Cardiology, Improving Throughput, Mythbusting

Yes, No, and Maybe – Magnesium for Afib RVR

I really, really, wanted this study to work.  Few things are more disheartening on an overnight observation shift than needing to place someone on a diltiazem drip after an inability to rate control. Ergo, I have been known to give a few grams of magnesium to try to decrease the likelihood of that happening. Therefore, on the surface, this study seems promising – it looks at standard of care for Atrial fibrillation with rapid ventricular response (dealer’s choice, metoprolol, diltiazem, or digoxin) given in combination with either one of 3 treatments: placebo, 4.5g of magnesium, or 9g of magnesium; with about 150 patients in each arm. This study took 5 years (!) over 3 academic centers in Tunisia, who’s ED’s service 90,000-110,000 patients per year. Patients needed to have a heart rate over 120 bpm, have a systolic BP >90 mmHg, and without: renal impairment, wide-complex tachycardia, decompensated CHF, acute myocardial infarction, or an impaired level of consciousness. All seems fair.

The results, at face value, seem great if you’re a magnesium believer: rate control at 24h of 83.3% for placebo, 97.9% for 4.5g MgSO4, and 94.1% for 9g of MgSO4. This is a great example of completely reading a paper before you start to fight about giving magnesium.

First, all groups used digoxin around 50% of the time for rate control.  This clearly does not mimic US practice. Nor does giving 4.5-9g of magnesium over 30 minutes.  Then the authors sneak this one in:

In a secondary analysis including only patients receiving beta blockers and calcium channel blockers, the obtained results were not significantly different compared to those found in the overall group.

This is sandwiched between mentions of adverse drug reactions (4% flushing in the 4.5g arm vs 12% in the 9g arm vs <1% in the placebo arm, and otherwise there was no significant difference between the 3 arms), and the discussion of 24h rate control. I am not 100% certain what they meant by this statement – were they referring to ADRs? Were they implying that there was no difference between metoprolol and diltiazem treated patients and placebo at 24 hours?  With only about 50% of patients per arm (~75 patients in total/arm) being treated with these agents, it would be hard to show a meaningful improvement.  Not to mention the fact that the actual data for this secondary analysis is nowhere to be found in this paper.  Nor have the authors responded to my email asking for it.

Then, of course, there are the prior trials with less than 60 patients / arm comparing diltiazem to metoprolol showing >90% efficacy with diltiazem.

And, of course, there is the next question, of are we doing any good?  Since rate control has not always shown to be in the patients best interest – a 6 fold higher rate of adverse events– and none of the ED AFib RVR magnesium studies look further out than 24 hours, perhaps we should cautiously, if at all, recommend magnesium, or even suggest waiting until long term outcomes are further elucidated.  Since this study took 5 years to complete, I do not see the desired study happening anytime soon.


HEART score predicts adverse events for no risk chest pain patients – for a whole 66 patients.

There has been some buzz about one particular HEART score paper on SoMe recently, and while touting the HEART score is all the rage, the excitement over a whopping 66 patients seems downright silly.

This study screened about 5000 patients and excluded roughly 4700 patients – without obvious good reason – as “inclusion criteria were satisfied if the provider ordered an ECG and troponin for the evaluation of ACS. Consistent with prior studies, patients were excluded for the following reasons: new ST -segment elevation > 1mm, hypotension, life expectancy <1 year, a non -cardiac medical, surgical, or psychiatric illness determined by the provider to require admission, prior enrollment, non -English speaking, and incapacity or unwillingness to consent.” Seems like most would be included then, right? Except that was not the case at all. I just do not see how >90% of patients could be excluded based on these criteria, in a study done in the United States.

So we are led to believe that this tertiary care center, which has >100,000 annual ED visits, somehow could only scrounge 282 patients with chest pain to recruit into this study. They randomized 1:1 into the HEART “pathway” (HEART score plus serial troponins – more on this later), with usual care per ACC/AHA guidelines – admit/obs, serial troponins, and provocative testing in consultation with cardiology. They assessed adverse events (MI, revascularization, cardiac death), objective testing (stress or angiography), and future hospitalizations / ED visits within the year.

While yes, all sixty-six patients with a HEART score of 3 or less and 2 negative troponins (yep, a whole 66 no/low risk patients at a 100k + visit ED), did have zero adverse events at 1 year, the question really is, who cares? This is not enough patients to be excited about, and besides, these are essentially no-risk chest pain patients that shouldnt have a high risk of adverse events anyway. They represent a group whom we should not be doing additional testing on anyway!

As for all the others, there was no change in adverse events between HEART vs usual care- about 10% of patients had adverse events in each arm. As such, I dont read this as the HEART pathway being awesome at reducing long term issues, but rather, more of the futility of advanced testing aimed at reducing adverse events; The HEART score is merely equivocal to our current tools at future risk stratification. While this is good, I doubt it will result in fewer downstream tests in “higher risk” patients, if only because old habits die hard, Americans like to do more, and ACC/AHA recommend doing so. Choose wisely, perhaps?

Laughably, the authors open their paper with this line: “Care patterns for the evaluation of Emergency Department (ED) patients with possible acute coronary syndrome (ACS) in the United States are heterogeneous, inefficient, and costly.” And yet, where did we get this “HEART pathway” from? The HEART score did not have two troponins. To boot, neither did the largest study published looking at the HEART score. So what does a second troponin get you? Well, if you believe this study of over 45,000 patients, in which *all* comers had 2 troponins and 2 ekgs, [patients only excluded if abnormal vital signs were present & defined as hypotension (systolic blood pressure <100 mm Hg), tachycardia (pulse >100 beats/min), tachypnea (respiratory rate >20 breaths/min), or hypoxemia (oxygen saturation level <95%), or if they had electrocardiographic ischemia, a left bundle branch block, or a paced rhythm], they only identified a primary end point event in 4 of 7266 patients, 2 of which were noncardiac and 2 of which were possibly iatrogenic.

So, I again ask, where did the two troponin issue come from? Well, here it is- in one singular study, not doing a second troponin would have missed 5 adverse events out of 899 patients. Because the total event rate was 12, the authors state that their sensitivity went from 58% to 100%. While this sounds nice, it can also be reframed as a 1.33% miss rate vs 0.78% miss rate – an overall improvement of…. 0.55% with a second troponin. And, this has not really been replicated to demonstrate the value of a second troponin. So, either use the HEART score as it was meant, or use two troponins and gestalt- both probably get you into trouble and add waste to the system and you reach the point of minimal gains. You’re testing 200 plus patients to find one more bumped troponin that may or may not get a meaningful intervention.

So I ask hospital administrators and EM & cardiology colleagues: is it worth the extra 4+ hours (3 hours for the second troponin, plus time for the draw to occur and test to get processed & resulted), plus all of the associated resources & space not allotted to other patients due to these 4+ hours that are given to thousands of patients annually… is a decrease of 0.55% worth a second troponin? I imagine if time and bed space was allocated to others, the 0.55% increase of adverse events would be more than made up for across the rest of the patients within the department by earlier recognition and treatment of just about every other disease entity within the department.  Sounds like, at a minimum, a time to introduce shared decision making (“hey, we catch one in two hundred with a second troponin, want to stay another 4 hours? and no, you can not go outside and smoke.  How about a nicotine patch and a tuna sandwich?”).

And lastly, no, you can not say the HEART score results in low risk of 1 year adverse events based on a single center study that failed to enroll more than 66 patients.

Cardiology, Improving Outcomes

Rising Risk Factors for CVD

This study looks at, a, um, rising star among cardiovascular risk factors:  erectile dysfunction.  ED and cardiovascular disease share many common risk factors (diabetes, smoking, obesity, etc), and prior studies have shown ED patients to have increased subclinical vascular disease such as increased coronary calcium scores, increased carotid plaque scores, etc.

Utilizing the MESA study, the authors followed ~1750 participants for 3.8 years on average, evaluating for cardiovascular disease (AMI, stroke, cardiac arrest, death) and coronary heart disease. Patients self-reported ED via the Massachusetts Male Aging Study.  Obviously this study is plagued by self-assessments which may or may not accurate, a composite endpoint, and is based on prior studies demonstrating the worsening surrogate markers; the authors do not tease out individual AMI, stroke or death risk from the composite endpoints either.

Ultimately, ED patients had more adverse cardiovascular events (6.3% versus 2.6%), resulting in an unadjusted hazard ratio of 2.6 and the risk persisted even after adjustment for traditional CVD risk factors, depression, and beta-blocker use.  Think of ED as an early warning sign of endothelial dysfunction, inflammation, and possibility, atherosclerosis.  ED is already in some UK risk stratification scores, will it make it to the US?


Cardiology, Improving Outcomes, Mythbusting

SVT: treat, wait, re-evaluate

What do you *really* need to do with your SVT patients? Well, this is a retrospective observational study of 633 consecutive SVT patients over 10 years seen in a single ED. This was more hypothesis generating than anything – they basically provide patient characteristics and try to tease out if labs / imaging were necessary.

Their mean age was 55, 62% of patients were female, 55% had prior SVT history, 31% had at least one cardiovascular risk factors (dyslipidemia, hypertension, diabetes, CHF, or vascular disease), and 9% had ischemic heart disease.

Some interesting lab nuggets:

-0.4% had a hemoglobin < 8g/L

-1.5% had a sodium >150 mmol/L, none <126

-no patient with severe hyperthyroidism

Chest Xray was obtained 30% of the time, and while it was abnormal 21.6% of the time (41 of 190), none of the time did it alter ED treatment – despite showing 14 cases of pulmonary edema, 4 cases of pneumonia, and 3 pleural effusions.

The authors conclude that patients with uncomplicated SVT are over-investigated, and that most have normal or near-normal results. While I tend to agree – for the 25 year old in SVT without a concerning story – the 55 year old diaphoretic (14% were diaphoretic) female with ischemic heart disease I’m going to work up. Chest films were only ordered on 30% of these patients – frankly in a US hospital, I’m thankful its not higher.

I know Billy Mallon loves his TSH, but why not get a better history to see if there are other concerning symptoms before sending off TSH… Speaking of which, maybe we could decrease those Chest films if we fixed the patient a bit, then reassessed to see if imaging is wanted. (ie, are you still short of breath?).

Finally, I think this study is plagued by premature closure, as they only searched for cases with a discharge diagnosis of paroxysmal supraventricular tachycardia. They’re likely missing at least a few patients who came in with SVT and were found to have actually have another diagnosis.

Ultimately, while this study should not change practice by any means, it should give us pause before shotgunning labs & chest films until after we treat the patient, re-evaluate, and get a better history. This could probably be said for many other diagnoses besides SVT.


Dedicated post-arrest services? meh.

Should we regionalize post-arrest care?  Well, if your facility does not have a cath lab, then the answer is yes.  But Academic Hospital A, which sees >100 arrests a year, just started advertising a fancy post-cardiac-arrest service.  Academic Hospital B also sees >100 arrests a year, but does not have a post-arrest service aside from their MICU.

You, being at hospital C without a cath lab, have just achieved ROSC in a witnessed arrest. Who do you transfer to?

This study looks at 987 post-arrest patients that survived to admission at 7 hospitals in and around Southwestern Pennsylvania. One of them is a regional referral center with post cardiac arrest services consulted on OHCA with ROSC, accepts sudden cardiac arrests from outside facilities, and is consulted on in-hospital arrests with ROSC. There are two additional tertiary care centers that see >100 SCA annually, and 4 “low volume” centers. They look at multiple variables, and evaluate discharge disposition, discharge CPC, and length of survival post-discharge.

They improved numbers of discharge CPC – the post arrest service center with a discharge CPC of 1 or 2 32% of the time vs 37% of the time for the other 6 facilities. More patients were discharged to home (41% vs 32%) from the post-arrest service center and survived for longer if they were treated with the post-arrest service.


While the authors claim similar patient characteristics between the post-arrest service center and the other 6 hospitals…. 46% of patients were transferred to the post-arrest service center vs 16% at hospitals 2-7 – perhaps skimming a healthier patient that made it through the transfer (remember- you had to survive to discharge to be counted) – the authors even acknowledge that their transferred patients did better than their other arrests.

Add in that the initial rhythm 51% of the time was VT/VF for the post-arrest service center vs 41% in the other six hospitals, and you’ve got plenty of confounders. Frankly, given all of this, it’s a bit strange that the proportion of patients surviving to discharge did not differ at all. One would think if you have a post arrest service and the scales are tipped in your favor to begin with, that you’d have a higher percentage of patients surviving.

Ultimately, patients lived longer post-arrest when treated at a facility with a post-arrest service, and the authors are touting this as reason to (further) regionalize post-arrest care.  Sure, there are slightly better neurologic outcomes, but the scales were tipped in their favor to begin with. I don’t trust this conclusion, especially when the post-arrest service had an advantageous patient population to begin with that should have led to a measurable increase in improved survival, in addition to an increase in length of survival.

Cardiology, Cardiology, Critical Care, Improving Outcomes, Improving Throughput, Mythbusting, Pulmonary, Radiology, Radiology

Probing the dyspneic patient.

For undifferentiated dyspnea, how would you like to have an accurate diagnosis in 24 minutes?

I love this study.

Basically, for all dyspneic patients (not trauma related, and over age 18), 10 EP’s were given an H&P, vital signs, and an EKG, as well as access to a Chest X-Ray, Chest CT, cardiologist performed echo, and labs including an ABG.

These same 2,683 patients, in tandem, had point of care ultrasound testing (lung, IVC, echo). Here’s the catch – the ultrasonographers were only provided the H&P, vital signs, and EKG then asked to make a diagnosis. The treating provider was blinded to POCUS diagnosis.

These numbers for diagnostic accuracy of POCUS are astounding.

+LR for acute HF? 22 (-LR 0.12)

+LR for ACS? 105 !!!

+LR for pneumonia? 10.5 (-LR 0.13)

+LR for pleural effusion? 95 (-LR 0.23)

+LR for pericardial effusion? 325!!! (-LR 0.14)

+LR for COPD/asthma? 22 (-LR 0.14)

+LR for PE? 345!!!

+LR for pneumothorax? 4635!!! (-LR 0.12)

+LR for ARDS? 90

Yes, for certain things like pneumonia, the difference in p-values between tradition means and POCUS diagnosis was not significantly different, but what about volume status? I cant imagine blindly giving 30 cc/kg would benefit the patient with a plethoric IVC and pleural effusion. There is some elegance a play here.

Additionally, sure, ED diagnosis for ACS had a higher LR, but they also had a cardiologist performing and interpreting echos in the ED (a rather rare siting in a US ED I would imagine) – without much improvement in their -LR (0.53 vs 0.48). For PE, the -LR of POCUS was predictably mediocre if not outright bad (0.6), while the -LR for ED diagnosis of PE, with the benefit of chest CT, was -0.10.

Now look, I get that these EP’s were quite sono-savvy. They all had 2+ years of experience, over 80 hours of ultrasound lessons & training, with at least 150 lung and 150 ED echo’s under their belt. The diagnosis was made in 24 minutes with POCUS in comparison to 186 minutes for traditional means. And while most of us can not do a year+ ultrasound fellowship, and neither can we all be as savvy with the probe as these authors (or Matt, Mike, Jacob, Resa, Laleh, etc) – it does not mean we shouldnt try. You can still greatly increase your yield just by practicing. To boot, the cognitive offload you experience by saving yourself a few hours by (correctly!) knowing which direction you are heading with a patient is an immense boon to both your mental heath & your patients well being.

Cardiology, Improving Outcomes, Improving Throughput

A chicken in every pot, and a cardiologist in every box.

I think the HEART score is useful, and an incredible start to getting everyone on the same page. Getting both an ED and consultant group to universally agree on a protocol, and implement observation / admission protocols off of it are probably a bit more difficult.

And this is only with a few “soft” variables– what exactly differentiates slightly from moderately suspicious anyway? As we all know, stories change (and not just from patients!).

This paper retrospectively looked at 6 months worth of ED chest pain charts which had a cardiology consult and tries to extract a HEART score based off the ED documentation as well as the cardiology consultation.

Unfortunately the retrospective nature and lack of a standardized “flow sheet” for history probably greatly contributes to cardiology/EP disagreement in the HEART score (like, say, documenting tobacco usage in the chart). History between EP and cardiology was in agreement 47% of the time, EKG interpretation agreement at 76%, and risk factor agreement at 85%. Overall HEART score agreement between EP’s and cardiology occurred 70% of the time, primarily with some mixture of cardiology consistently downplaying elements and/or EP’s upselling some.

Of those who had a phone consultation with cardiology, only 5.4% were discharged, vs 45% discharged when physically seen by cardiology. Only 9% were admitted after in-person cardiology evaluation vs 77% for those with phone consultation. Of those who received further testing, 45% of the cardiology phone consultations were discharged, vs 87% discharge rate for those who received additional testing after an in-person cardiology consultation…. Seems like cardiology is scared to discharge without seeing the patient, and that we are probably upselling the patient a bit.

Regardless, this is hypothesis generating at best, particularly with such low numbers to evaluate (33 patients evaluated by cardiology and EP’s over this 3 month period!), and frankly, the retrospective data extraction without a clear checklist for HEART scores makes me question the validity of their conclusions. Nonetheless, I hold hope that cardiology and EM can live in harmony at some point in the future.