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.

Improving Outcomes, Mythbusting, Pulmonary

Sono-guided ACLS

This study demonstrates what many of us have probably suspected – the absence of cardiac activity on ultrasound portends a grave diagnosis; but this study really is so much more.

Utilizing 20 sites across the US and Canada from May 2011-Nov 2014 looked at all nontraumatic in-ED and out of hospital cardiac arrests that arrived to the ED in either PEA or asystole, and whether or not POCUS demonstrated a potential role in resuscitation.

953 patients, 793 used for final analysis (106 not included due to resuscitation under 5 minutes, 8 patients DNR, 1 uninterpretable sono, 3 with incomplete timing data, 42 for no ACLS meds given) – had a cardiac sono at the “beginning and end of ACLS.” The primary outcome was percentage of patients that survived to hospital admission, with secondary outcomes of survival to discharge and ROSC. Unfortunately, neurologic intact survival was not evaluated. The treating EP’s were credentialed in POCUS at their local institutions and unblinded. Digital clips were reviewed by a single reviewer in a blinded fashion for agreement (which was deemed to be “substantial agreement”).

The data (numbers are percentage, such that “28.9” = the percentage of patients with cardiac activity on POCUS during the resuscitation who survived to admission):



Cutting to the chase, this study brings up a number of key points:

-PEA on the monitor may not necessarily be PEA, with a whopping 54% of patients having cardiac activity on POCUS

-asystole on the monitor may not be cardiac standstill, as 10% had cardiac activity on POCUS

– survival to admission with cardiac activity on POCUS is MUCH higher – 28.9% vs 7.2%, but….

– cardiac activity on POCUS for PEA/asystole portends only a 3.8% survival to discharge

-no cardiac activity = poor prognosis, 0.6% of patients survived (3 out of 530). With two of the three patients were Vfib at some point during EMS working on them.

-pericardial effusion was seen in 34 patients (4.3% of those in the final analysis). 15.3% of patients whom had a pericardiocentesis performed survived to discharge.

– only 15 patients received lytics for suspected PE, with only one (6.7%) surviving to discharge. (which was almost the MORTALITY rate of PEAPETT)


Whew. This is a lot to digest. Let’s just say that ultrasound helps you tease out a spectrum of disease and further characterizes what you are dealing with. I’m looking at POCUS in codes as a risk stratification tool. Is there a prolonged time without cardiac activity without a potentially reversible causes? Might want to consider calling it earlier since survival to discharge is abysmally low. And sheesh… 1 out of 25 cardiac arrests had a pericardial effusion??? Wow. Time to brush up on those pericardiocentesis skills.

Caveats- this was done by EP’s credentialed for POCUS, so they’re likely more talented than the rest of us.  Dont let that scare you though, rather, this.  Perhaps seeing cardiac movement on ultrasound lends a “bridge to hope” and the team puts in a more-heroic-than-usual effort.

And of course, this also leads to more questions- of those 28.9% with cardiac activity that survive to admission, what if they are brought straight to the cath lab? Or started on ECMO? Would this potentially alter survival rates and neurologically intact survival in meaningful ways? Time shall tell.  Until then, cut that KT window, pick up the probe, and have your TPA & long pericardiocentesis needle ready.

Cardiology, Improving Outcomes, Mythbusting, Neurology

Chronic viral infection & Coronary disease.

Are you openly ignoring a cardiac risk factor that is in the ballpark of smoking or early family history?   Even after controlling for numerous factors, well controlled HIV has a significantly higher cardiovascular MORTALITY rate – with an adjusted rate ratio of 1.53, while poorly controlled patients even moreso, with an adjusted rate ratio of 3.53, according to this paper.  It should be noted that this is one of several papers looking into HIV as a risk factor for early cardiac disease and death.

It is important to realize the limitations of our tools that we have at our disposal.  For instance, PERC and HEART are not validated in an HIV population.

I suspect many if not all chronic viral infections will portray a similar trend. It is already seen in HepC, albeit to a lesser extent. It will be interesting to see if the new age HepC drugs decrease the known risk of increased coronary artery disease and cerebrovascular disease after treatment.

Cardiology, Critical Care, Improving Outcomes

Brady arrest? Go Full Bore.

Do you believe in full bore medicine?

(hat tip to SMACCdub for that line)

This paper puts those thoughts under the microscope a bit, and challenges us to think ahead and be prepared.

They looked at all OHCA from 2006 to 2012 with initial brady/asystolic arrests to determine if they may benefit from pre-hospital pacing, and to look at survival rates associated with various rhythms. Clear non-cardiac causes (trauma, drowning, respiratory, neurologic, suicide) were excluded.

7925 OHCA in the Netherlands

less non-cardiac (6681 patients)

less those without EKGs (~500 patients)

less ~3000 patients with VF/VT (now at 2643 patients)

less those with normo/tachycardia and those with pacers previously placed (~300 patients)


This leaves us with 2333 brady/asystolic (idioventricular, junctional, sinus brady, 3rd degree with/without escape, asystole) patients – or, about 30% of their OHCA.

Unwitnessed arrest still protends a poor outcome, with survival about 0.5%. However, for witnessed arrests, they report 4% survival for idioventricular / junctional arrests and 6.8% for sinus brady arrests. This seems consistent with prior studies. However, for a study trying to determine whether or not pacing is beneficial, their pace rates were quite low. They paced 11 of 220 sinus brady patients and 41 of 452 idioventricular / junctional patients, with a delay of 30.1 and 16.5 minutes to pacing respectively – with an electrical capture rate of 55% and 70% to boot.  Esssentially, they can’t answer the question “Does pacing help” with such a care gap.

So, why is this? For sinus brady, maybe patients are hanging in the 40’s-50’s and felt to be quasi-stable. Maybe its the angst of floating a pacer. Perhaps the lengthy delay for sinus brady is giving atropine, then giving it again… and maybe again- akin to pressor-angst for sepsis (giving a 4th, 5th, and 6th liter rather than starting pressors or a central line).  I imagine there is a mental barrier – whether it be not thinking about pacing or passing the buck (“I’ll let the ICU figure it out.”). The evolution of the ED-ICU model (and perhaps UPMC’s cardiac arrest unit) may be the best place to look at this type of “full bore” medicine and whether or not it would be beneficial.

But for now, there is a large gap in care. Bradycardic arrests represent about 10% of arrests, have a reasonable survival rate, and are (potentially) suboptimally managed – and you have the tools to potentially improve an outcome.  We can not say whether or not pacing is futile care for this condition.

Until then, go full bore. Your patients & their families deserve it until pacing is demonstrably shown to not be beneficial in bradycardic arrests.