most notably, the average length of stay for the ED observation group was 12.6 hours (median, 10.1 hours) vs 50.1 hours (median, 25.2 hours) for the routine care group. The findings at follow-up were similar between the ED observation and routine care groups: AF recurrence, 11% vs 10%; return visits, 33% vs 35%;

and adverse events (MI, CHF, stroke, death), 0% vs 1%, respectively.

The authors do not purport that the observation unit protocol and ECV are necessarily better than routine in-patient care, given that conversion rates and follow-up ended up being approximately equivalent. The protocol clearly demonstrated, however, that their observation unit protocol and early use of ECV resulted in a shorter hospital length of stay and avoided

The authors of this trial from Oxford provide yet another blow to the use of amiodarone for stable VT. They retrospectively evaluated 41 consecutive emergency admissions for sustained, hemodynamically stable VT that were treated with bolus dose intravenous amiodarone 300 mg, the current recommended treatment according to the UK advanced life support practice guidelines. The average heart rate was 174 beats/min and average SBP was 112 mm Hg. Pharmacologic termination of VToccurred within 20 minutes in only 6 (15%) of 41 patients and within 1 hour in only 12 (29%) of 41 patients. The 1-hour success rate is especially important to notice as one of the supposed drawbacks of procainamide is that it requires a relatively long time to work–the infusion takes 30 to 45 minutes in most patients. Yet in this study, not only did amiodarone fail to work in most cases, but even when it did work it was not rapidly effective in most cases. Another purported benefit of amiodarone is that it is fairly hemodynamically stable. In this study, however, Hemodynamic deterioration requiring emergency direct current cardioversion occurred in 7 (17%) of 41 patients. Hemodynamic deteriora- tion in patients receiving amiodarone may actually not be surprising. The authors state, “…it is well recognized that intravenous amiodarone acutely depresses myocardial contractility and may cause haemodynamic deteriora- tion or even circulatory collapse in patients with VT.”

Before amiodarone is completely discarded, remember that this study only relates to the short-term use of amiodarone. Long-term oral use of amiodarone and also prolonged infusions over hours to days may still be effective in the suppression of recurrent hemodynamically destabilizing ventricular tachy- dysrhythmias. “Whereas chronic administration of amiodarone prolongs the action potential duration and refractoriness of ventricular myocardium, bolus intravenous administration exerts predominantly anti-adrenergic effects and is therefore unlikely to interrupt a macro-reentrant arrhythmia.” In other words, the short- and long-term mechanisms of actions of amiodarone are different, and amiodarone appears to work better when it is used chronically.

We probably will never know with complete certainty which is the best drug for Pharmacologic conversion of stable VT without large randomized blinded studies. However, the literature appears to favor procainamide–and recent cardiology guidelines support this as well [27]. Amiodarone, generally presumed to have a more rapid action and greater hemodynamic stability in the acute setting, actually appears to have neither of these benefits. We all should definitely be reacquainting ourselves with procainamide.

numerous admissions without any change in utilization of health care

resources during the 6 months of follow-up. This translates into saving money and saving Hospital beds for other patients.

As we have stated before in prior literature reviews [23] on AF, standard ED care for AF is changing. It is not going to be just “rate- control and admit” in the coming years. Emergency physicians will see an increasing push for patients with new “uncomplicated” AF to undergo ED or observation unit cardioversion protocols, followed by early discharge (make sure to review exclusion criteria).

Tomlinson DR, Cherian P, Betts TR, et al. 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.

Amiodarone has been touted as safe and effective for just about every dysrhythmia imaginable, especially ventricular dysrhythmias. It turns out that the recommendations for use of amiodarone in Ventricular tachycardia are actually based on “expert” opinion, not on actual evidence. For readers of this forum over the past couple of years, you will recall a study published in Annals of Emergency Medicine [25] which demonstrated that amiodarone’s success rate in converting stable VT was only 29%. The accompanying editorial [26] indicated that the inclusion of amiodarone in the AHA guidelines was based on old studies indicating that amiodarone was only 40% to 60% successful in terminating VT. Based on this type of evidence, the AHA, the ACC, and the European Society of Cardiology (ESC) developed new guidelines in 2006 recommending procainamide as the preferred antidysrhythmic for patients with stable monomorphic VT instead of amiodarone [27]. Procainamide appears to have a longer history of success, with conversion rates as high as 80% in a randomized study [28].

Gallagher MM, Yap YG, Padula M, et al. Arrhythmic complications of electrical cardioversion: relationship to shock energy. Int J Cardiol 2008;123:307-312.

Traditionally, guidelines regarding ECV of patients with atrial dysrhythmias have recommended starting with low energy (eg, 50 J-100 J) and increasing sequentially if initial shocks fail. This recommendation is largely based on fears that high-energy shocks might induce myocardial damage or induce ventricular fibrillation (VF). More recent guidelines have recommended initial shocks for AF with higher energy levels, but the guidelines still recommend levels as low as 50 J for atrial flutter and SVT

[29] because of the concerns noted above. These concerns, however, are not based on human data but rather on small-animal models using shocks of far greater energy levels than those used in humans. In one study, for example, dogs received shocks of 120 J/kg of body weight [30].

The authors of this study proposed that higher energy levels might actually be safe and perhaps more effective than lower energy levels. To evaluate this hypothesis, they collected data on shocks delivered to 1896 patients who underwent transthoracic ECV for various atrial dysrhythmias. In 2522 attempts at ECV, 6398 shocks were delivered, 1243 for atrial flutter or atrial tachycardias and the others for AF. They found that, overall, VF was more common after shocks of less than 200 J (5 of 2959 shocks at less than 200 J vs 0 of 3439 shocks at greater than 200 J; P b .05). Conversion of atrial flutter or atrial tachycardia to AF was also more common at less than 200 J (20 of 930 shocks at less than 200 J vs 1 of 313 shocks at greater than 200 J; P b .05). Sinus bradycardia or sinus arrest was an extremely rare complication (0.95%), unrelated to the energy used, and in no cases required emergency pacing. embolic complications occurred in 14 patients and were not related to the energy used either.

The energy levels noted above relate to monophasic defibrillators. For biphasic defibrillators, the guidelines for ECV of AF [29] suggest starting at 200 J, which is equivalent to monophasic shocks of 360 J. Because the authors caution against using monophasic shocks less than 200 J, they correspondingly caution against using Biphasic shocks of less than 100 J.

In the discussion, the authors actually make an interesting point, stating that “It has been shown that the initial use of a higher energy setting reduces the number of shocks required to effect [successful] cardioversion and in many cases [actually] reduces the total energy delivered” [31]. So it appears that higher energy levels are more effective and associated with slightly fewer complications, with the potential ultimately of less cumulative energy used [29].

1. Cardiac arrest

Sasson C, Hegg AJ, Macy M, et al. prehospital termination of resuscitation in cases of refractory out-of-hospital cardiac arrest. JAMA 2008;300:1423-1438.

High-speed transport of prehospital patients with lights and sirens has been shown to pose hazards for emergency medical services (EMS) personnel and the public [32]. Therefore, it makes sense to limit rapid transport to those cases in which the benefit to the patient outweighs the risk to the patient, health care providers, and the public. As previously discussed, resuscitation rates for prehospital cardiac arrest are generally reported as less than 10% [33]. Although it is true that our society favors making every possible attempt to save lives, there are scenarios in which resuscitation from CA is futile and the risk of transport outweighs the benefit.

The Ontario Prehospital advanced life support study group has recently proposed 2 rules for termination of prehospital resuscitation (TOPR) of victims of CA. The rules were derived from evaluation of their large CA registry. The first of the rules is intended for basic life support (BLS) responders who are equipped with an Automated external defibrillator [34]. The BLS rule suggests TOPR if 3 conditions are met: (1) event not witnessed by EMS personnel, (2) no AED used or manual shock applied in prehospital setting, and (3) no return of spontaneous circulation (ROSC) in prehospital setting. The second rule is intended for use by Advanced life support responders [35]. The ALS rule suggests TOPR if 5 conditions are met: (1-3) all of the BLS rule’s conditions, plus (4) arrest not witnessed by bystander and (5) no bystander-administered cardiopulmonary resuscitation performed. These criteria are summarized in Table 1.

Sasson and colleagues performed a retrospective evaluation of 5505 cases of prehospital CA that were part of a large registry drawn from 19 EMS agencies in 8 US cities to assess the validity of the BLS and ALS rules. Cases of CA had been excluded if (1) EMS personnel determined that arrest was due to a noncardiac etiology (eg, trauma, electrocution, drowning, or respiratory arrest); (2) prehospital resuscitation was not attempted based on other local EMS TOPR protocols (eg, Rigor mortis, lividity); or (3) the patient was younger than 16 years. The overall rate of survival to hospital discharge was 7.1%, similar to other prehospital data [33]. Emergency medical services personnel pronounced 947 patients (17.2%) dead in the field based on local EMS agency protocols. How did the rules perform?

Table 1 Rules for TOPR

BLS ALS

Event not witnessed by EMS Event not witnessed by EMS personnel personnel

No AED used or manual shock No AED used or manual shock applied in prehospital setting applied in prehospital setting

No ROSC in prehospital setting. No ROSC in prehospital setting

Arrest not witnessed by bystander No bystander-administered CPR performed

The BLS rule would have recommended TOPR in 2592 cases (47.1%). Seventy patients who met BLS rule criteria for TOPR survived to hospital admission and 5 (0.2%) survived to hospital discharge. Of the 5, 4 were documented as having Good neurologic outcome with a cerebral performance score of 1 (1 = “conscious, alert, able to work and lead a normal life). If the BLS rule had been applied, it would have terminated efforts in an additional 1645 cases, increasing the number of prehospital pronouncements from 17% to 47% (again, at the expense of pronouncing dead the 5 patients who ended up surviving to hospital discharge).

The ALS rule performed even more impressively. It would have recommended TOPR in 1192 cases (21.7%). Twenty-four of the patients who met ALS rule criteria for TOPR survived to hospital admission but NONE survived to hospital discharge. If the ALS rule had been applied, EMS personnel would have terminated efforts in an additional 245 cases, increasing the number of prehospital pronouncements from 17% to 22%. The overall results of the study are similar to the original Ontario Prehospital Advanced Life Support study group results: they demon- strated that of 776 patients for whom the BLS rule recommended TOPR, only 4 (0.5%) of patients survived to hospital discharge; [34] and none of the patients who met the ALS rule for TOPR survived to hospital discharge [35].

In the discussion section, these authors argue for implementation of the BLS rule in EMS systems despite the misclassification of the few survivors. They argue that the ALS rule is too conservative because it warrants transport for any patient in whom bystander CPR is initiated and that the 99.8% predictive value of the BLS rule is sufficient to accept. Our society may have a difficult time accepting this argument given that 4 of the 5 BLS rule misses ended up with outstanding Neurologic recovery. Perhaps we need to focus on adjusting the ALS rule so that bystander CPR alone does not mandate transport.

Regardless, it certainly seems sensible that all preHospital systems should adopt these or similar rules for TOPR. As the authors argue, there are many benefits: (1) reduced risk to EMS personnel and the public during high-speed transport, (2) decreased risk of occupational exposure to contaminated body fluids, (3) decreased pressure on overburdened EMS systems, (4) decreased pressure on overburdened EDs to provide care that is likely futile and allowance of ED staff to focus instead on patients who have greater odds of survival, (5) decreased admissions to Intensive care units of patients who have little chance of survival to discharge, and (6) decreased utilization of Health care resources and monetary funds.

Sayre MR, Berg RA, Cave DM, et al. Hands-only (compression-only) cardiopulmonary resuscitation: a call to action for bystander response to adults who experience out-of-hospital sudden cardiac arrest. Circulation 2008;117:2162-2167.

Last year we discussed a handful of articles that indicated that many victims of CA receive no CPR from bystanders [23]. A reason commonly cited for lack of bystander action, even when bystanders have been properly trained in CPR, is fear of performing mouth-to-mouth ventilations (MTMVs). Many laypersons and even health care providers fear disease transmission during MTMV, and there are additional concerns from laypersons regarding improper performance of the MTMV. As a result, they do not perform any CPR at all–and not surprisingly, these patients have poor outcomes.

In contrast, when bystanders perform chest compressions only, resuscitation outcomes are superior compared to when no compressions are performed, and in fact the outcomes are often equivalent to or even better than when full CPR (with MTMV) is performed. The fact is that most victims of CA have sudden VF, and these patients usually have normal oxygen saturations in the central circulation at the time of arrest. As a result, MTMVis probably not helpful for most arrest patients during the first several minutes before arrival of EMS. Furthermore, studies have also demonstrated that MTMVoften results in a slower compression rate and increases intrathoracic pressure, resulting in decreased preload, cardiac output, and coronary

perfusion. It is important to realize, though, that MTMV is clearly important for patients with prolonged CA, for pediatric arrest (which is usually due to respiratory causes), and for other suspected cases of respiratory arrest (eg, drowning, opiate overdose).

Given that compression-only CPR often produces reasonably good resuscitation rates and that the requirement for MTMV often results in no bystander CPR at all, the AHA has reevaluated its recommendations for public intervention in cases of CA. They acknowledge that further simplification of CPR instructions might encourage more bystanders to take action.

This document, “A Science Advisory for the Public from the American Heart Association Emergency Cardiovascular Care Committee,” clarifies the recommendation and reviews the most recent literature since the last set of AHA Guidelines for CPR and Emergency Cardiac Care were published in 2005. The recommendations and “call to action” can be summarized as follows:

• When an adult is witnessed to collapse, trained or untrained (in CPR) bystanders should activate EMS and provide high-quality compres- sions–push hard, push fast, and minimize interruptions of compres- sions. This intervention should be performed until an AED is obtained and/or EMS arrives.
• If a bystander is not trained in CPR, compressions-only CPR should be initiated until help arrives.
• If a bystander was previously trained in CPR and is confident in his or her abilities to provide full CPR with MTMV and minimal interruptions in compressions, then full CPR should be used with a 30:2 compression/ventilation ratio until help arrives.
• If the bystander is not confident in his or her ability to provide full CPR, then chest compressions-only CPR should be used until help arrives.

The document again emphasizes that “this ‘call to action’ does NOTapply to unwitnessed cardiac arrest [because of the unknown duration], cardiac arrest in children, or cardiac arrest presumed to be of nonCardiac origin.”

Kellum MJ, Kennedy KW, Barney R, et al. Cardiocerebral resuscitation improves Neurologically intact survival of patients with out-of-hospital cardiac arrest. Ann Emerg Med 2008;52:244-252.

Sanders AB. Progress in improving Neurologically intact survival from cardiac arrest. Ann Emerg Med 2008;52:253-255.

Cardiocerebral resuscitation (CCR) consists of 3 major parts: (1) Continuous chest compressions with no early ventilations pre- and postshock; (2) delayed intubation; and (3) early use of epinephrine (EPI). The concept of CCR, first developed in 2003 at the University of Arizona, is based on early concerns that we now know are true–that early ventilations contribute no increase in survival and may actually be detrimental because of decreased compression rates and elevated intrathoracic pressure, which results in decreased venous return to the heart.

The authors of this study from rural Wisconsin report on 3 years of data before and 3 years of data after initiation of CCR for out-of-hospital CA. Emergency medical services personnel responding to the scene would initiate 2 minutes of chest compressions before the first Rhythm analysis. If the initial rhythm was “shockable” (ie, VF or pulseless VT), the patient would get 1 shock (maximum joules) followed by 2 more rounds of compressions with additional Electrical shocks before receiving any invasive airway management or assisted ventilation, and also before leaving the scene. If a second rescuer was present, he or she would provide an oral airway and oxygen via non-rebreather face mask only. In other words, if the initial rhythm was “shockable,” the patient received no airway intervention aside from face mask oxygen for the first 6 minutes. If a “nonshockable” rhythm was present, then intubation and positive pressure ventilation (rate, 8-10 per minute) was initiated after the initial 2 minutes of compressions.

The authors separated the data into several categories: witnessed vs unwitnessed arrest, and “shockable” vs “nonshockable” initial rhythm. They also evaluated the neurologic outcome of the patients. A total of 268 patients were included from the initial 3-year period of time when standard CPR was performed, and 230 patients were included from the 3-year period after CCR was initiated. The first interesting point from the overall data was that if the patient’s CA was not witnessed and the initial rhythm was “nonshockable,” the patient never survived: 0 of 167 patients. In fact, even if the arrest was witnessed, if the initial rhythm upon EMS arrival was “nonshockable,” it was extremely rare that the patient survived: 2 of 108 patients. A patient’s best chance of survival was if the arrest was witnessed and the initial rhythm upon EMS arrival was “shockable.”

Among this “witnessed, “shockable” group, how did CCR compare vs CPR? Of patients receiving standard CPR, 18 of 92 (19.6%) patients survived vs 42 of 89 (47.2%) surviving patients who received CCR. Neurologic survival with good cerebral performance (alert, work, and live normal life with minimal deficits) was similar in terms of percentages for those who survived (14/18, or 77.8% of CPR patients; 35/42, or 83.3% for CCR patients). Looking at overall numbers, however, CPR resulted in 15% of patients surviving neurologically intact, whereas CCR resulted in 39% of patients surviving neurologically intact.

The authors of both articles suggest that waiting for new guidelines to be published every 5 years is not appropriate; we should use new strategies that make sense, such as CCR, as soon as possible.

Lloyd MS, Heeke B, Walter PF, et al. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation 2008;117:2510-2514.

Kerber RE. “I’m clear, you’re clear, everybody’s clear“–a tradition no longer necessary for defibrillation. Circulation 2008;117:2435-2436.

Significant changes have been made to AHA guidelines in recent years that emphasize the importance of minimizing interruptions in chest compressions. There is no question that rapid defibrillation is also a critically important intervention as well for patients with VF/pulseless VT. The 2005 AHA guidelines, however, have even deemphasized some of the traditional teachings regarding defibrillation of patients with VF/pulseless VT to maximize compression rate: (1) stacked shocks are no longer recommended in favor of performing only single shocks followed immediately by compressions; (2) defibrillation for patients with VF/ pulseless VT of unknown duration or of duration greater than 5 minutes is no longer recommended until after 2 minutes of chest compressions have been performed; and (3) pulse and rhythm checks immediately after defibrillation is no longer recommended until after 2 minutes of chest compressions have been performed. Given that compressions are generally interrupted during defibrillation, the act of defibrillation actually produces a temporary period of absent circulation during critical moments of pulselessness. But do the compressions really need to stop? If a rescuer is performing compressions during the delivery of the shock, is there really a danger to the rescuer?

The authors of this study decided to investigate whether rescuers really are at risk of harm with modern-day defibrillators. Thirty-nine patients who were undergoing elective cardioversion for AF/flutter or external cardiover- sion/defibrillation during electrophysiology studies were chosen for the study. Rescuers applied approximately 20 lb of downward force on the lower sternal area with their palms to simulate the compressions during the shocks. In addition, to simulate an inadvertent conductive contact between the patient and rescuer, a skin electrode was connected between the patient’s shoulder and the rescuer’s thigh. The external defibrillator used was Lifepak

12 biphasic defibrillator (Medtronics Physiocontrol, Minneapolis, MN 55432-5604, USA). Standard gloves were worn by rescuers and standard self-adhesive defibrillation pads were used.

Forty-three hands-on shocks were delivered in these 39 patients. Four shocks were applied at 100, 200, and 200 J, and 8 at 360 J. None of the shocks were perceptible to the rescuers. The authors also measured the

average leakage current flow through the rescuer’s body for each phase of the waveform and found it to be well below the allowable standards used for household and business equipment and also below the usual threshold for human perception. As an example, the authors cite that the average leakage current was below the average amount of current exposure from a home body fat monitoring scale.

The authors of the study as well as the editorial highlight some caveats to consider before acceptance of the findings. First, the rescuers wore gloves. Second, the shocks were delivered through self-adhesive pregelled pad electrodes. Finally, the authors used a biphasic defibrillator. Although these caveats are not necessarily applicable in most US settings, the editorial reminds us that handheld and monophasic defibrillators are still in use in many international and some US settings, and in some places gloves may not even be the norm. Nevertheless, the editorialist believes that the study should lead the AHA to consider a modification of the 2005 guidelines when gloves, self-adhesive pad electrodes, and Biphasic defibrillation is available. This study may very well support another important advance toward further minimizing interruptions in chest compressions.

Gueugniaud PY, David JS, Chanzy E, et al. Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation. N Engl J Med 2008;359:21-30.

Epinephrine has long been considered a standard drug for patients in CA, although there has never been adequate evidence that EPI, regardless of dose, increases survival to hospital discharge or produces a good neurologic outcome. Epinephrine’s ?-adrenergic effect should theoreti- cally produce mostly beneficial effects–increased diastolic blood pressure and improved coronary perfusion pressure. On the other hand, the ?-adrenergic effect would appear to be harmful–increased myocar- dial oxygen consumption and postresuscitation ischemia. Two research- ers, Lindner and Wenzel, then studied the use of vasopressin (VP) instead of EPI for CA. Vasopressin works via V₁ receptors in smooth muscle, which at high dosages produces Peripheral vasoconstriction much more than central action, resulting in the same type of beneficial effects of EPI but without the adverse ? effects. Studies in a pig model for CA confirmed this theory–VP was superior to EPI in terms of improved coronary perfusion pressure and vital organ blood flow, and it resulted in improved cerebral oxygen delivery, ROSC, and neurologic outcome [36- 39]. When the effectiveness of VP was studied in humans, it was found to produce no Survival benefit whether in or out of the hospital [40,41]. In one of these clinical studies [40], however, the authors conclude that when VP was combined with EPI in patients with asystole, it produced improved Survival to admission and hospital discharge. Notably, this benefit of VP was not found for patients with VF or Pulseless electrical activity , but only for asystole. Also, the surviving patients receiving VP tended to have a worse neurologic outcome.

And that leads us to the current study that randomly assigned victims of out-of-hospital CA to receive either 1 mg EPI plus 40 IU (40 IU is the standard dose) VP vs EPI and saline placebo. Subsequent dosages continued to be the same combination, depending on the group the patient was in. A total of 1442 patients received EPI and VP, and 1452 received only EPI. Overall, 80% of patients presented with asystole. There was no significant difference between the groups in terms of Survival to hospital admission, ROSC, survival to hospital discharge (1.7% vs 2.3%), 1-Year survival (1.3% vs 2.1%), or good neurologic recovery at hospital discharge among survivors (37.5% vs 51.5%; relative risk, 1.29; 95% confidence interval, 0.81- 2.06). Just like the study noted above, the use of VP appears to produce at least a trend toward worse neurologic outcome among the survivors, without improving overall survival.

There are now 2 consecutive large randomized studies that indicate that VP is associated with worse neurologic outcomes. Unless an even larger study clearly overturns the results of these 2 published studies, the use of VP should probably be abandoned. (Adapted from Mattu A. Should a moratorium be placed on the use of vasopressin for CA. From

Medscape, Emergency Medicine Viewpoints, January 2009: http://www. medscape.com)

Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med 2008;359:2651-2662.

The researchers performed a randomized, double-blind, multicenter (involving 66 EMS systems throughout Europe) trial of adult patients with witnessed out-of-hospital CA of presumed cardiac origin and with initiation of BLS or ALS care within 10 minutes of collapse. Patients received standard ALS according to international guidelines as well as either tenecteplase or placebo during CPR. resuscitation attempts were continued for at least 30 minutes after the study drug was given. Initially, all CA rhythms were included, but then after the first 443 patients were enrolled, the data and safety monitoring board recommended discontinuing enrollment of asystolic patients because of low survival. In the end, 1050 patients were enrolled (525 in each group) before the trial was terminated prematurely for futility. The researchers found no difference between the tenecteplase group or placebo group in terms of 30-day survival, survival to hospital discharge, hospital admission, ROSC, or neurologic outcome.

Although the findings suggest that thrombolytics are not effective in undifferentiated causes of CA, this should not be interpreted to mean that thrombolytics must be withheld in CA that is caused by specific conditions that are known to be responsive to thrombolytics. For example, patients with STEMI who develop CA have been shown to benefit in terms of 6- month survival and neurologic outcome when treated with thrombolytics [42]. But for routine, undifferentiated victims of CA, despite our best efforts to find advanced therapies that will save lives, it seems we just keep coming full circle back to the same inexpensive basic therapies that actually work: adequate chest compressions, early electrical defibrillation, and therapeutic hypothermia.

Kilgannon JH, Rberts BW, Reihl LR, et al. Early arterial hypotension is common in the Post-cardiac arrest syndrome and associated with increased in-hospital mortality. Resuscitation 2008;79:410-416.

One of the hot topics in emergency cardiology and resuscitation is the management of post-CA patients. The literature is increasingly focusing on the importance of oxygenation, glucose levels, body temperature, and early PCI for survivors of CA, and “post-resuscitation care” is now regarded as the “final link in the Chain of survival paradigm” for treating CA and saving lives [43]. An “early goal-directed treatment strategy for post- cardiac arrest syndrome” appears to be on the horizon. The authors of this study have possibly identified one more target for treatment in CA survivors: arterial hypotension.

The authors retrospectively evaluated 102 adult patients who had ROSC after nontraumatic CA. Patients were separated into 2 groups based on the presence of hypotension (arterial or cuff) within 6 hours of ROSC: group 1 consisted of patients who had 2 or more readings of systolic blood pressure of less than 100 mm Hg (the “hypotensive group”); and group 2 consisted of patients with 0 or 1 reading of SBP less than 100 mm Hg (the “nonhypotensive group”). The primary outcome was in-hospital mortality, and the secondary measure was rearrest within 72 hours of the initial ROSC. Overall mortality was 75%. The hypotensive group was composed of 66 patients (65%) of the total group and had a significantly higher mortality and rate of rearrest (83% mortality, 32% rearrest) compared to the nonhypoten- sive group (58% mortality, 11% rearrest). The authors used multivariate logistic regression to control for common confounding variables (age, arrest rhythm, use of induced hypothermia, prearrest functional status) and found that early hypotension was a strong and independent predictor of in-hospital death (odds ratio, 3.5). The authors also found that patients with distinct separate episodes of hypotension had the same mortality as patients who had

persistent hypotension.

The study has some obvious limitations, even despite the statistical accounting for confounders. It is impossible to know for sure in this retrospective study whether the hypotension contributed to the increased mortality or whether the hypotension was simply a marker of more ill patients. The authors also could not comment on “the impact of depth and duration of post-ROSC hypotension (ie, akin to a dose-response effect).” Nonetheless, this study adds to the work of other authors that have associated post-ROSC hypotension with poor outcomes, including death and multiorgan failure [44] and poor 6-month neurologic outcome [45]. These studies indicate that post-ROSC hypotension is an important determinant of outcome, and it stands to reason that aggressive early management of hypotension just might make a difference.

1. Syncope

Costantino G, Perego F, Dipaola F, et al. Short- and long-term prognosis of syncope, risk factors, and role of hospital admission: results from the STePS (short-term prognosis of Syncope) Study. J Am Coll Cardiol 2008;51:276-283.

Brignole M, Shen WK. Syncope management from emergency department to hospital. J Am Coll Cardiol 2008;51:284-287. (editorial accompanying article above)

The authors of this Italian study sought to answer 3 questions regarding Patients with syncope. (1) What are the risk factors for adverse outcome within 10 days? (2) What are the risk factors for adverse outcome within 1 year? (3) Does hospital admission favorably influence the outcome at 10 days and 1 year? To address these questions, they screened 2775 consecutive patients presenting with syncope at 4 EDs between January and July 2004. They excluded patients for whom diagnoses were confirmed in the ED that would have required admission regardless of the syncope (eg, acute MI [AMI], pulmonary embolism (PE), stroke). They also excluded patients with terminal diseases, those with nonsyncopal syndromes (eg, vertigo, seizures, coma, shock), and patients with presyncopal head injuries. Essentially, then, these were just patients with syncope of uncertain cause in the ED. (Note that this contrasts with many other studies of syncope patients, including the San Francisco Syncope Rule study, which tend to enroll almost any patient with syncope, even those with obvious ED diagnoses of deadly conditions [eg, AMI, PE].) They followed up the patients for “severe adverse outcomes” that included death, need for major Therapeutic procedures (CPR, pacemaker or implanted cardioverter-defibrillator insertion, ICU admission, and acute antiarrhythmic therapy), and early (10-day) readmission to the hospital. Electrocardiograms were obtained and considered abnormal if they had any atrial tachydysrhythmia, sinus pauses greater than 2 seconds, sinus bradycardia less than 45 beats/min, conduction disorders, evidence of prior MI or ventricular hypertrophy, or multiple premature ventricular contraction (PVC). A total of 676 patients were enrolled.

The authors found that a total of 41 patients (6.1%) who exhibited Severe outcomes within 10 days, 5 (0.7%) of whom that died. Of note, 4 of the 5 deaths occurred within 48 hours. On multivariate analysis, independent risk factors for severe adverse Short-term outcomes were (1) Abnormal ECG at presentation (which had the highest associated odds ratio at 6.9), (2) concomitant trauma (sustained trauma during syncope), (3) absence of preceding symptoms (ie, no prodrome of lightheadedness, palpitations, chest pain, etc), (4) and male sex. It is interesting to note here that this list of risk factors for short-term adverse outcomes minimally overlaps with Quinn’s San Francisco Syncope Rules [46]–the overlap only occurring in terms of ECG abnormalities as a risk factor. Independent risk factors for severe adverse long- term (from 11th day up to 1 year after ED visit) outcomes were age greater than

65 years of age, coexistence of neoplasms, cerebrovascular diseases, or ventricular dysrhythmias.

Did hospital admission have an effect on the prognosis? This query was clearly a more difficult question to answer because there is a clear bias in terms of admission of sicker, older patients: approximately half of admitted patients were older than 65 years and possessed more

comorbidities than discharged patients. On analysis, the authors found that within 10 days of syncope, the rate of the adverse outcomes was significantly greater in admitted patients (14.7%) than in discharged patients (2.0%). However, the 10-day mortality rate for admitted patients was not much higher in hospitalized patients (n = 3, 1.4%) than in discharged patients (n = 2, 0.4%), suggesting that the hospi- talization did in fact make a short-term difference in terms of mortality. On the other hand, the 1-year mortality in admitted patients was actually much greater (n = 32, 14.7%) than in discharged patients, suggesting that the admission did not help long-term outcome as much. The bottom line here regarding the role of admission is that “hospital admission seems to favorably modify the short-term prognosis of syn- cope possibly because of the promptly undertaken life-saving mea- sures,” long-term prognosis is much more dependent on age and comorbidities. This study also demonstrates that risk factors for short- term adverse outcome are markedly different than risk factors for long- term adverse outcome.

The accompanying editorial reviews this study, the San Francisco Syncope Rules, the 2007 ACEP Clinical Policy that we reviewed last year, as well as the ESC guidelines. They also discuss the Syncope Evaluation in the Emergency Department Study [47], which demonstrated that a syncope observation unit in the ED could be an effective method of providing rapid risk stratification and diagnosis of patients. The observation unit concept, while appealing, is limited by the availability of resources in most EDs: the proposed unit uses continuous cardiac monitoring for up to 6 hours, hourly vital signs and orthostatic blood pressure evaluations, and echocardiogram for patients with abnormal cardiovascular examinations or abnormal ECGs. Tilt-table testing, carotid sinus massage, and electrophysiology consultation were also available.

The ACEP Clinical Policy recommends hospitalization for patients who are risk-stratified to a high level, which includes (1) older age and associated comorbidities; (2) abnormal ECG, including ischemia, dysrhythmias, or significant Conduction abnormalities; (3) hematocrit less than 30% if obtained; and (4) history or presence of heart failure, CAD, or structural heart disease. Does that mean that anyone who does not meet any of these 4 criteria can be discharged? That answer is not provided.

The ESC guidelines “strongly recommend” admission (for diagnostic purposes; there are more recommendations for admitting patients for treatment purposes) if patients have (1) suspected or known significant heart disease, (2) ECG abnormalities suggesting dysrhythmic syncope, (3) syncope occurring during exercise, (4) syncope causing severe injury, and

(5) strong family history of sudden death. Unfortunately, the ESC guidelines then go on to broaden things even more by listing another set of criteria for which patients “occasionally” may need to be admitted. “Occasionally” is not particularly helpful. Does this statement mean that the emergency physician should use clinical judgment as the primary guide to disposition determination? If so, “what’s the point of these criteria if it will boil down to clinical judgment anyway?”.

The problem with all of these rules, guidelines, and policies is that they are so terribly broad and inclusive that it is doubtful that they increase our sensitivity for admitting patients who are going to have bad outcomes. In other words, it is doubtful that these recommendations tell us to admit patients who are destined for adverse outcomes that we were planning on sending home. Did you need a rule or policy to tell you to admit a patient presenting for syncope who is older than 65 years? Or a patient who has CHF? Or a patient who has an abnormal ECG? Or a patient who is anemic? It is also unclear whether these rules allow us to safely discharge patients who we were originally planning to admit. In summary, it is unlikely that these rules and policies are better than the clinical judgment of an experienced emergency physician who reads these cardiology updates. In the end, we believe that these rules and policies primarily serve 2 purposes: (1) to provide guidance to health care providers that are not experienced in managing patients presenting after syncope and (2) to reaffirm what most of us already do–apply clinical judgment in your medical decision-making. Nonetheless, such rules and policies provide a framework on which to construct one’s clinical judgment.

1. Congestive heart failure

Peacock WF, Hollander JE, Diercks DB, et al. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med J 2008;25:205-209.

A close review of the literature shows that there’s no good evidence to support the practice of treating heart failure patients with morphine, and there is mounting evidence to show that his practice is potentially dangerous. This article may be the strongest evidence against using morphine so far. The researchers retrospectively analyzed patients from the Acute Decompensated Heart Failure National Registry (ADHERE) registry (a large registry of patients admitted with decompensated CHF) and found 20 782 patients (14.1% of patients overall) that received morphine (compared to 126 580 patients–85.9%–that did not). There was no significant difference in the groups in terms of age, vital signs, renal function, hemoglobin, ejection fraction, AF, or other comorbidities. Morphine use was found to be an independent predictor of mortality. Overall, 13.0% of morphine patients died vs 2.4% of nonmorphine patients. Morphine use was also associated with an increased need for mechanical ventilation (15.4% vs 2.8%), increased days in the hospital (5.6 days vs 4.2 days), and increased need for ICU admission (38.7% vs 14.4%).

The lack of difference between the standard oxygen group and the NIV group cannot be explained by the fact that the patients were not that ill. The mortality rates (9%-10% within 1 week) suggest that these patients were, in fact, quite ill. Furthermore, the average admission heart rates (112-114 beats/ min), SBPs (160s), respiratory rates (32-33/min), and peripheral oxygen saturations (90%-91%) suggested that the patients were fairly ill at the time of arrival. The bottom line is that NIV did not harm the patients and did produce slightly more rapid subjective improvements, but NIV did not reduce endotracheal Intubation rates or mortality.

Although this study is not a total and complete support for NIV, it does report that the patient’s overall condition does improve with this intervention. Would you, the emergency physician, rather perform emergent endotracheal intubation on a patient with acute respiratory failure or, alternatively, do such in a semielective fashion? Furthermore, would you, the emergency physician, rather perform paralytic-assisted endotracheal intubation on a poorly perfused, acidotic, and hypoxic patient or, alternatively, provide the same intervention in a patient who has experienced improvements in systemic perfusion, acid-base status, and oxygenation? The answer to both these queries is self-evident.

1. Diagnostic testing

Although this study has the typical limitations of a retrospective study,

the researchers did a good job of accounting for many of these shortcomings. For example, to account for the possibility that morphine use may simply have been used in more ill patients, the researchers evaluated patient mortality after adjusting for admission blood urea nitrogen, admission creatinine, and admission SBP (the 3 factors that are most correlated with in-hospital mortality) as well as age, dyspnea at rest, chronic dialysis, heart rate, inotrope or vasodilator use, troponin level, ejection fraction, rales, and congestion on chest radiograph. They found that the morphine use remained associated with mortality across all risk groups, with odds ratios for mortality in the morphine group of 4.84 after all of these factors were analyzed. The researchers even considered the possibility that morphine may have been used as an adjunct for intubation so they repeated the analysis excluding all patients requiring intubation and still found that the use of morphine was associated with higher mortality (odds ratio, 5.75).

Gray A, Goodacre S, Newby DE, et al. noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med 2008;359:142-151.

Three recent meta-analyses [48-50] and a prehospital trial [51] have all suggested reductions in intubation rates and improvements in mortality when Noninvasive ventilation is used early in patients with cardiogenic pulmonary edema (CPE). The authors of this study conducted a prospective randomized trial of 1069 patients with cardiogenic pulmonary edema to see whether NIV truly does improve mortality and intubation rates in the short term (within 7 days) and also to evaluate if there was a difference between continuous positive airway pressure (CPAP) and Bilevel positive airway pressure .

A total of 367 patients received standard oxygen therapy, 346 patients received CPAP (5-15 cm H₂O), and 356 patients received BiPAP (inspiratory pressure 8-20 cm H₂O, expiratory pressure 4-10 cm H₂O). All patients received standard medical therapies (nitrates, etc) as well (groups were fairly equal in terms of the therapies they received). The authors found no significant difference in 7-day mortality between patients receiving standard oxygen therapy (9.8%) and those receiving NIV (9.5%), nor was there a difference in 7-day intubation rates (2.8% vs 2.9%, respectively). In addition, there was no difference in the combined end point of death or intubation within 7 days between CPAP (11.7%) vs BiPAP (11.1%). They did, however, note that patients receiving NIV had greater mean improvements at 1 hour in terms of patient-reported dyspnea, heart rate, acidosis, and hypercapnia. These metabolic differences were statistically significant although probably clinically irrelevant because they were small. No treatment-related adverse effects were noted.

Saenger AK, Jaffe AS. Requiem for a heavyweight—the demise of creatine kinase—MB. Circulation 2008;118:2200-2206.

Creatine kinase-MB (CK-MB) has been heavily relied upon over the years to make the diagnosis of acute myocardial infarction. However, over the years, the literature has dealt some major blows to the diagnostic utility of CK-MB, and now many cardiologists are calling for an end to the CK-MB era. Creatine kinase-MB and troponin (TN) are trading places as the cardiac biomarker of choice for patients with cardiovascular issues. The authors of this editorial provide the reasons. There are 81 references in this 4-page editorial. The interested reader should refer to the manuscript for the specific references; a summary of their comments follows:

• Troponin is now the preferred marker of all of the organizations that are involved in creating the major guidelines for AMI: the ACC, AHA, ESC, and National Academy of Clinical Biochemistry. The World Health Organization has also adopted TN, not CK-MB, into its definition for MI.
• Assays now detect TN elevations as quickly as they detect CK-MB.
• Troponin is predictive of in-patient and long-term prognosis in patients with ACS and non-ACS Cardiac conditions. The same is not true for CK-MB.
• In 10% of cases of ACS, CK-MB may be positive with a negative TN. However, the prognosis of these patients correlates with the negative TN, not with the positive CK-MB; so it appears that even in these cases, the presence of the positive CK-MB is not helpful.
• Troponin predicts infarct size as well as or better than CK-MB.
• Troponin is more cardioselective than CK-MB (although neither is perfect).
• Quality control of CK-MB assays is waning, perhaps partly because the industry also believes that there is little future in CK-MB. As a result, there is greater machine-to-machine variability in CK-MB values.
• Proper use of TN makes this test at least as useful, if not more, compared to CK-MB for detecting reinfarction and in evaluating patients post-PCI and post-CABG.
• Overall, CK-MB appears to increase costs without providing any additional diagnostic or prognostic benefit.

The authors argue that one of the main reasons that CK-MB is still around is because physicians have been so accustomed to CK-MB that they simply are unwilling to remove it. Creatine kinase-MB has certainly served its purpose well for many years. Perhaps now, however, it is time to allow CK-MB to enter retirement.

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