UMEM Educational Pearls - By Amal Mattu

As many as 1/3 of patients with proven ACS have no chest pain at presentation. Among the more common alternative presentations (anginal equivalents) are dyspnea, diaphoresis, nausea/vomiting, and syncope/near-syncope.

Note also that the absence of pain does not confer a better prognosis. The overall in-hospital mortality rate for patients with painless presentations is 13% vs. 4.3% for patients with chest pain.

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We've noted studies in recent years indicating that cardiac risk factors are ineffective at predicting the likelihood of ACS in patients with acute chest pain (in other words, it's all about the HPI and EKG!). Now there's evidence also that cardiac risk factors are ineffective at predicting in-hospital mortality in patients that rule in for acute MI. [1]  In fact, this study actually demonstrated that in-hospital mortality is inversely related to the number of cardiac risk factors!

The bottom line is simple: cardiac risk factors are useful at predicting long-term risk for development of coronary artery disease, but they are NOT useful at in the acute setting.

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Patients with ACS are often treated early with clopidogrel. However, if the patient with ACS appears to be developing cardiogenic shock, its probably best to withhold the early clopidogrel. The literature indicates that patients with cardiogentic shock benefit most from emergent PCI, and many of these patients will need CABG. Generally it's best to avoid clopidogrel in patients heading for CABG.

The use of clopidogrel in patients with cardiogenic shock can be deferred to the cardiologists in the cath lab once they decide whether the patient will need CABG or not.

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Feeling a bit guilty about over-eating during these holidays? Here's a study that might make you feel just a tad bit better about those extra pounds. (Just a tad.)

Auer and colleagues reviewed coronary angiograms of over 1000 patients and correlated them with body fat percentage. After statistical analysis, they found that body fat was not associated with the presence (or absence) or severity (size of coronary lesions) of atherosclerosis in men or women. Furthermore, the results did not differ based on age.

What's the takeaway point? Simple: go ahead and have that second serving of ham and eat that extra slice of cake!

[disclaimer: This study has not necessarily been reproduced, and is not intended to give free license to gorge after the holidays are done. It is fully expected that starting on January 2 you will immediately forget all of the above and renew your commitment to a healthy lifestyle consisting of a bland diet and P90X or Insanity workouts on a daily basis. But until then, forget the guilt!]

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There are a handful of conditions associated with a rightward axis on the ECG: left posterior fascicular block, ventricular ectopy, lateral MI (old), pulmonary hypertension (acute or chronic), right ventricular hypertrophy, hyperkalemia, misplaced leads, and toxicity of sodium channel blocking drugs, to name a few.

When you notice that the rightward axis is NEW compared to an old ECG, and there's nothing else on the ECG that's obviously diagnostic (e.g. hyperkalemia would also show peaked Ts; ventricular tachycardia would be wide complex and fast, etc.), in emergency medicine you should always think first and foremost of the following three possibilities:
1. acute pulmonary embolus
2. toxicity of a sodium channel blocking drug
3. misplaced leads

Pay attention to axis! Using the above rule can make rightward axis very simple and useful.

AM
 

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Minimizing interruptions in chest compressions during CPR is critically important. As an example of the adverse consequences of interruptions, consider the following finding from Edelson (Resuscitation 2010): for every 10 seconds of hands-off time during cardiac arrest, the patient's chances of successful return of spontaneous circulation decreases by 50% due to reductions in cerebral perfusion.

Next time you are involved in a code, keep this in mind, and do EVERYTHING POSSIBLE to minimize those interruptions in chest compressions.

 

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Right heart endocarditis is much more common in patients that are injection drug users. Fortunately for them, they have a lower mortality than patients with left heart endocarditis because they have a lower rate of developing heart failure. This is a reminder that the most common cause of death from endocarditis is heart failure.

Reasons for acutely elevated troponins
ACS
Acute heart failure
PE
Stroke
Aortic dissection
Tachyarrhythmias
Shock
Sepsis
Perimyocarditis
Endocarditis
Tako-tsubo cardiomyopathy
Cardiac contusion
Strenuous excercise
Sympathomimetic drugs
Chemotherapy

I guess that means that your history, physical, and clinical judgment still supersede the lab test.

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The 30-day mortality for patients < 65 years of age who are diagnosed with and treated for acute MI is 3%. In contrast, the 30-day mortality for patients > 85 years of age who are diagnosed with and treated for acute MI is 30%! Obviously the mortality is far higher if the patient's diagnosis is delayed or missed; or if the patient is not treated appropriately.

This simple statistic highlights the critical importance of being aggressive with diagnostic and therapeutic planning for elder patients with potential ACS. We cannot afford to be cavalier in their evaluation or treatment.

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Blood pressure cuffs tend to OVERESTIMATE true blood pressure in obese patients. Even larger cuffs tend to do this as well. While low blood pressures are often reliable in diagnosing shock, be wary of  assuming a "normal" blood pressure (e.g. SBP 100-120s) rules out shock in an obese patient who is sick. A-lines might be necessary to accurately assess the blood pressure.

[adapted from ACEP talk by Dr. Tiffany Osborn]

Today's cardiology pearl provided by EMS guru Dr. Ben Lawner. Consider this one if you are caring for a patient with what appears to be shock-resistant VFib.

An intervention that has its roots in the electrophysiology lab has now gained traction on the front lines of resuscitation: double sequential defibrillation. Prospective studies are currently underway to examine the feasibility of this technique. New Orleans (LA) EMS boasts several anectodal accounts of survival, with neurologically intact recovery, from refractory ventricular fibrillation. The next time you can’t stop the fibbing, consider this:

·       Apply TWO sets of defibrillator pads to the patient; one in traditional sternum/apex configuration and the other in anterior/posterior configuration

·       If ventricular fibrillation persists despite several shocks, coordinate the simultaneous firing of BOTH defibrillators

Some caveats:
This treatment is based upon EP lab data; each MONOPHASIC defibrillator was set at 360J. EMS services in New Orleans and Wake County (NC) have used two biphasic defibrillators, each set a 200J. There is not sufficient data to make any widespread recommendation, but the idea of double sequential defibrillation may be another tool in a limited ACLS bag of tricks for patients who simply cannot come out of V-fib. New Orleans EMS has initiated the double-defib protocol after four shocks, and Wake County’s protocol recommends initiation after five. Wake's protocol also recommends firing the defirbillators "as synchronously as possible."

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"Women experience higher mortality rates and more adverse outcomes after acute MI than men, despite less obstructive CAD and plaque burden."(1)

How can this be explained? It turns out that women have more frequent coronary remodeling of vessels. "Remodeling" refers to the concept that as plaques grow, they tend grow into the vessel wall causing outward bulging of the wall, rather than growing into the vessel lumen. That means that standard coronary angiography and even stress testing often miss significant lesions because they only evaluate lumen obstruction....which is not directly reflective of plaque size/burden.

The net effect of the above is that women are more likely to have false negative stress tests and angiograms that appear to show non-significant occlusions. Until we have reliable tests that evaluate true plaque burden rather than just vessel occlusion, we can't completely rely on stress testing and angiography to rule out the the presence of significant plaques.

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Elevated BNP levels are found in conditions besides acutely decompensated CHF. These conditions can include:
Older age
Renal failure
Severe sepsis
PE
Chronic CHF

These conditions will often produce BNP elevations in an intermediate range, but if the elevation is markedly positive, the acutely decompensated CHF is much more likely.

[adapted from ACEP speaker Matthew Strehlow, MD]

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ST depression in the right precordial leads can be anteroseptal ischemia, but it can also be a posterior STEMI. What are the clues to posterior STEMI?

• tall R waves in these leads is highly suggestive of posterior STEMI
• upright T-waves in these leads is also suggestive of posterior STEMI

Posterior leads (a couple of leads placed in the left mid-back area below the tip of the scapula) can help confirm posterior STEMI if there's STE in those leads. If there's no STE, call it just ischemia!

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Hostile behavior appears to be a predictor of ischemic heart disease and myocardial infarction. Prior studies have demonstrated this association, and now one more study has supported this. In short, researchers from Nova Scotia demonstrated that observed hostility was a predictor of ischemic heart disease and myocardial infarction (2-fold), independent of age, sex, Framingham Risk Score, and other psychosocial risk factors.

The key takeaway point of this fun, but validated concept, is that in addition to exercising and eating right, we all just need to relax a bit more. And the next time you have to deal with an angry consultant, just tell him to chill out or he'll die!

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Elderly patients in general have a lower baseline body temperature than younger patients. Consequently, it makes sense to redefine the definition of what constitutes a "fever" in the elderly. Rather than using the typical oral temperature cutoff of 38^o C (100.4^o F) for defining a fever, instead consider using 37.2^o C (99^o F). Redefining fever in this way increases the sensitivity for detecting bacterial infections from 40% to 83% while retaining an 89% specificity.

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A patient presents to the ED in pulmonary edema, hypotensive, and has JVD. There's a new systolic murmur. The patient had an acute MI 7-10 days ago and had appropriate treatment and uncomplicated course, then discharge. What's the diagnosis and what do you do?

Step 1: Sign out immediately.

Step 2: If it's not time to sign out (just kidding about step 1), listen carefully to the murmur. If it's heard best at the lower sternal border, it's probably a ruptured papillary muscle with acute MR. If it's a "machinery" type murmur heard throughout the precordium loudly, it's probably an acute VSD.

Step 3: VSD patient is likely to die, but with either one, you've got to move quickly. IMMEDIATELY call cardiology AND cardiac surgery. The patient is in need of a balloon pump and OR.
All you can do is buy time until the patient goes upstairs....pressors for BP, IV NTG as tolerated for preload reduction, and be judicious with diuretics. Vasodilators might help unload the heart also. This patient may end up on 2-3 drips, and make sure ALL meds are titrateable. And just keep your fingers crossed!

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SVT is rarely, if ever, the presenting rhythm associated with an acute MI. As a result, physicians should not feel compelled to send troponin levels and perform rule-outs purely based on an SVT presentation. Instead, the decision to rule out a patient presenting with SVT should be based on whether there is a constellation of other concerning symptoms, exclusive of the SVT (e.g. if the patient presented with chest pressure radiating down the arm and diaphoresis, in addition to the SVT).

Two recent studies confirmed that routine troponin testing in patients with SVT is extremely low-yield, and instead often produces false-positive troponin results that lead to unnecessary admissions and workups. In other words, mild troponin elevations may occur in SVT but they do not correlate with true ACS.

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Approximately 7-10% of cases of ACS are not related to atherosclerotic coronary disease. Some other causes of ACS include the following:
trauma
vasculitis
congenital abnormalities
emboli (e.g. bacterial)
thoracic aortic dissection
infectious diseases
DIC, TTP

These conditions can produce ST-segment changes that resemble those of true STEMI or non-STEMI, and therefore some of these patients are diagnosed retrospectively after a negative catheterization.

 

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If you're like me, you've been a bit confused about what exactly defines "coma" in the current recommendations for post-arrest hypothermia in "comatose" patients with return of spontaneous circulation. Fortunately, a recent NEJM article has helped clarify this by suggesting that hypothermia should be induced in these post-arrest patients with either:

1. GCS < 8
2. "patients who do not obey any verbal command at any time after restoration of spontaneous circulation and before initiation of cooling."

Naturally, if the patient was comatose before the arrest, don't bother.

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