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A number of you have asked for a recap on Dr. Hollander’s approach to treating NSTE ACS. You can download the audio from his talk on the Conference website. I’ve gone through it again and have some citations below. His talk is indeed guideline-based (all from the ACC/AHA 2007 NSTEMI / UA guidelines — familiarize yourself with their classes of recommendations and their grading the level of evidence) but also this portion of his talk was explicitly featured in a pharmaceutical-industry sponsored event. So, as always, approach this with a skeptical mind, and please share your findings in the comments section:

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So, lots of big things were discussed today, but I’m going to focus on Dr. Judd Hollander’s talk, as it was crammed with insight on a very common problem – achieving disposition on the 8 million patients we seen annually with chest pain (this is national, not just Sinai). Of these 8 million, 3 million are sent home and so we admit 60-65% of chest pain, of which only 15% have real disease… Cardiologists hate us for this, but is there an alternative? What’s the evidence behind what we do?

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Today’s simulation led to a discussion of the optimal therapy for treatment of the acutely dyspneic, diaphoretic, tachycardic, hypertensive distressed patient with acute pulmonary edema. After discussing the routine medical therapies — nitro SL, nitro gtt, ACE inhibitors, and furosemide — the discussion turned to the role of non-invasive ventilation (NIV).

It is no longer thought to be controversial that a trial of NIV is a crucial intervention for patients presenting with acute pulmonary edema prior to committing to endotracheal intubation (assuming that the patient has the mental status to tolerate NIV). The controversy lies in which modality of NIV to use — continuous positive airway pressure (CPAP) vs. bilevel non-invasive positive pressure ventilation (NIPPV), commonly referred to by the proprietary name BiPAP®.

Theoretically, it seems that BiPAP would be superior to CPAP since in addition to the basal positive pressure of CPAP which helps to stent open alveoli prone to collapse due to the weighty edema filling the lungs, there is an augmentation with positive pressure during inhalation to reduce the work of breathing. It would seem to follow that BiPAP would likely be superior to CPAP in reducing rates of intubation and possibly even mortality, while both modalities would be superior to just oxygen alone as they prevent derecruitment of alveoli.

Numerous trials have studied whether NIV is superior to oxygen alone when used to augment medical therapy for APE. Recent meta-analyses in JAMA (PMID: 16380593) and Critical Care (PMID: 16646987 and 16569254) have concluded that both CPAP and BiPAP are effective in the treatment of acute pulmonary edema with respect to the endpoints of mortality and subsequent need for intubation. However, all three meta-analyses find that BiPAP is not superior to CPAP with respect to either of these two endpoints.

All three articles make mention of a 1997 comparison study of BiPAP and CPAP by Mehta, et al. published in Critical Care Medicine (PMID: 9142026) which was terminated after interim analysis indicated that the patients randomized to the BiPAP arm of the study suffered greater myocardial infarction rates than those receiving CPAP (71% vs 31%). The articles mention that subsequent studies have failed to show this disparity and that the numbers in this trial we very small. Despite these assurances, none of the authors’ conclusions recommend a strategy of BiPAP over CPAP in lieu of the fact that the “physiological benefits [of BiPAP] did not translate into primary outcomes.” (JAMA). The JAMA article goes on to conclude that

the question of whether one technique offers advantage over the other and what subset of patients would benefit more with either one of these techniques remains unresolved.

The first of the Critical Care articles concludes that CPAP should be the NIV of choice because “from a practical point of view CPAP has been shown to be cheaper and easier to use” while the second recommends whichever modality is available.

ACEP also weighed in on this controversy in early 2007 when it published its Clinical Policy on patients presenting to the ED with acute heart failure syndromes. ACEP recommends the use of CPAP as a level B recommendation and downgrades the use of BiPAP to a level C recommendation citing the possible increase in myocardial infarction in conjunction with the lack of observed benefit over CPAP in the two main endpoints, mortality and reduction in the need for intubation.

Bottom line: It’s the smart and safe move to favor CPAP over BiPAP unless and until BiPAP is shown unequivocally to be more effective than CPAP with similar safety profile.

During cardiology conference one of the senior cardiology fellows mentioned that we have seen several cases of patients presenting with new right bundle branch block in the setting of acute MI who had complete arterial occlusion requiring coronary reperfusion (PCI or thrombolytics). While the traditional teaching is that new left bundle branch block in the setting of a clinical presentation suggestive of myocardial infarction mandates immediate reperfusion therapy, the point was made that a new RBBB may also suggest significant myocardial infarct territory, and coronary reperfusion in this setting should be considered.

This reminded me of a conversation I had a few years ago about guidelines for coronary reperfusion in the setting of ACS. The gist of that conversation was that only 1 of the major societies that issues these guidelines suggests consideration of a new RBBB for immediate reperfusion — ACEP.

I pulled the major guidelines to determine why they differed on this issue, and more importantly, why ACEP felt it necessary to broaden the indication for coronary reperfusion to include new RBBB. The first thing to note is that ACEP certainly does not enthusiastically endorse reperfusion therapy in the setting of RBBB given that it is given only a level C recommendation (based on preliminary, inconclusive, or conflicting evidence or expert opinion). Here is their rationale as quoted from the ACEP Clinical Policy:

…only 6 of the 9 trials included in the FTT analysis included BBB as an entry criteria and none of these studies made a distinction from right, left, or atypical, and from new or old. There were only 2,146 (4%) patients with BBB out of a total of 58,600 patients. In this undifferentiated group of BBB, mortality was 18.7% in the fibrinolytic treated patients versus 23.6% in controls…Due to the relatively small number of these patients included in the FTT report, it suggests that these patients with undifferentiated BBB most likely had symptoms strongly suggestive of AMI in order to be enrolled in these clinical trials. Studies since the FTT report have failed to clarify this issue, and it has become commonplace for clinical trials in AMI to either exclude all BBB patients or to include only patients with new or presumably new LBBB as one of the entry criteria.

In essence, ACEP concludes that the FTT analysis (PMID: 7905143) reviewed trials in which the BBB included was undifferentiated, and given that those patients did better with reperfusion therapy and that more recent trials exclude patients with RBBB, evidence is inconclusive to support excluding patients with new RBBB from consideration for reperfusion therapy. Given the acknowledged evidentiary weakness of the this claim, it is given a level C recommendation.

Reviewing the AHA/ACC Practice Guidelines and the European Society of Cardiology Guidelines, there is consensus recommendations on the use of reperfusion therapy for new LBBB or ECG-demonstrated STEMI. The AHA/ACC guidelines do not ever mention the case of new RBBB, and while the ESC guidelines mention the same shortcomings (patients with undifferentiated BBB) in the data reviewed in the FTT analysis, they stop short of recommending consideration of reperfusion therapy for new RBBB (at least in the text, although there is an ambiguous chart on page 38).

The bottom line is that ACEP has put this into a clinical policy which may hold medicolegal weight, although in clinical practice the entire controversy may be moot. This is because unlike in a LBBB, it is still possible to decipher true, ischemic ST elevations in the setting of a RBBB. Thus patients with new RBBB resulting from complete occlusion of a coronary vessel will have ST elevations that should be interpretable despite the right bundle and therefore qualify for reperfusion based on that well-accepted criteria.

There is a new article in JAMA published this week that attempts to make estimates for the risk of development of malignancy in patients as a result of a single coronary artery CT scan (CTCA) for evaluation of possible coronary artery disease. The is an especially prescient article for emergency medicine physicians given the large number of chest pain complaints that present to EDs and also specifically at our institution since we have now started to perform this test (not to mention that one of the co-authors of the paper is based at our medical center).

Briefly, the paper uses statistical risk modeling (called the Monte Carlo method, more about that later) to make estimates about the risk of development of malignancy as correlated with the level of radiation exposure from each of 4 different type of CTCAs and the age of the patient when the scan was done. Unsurprisingly, the risk of cancer development increased the earlier that the scan was done, but somewhat surprisingly the curve was quite concerning for patients dosed with radiation early in life. Particulary concerning were young females (20 years old) who had twice the RR and thrice the RR of their 40-year old and 60-year old counterparts, respectively, for the development of cancer during their lifetime.

Regarding the statistics, what is interesting is the Monte Carlo method was used for statistical modeling. This is the same mathematical modeling used for risk modeling in the insurance and financial industries, and the results bear striking resemblance. Much as the power of interest compounded over time is the great wealth creator, it seems that the effect of early radiation compounded over time is similarly potent for causing malignancy in later life.

This study is certainly limited in that it studied no real patients and simply extrapolated data from mathematical models. Further the authors did not compare this test with others that may employ similar or slightly lesser amounts of radiation. That being said, it should give pause that all the imaging that is ordered is not without risk, and even if that risk is small for the individual, the population-based risk — given the fantastic numbers in question — is not small indeed.

Ordinarily I like to write a conference follow up on the same day as conference to review clinical information or research relevant to the topics that were covered that day. Yesterday, however, I was working overnight and just didn’t have the time to put anything together. As fate would have it, I saw something during that very shift that was very apropos to our cardiology board review. There is no better way to learn something in medicine that to review it and then see it clinically, which is what happened in this case.

As you may recall, I mentioned numerous times during the board review that a new left bundle branch block in patients with no prior EKG and symptoms of acute coronary syndrome should be treated as an STEMI and receive treatment with thrombolytics or mobilization of the cath lab (owing to journal club yesterday, I’ll say either-or since we all seemed to agree that doing both is not yet supported by the evidence).

Well, at the end of my shift, a 58 yo smoker with DM and HTN happened to come in with chest pain and SOB for the last 75 minutes upon awaking. The pain was in the left chest without radiation, pressure-like. Vital signs were HR 120, BP 176/98, O2 sat 100% on RA, RR 18. The initial EKG while having pain was:

Note the LBBB with the wide QRS, notched R waves in I, V5, V6 with deep S waves in the early precordium V1-V3. The patient denied prior history of heart disease or myocardial infarction and had never been to this facility before. At this point, the patient was moved into the Resus area and the cardiac cath team was called. Aspirin, beta-blocker, and nitro were administered. Shortly thereafter, the patient reported being pain-free. A repeat EKG was obtained:

Whoa!?! What is going on here? Where’s the bundle? Is this the same patient? If it is, this would seem to be reassuring since the pain is now gone and the left bundle has resolved. Just get two sets and stress or even send for follow up as an outpatient, right?

Actually no. This is what is known as having “dynamic EKG changes” and is very concerning and would seem to indicate that the LBBB is indeed new and is related to a dynamic lesion in the heart. Presumably, the pain and LBBB resolved because the 100% stenosis auto-lysed (or maybe with the help of the aspirin) and the patient’s underlying, native rhythm can be seen on the second EKG. So this is worrisome and indicates that this patient should be evaluated urgently for a critical lesion. In this case, the cath was performed and the patient was found to have a single-vessel coronary disease with 60-70% stenosis in the LCx. Again, presumably no 100% lesion was found in any vessel owing to the pre-cath lysis of the clot which was causing the LBBB.

So in summary, new LBBB is bad and should be treated with the same urgency as an STEMI. It also highlights the importance of the repeat EKG. No matter how tedious it may seem, you can’t see dynamic EKG changes without repeats.

This month’s journal club presentation began with what I believe was a discussion of blood clots in Cro-Mags before touching upon late 19th century versions of CPR, the landmark closed-chest cardiac massage paper, and eventually, a comparison of ROSC (return of spontaneous circulation) in real patients vs. as seen on television. Chad then led the group in a discussion of a new meta-analysis by Xin Li et al appearing in a recent issue of Resuscitation (2006: Vol 70, pp31-36) on the topic of CPR with and without thrombolytics.

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